COURSE PRICE: $35.00
CONTACT HOURS: 5
This program has been pre-approved by The Commission for Case Manager Certification to provide continuing education credit to CCM® board certified case managers.
Wild Iris Medical Education, Inc. is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.
Course Availability: Expires February 2, 2016. You must score 70% or better on the test and complete the course evaluation to earn a certificate of completion for this CE activity. Wild Iris Medical Education, Inc. provides educational activities that are free from bias. The information provided in this course is to be used for educational purposes only. It is not intended as a substitute for professional health care. Medical Disclaimer Legal Disclaimer Disclosures
Copyright © 2013 Wild Iris Medical Education, Inc. All Rights Reserved.
COURSE OBJECTIVE: The purpose of this course is to help healthcare professionals understand the causes of and the current treatments for chronic obstructive pulmonary disease (COPD).
Upon completion of this course, you will be able to:
Chronic obstructive pulmonary disease (COPD) is a condition that makes it difficult to move air into and out of a person’s lungs. Difficulty moving air in the lungs is called “airflow obstruction” or “airflow resistance.” COPD is characterized by a progressively increasing airflow obstruction that cannot be fully reversed, although it can sometimes be temporarily improved by medications. In almost all cases, COPD has been caused by the long-term inhalation of pollutants, especially cigarette smoke (Punturieri et al., 2009; Barnett, 2012a).
The specific form that COPD takes can range along a spectrum. At one end of the spectrum, people get emphysema, the destruction of small respiratory units (alveoli and respiratory bronchioles) and the formation of large, useless air spaces in the lung. At the other end of the spectrum, people get chronic bronchitis, narrowed inflamed airways filled with mucus, accompanied by a chronic, phlegmy cough. Many people with COPD have a mix of both emphysema and chronic bronchitis.
Regardless of its form, COPD causes dyspnea (difficulty breathing). The dyspnea of COPD feels like shortness of breath. Initially, shortness of breath occurs only during vigorous exercise. Subsequently, the dyspnea begins to happen with mild exercise. Eventually, normal activities of daily living (ADLs) cause dyspnea. Finally, a person with COPD is short of breath even when at rest. This relentless increase of dyspnea gradually limits a person’s activities, and at some point it becomes hard for a person with COPD to do anything but sit or lie down (Barnett, 2012a).
Patients with COPD have little or no reserve capacity in their lungs and they can be living on the verge of hypoxemia. Respiratory infections, increases in inhaled pollution, and the occurrence of other medical problems will further reduce their ability to absorb oxygen and to expel carbon dioxide. These problems can send COPD patients into hypoxemia. Such stresses are unavoidable, so COPD patients suffer repeated episodes of significantly worsened symptoms called “acute exacerbations.” Acute exacerbations resolve slowly over weeks or months even with medical treatment, and sometimes acute exacerbations must be managed in a hospital.
After COPD has become symptomatic, the disease is treated with bronchodilators, which can ease the patient’s dyspnea so that a wider range of activities remains tolerable. However, COPD follows a relentless downward course. Supplemental oxygen therapy can prolong some patients’ lives, and a few select patients can benefit temporarily from lung surgery. Acute exacerbations continue for all patients, and most patients eventually succumb to an acute exacerbation that cannot be reversed (Barnett, 2012b).
The specific form that COPD takes varies from person to person. The predominant forms of COPD are emphysema (destruction of alveoli) and chronic bronchitis (inflammation of the conducting air tubules).
For some people, COPD causes significant destruction of the terminal airways and air sacs (alveoli). This form of COPD is called emphysema. In emphysema, the overall architecture of the lung is altered dramatically, and the lung becomes honeycombed with useless spaces. These air spaces are created when the walls of the small respiratory airways and their alveoli are torn, allowing neighboring airways and alveoli to merge. In the process, the surrounding capillaries become damaged and the new larger air spaces become useless for gas exchange. Another characteristic of emphysema is decreased elasticity of lung tissue. Besides reducing the lung area available for gas exchange, emphysema leads to hyperinflated lungs and obstructed airflow (Ignatavicius & Workman, 2010).
The other main type of COPD involves inflamed airways that become clogged with mucus. Patients with this variant of COPD develop a chronic cough that brings up sputum. This manifestation of COPD is a form of chronic bronchitis, which is defined as a persistent mucus-filled cough that has occurred frequently for at least two years and that is not caused by another disease such as an infection, cancer, or congestive heart failure. It is characterized by an increase in the number and the size of mucus glands in the airways of the lung.
Chronic bronchitis can occur without COPD. More than one third of smokers have chronic bronchitis, but the disorder is only considered a form of COPD when there is also significant obstruction to airflow within the lungs (Kamanger et al., 2009).
In the past, COPD patients with emphysema were said to have type A COPD and were sometimes called “pink puffers.” COPD patients with chronic bronchitis were said to have type B COPD and were sometimes called “blue bloaters.”
Although these names are still used, the division of COPD into two alternative types is too simple because many patients have a mix of emphysema and chronic bronchitis. Currently, the emphasis is on the common feature of all COPD patients: airflow obstruction. Whether it appears as emphysema, as chronic bronchitis, or as a mixture of the two, COPD is characterized by chronic, worsening, and irreversible airflow obstruction.
COPD can be almost entirely prevented by avoiding long-term inhalation of pollutants, mainly cigarette smoke. As they age, all people suffer a decline in their lung functions. Smokers who quit before developing symptoms of COPD can often reduce the decline in their lung functions to nearly normal levels within a few years of remaining smoke free (ALA, 2012a).
COPD is the most common serious lung disease in the United States. Over the last few decades, there has been an increase in the percentage of Americans with COPD. Currently, 13.1 million adults in the United States have a diagnosis of COPD, and an equal number of Americans with COPD may still be undiagnosed. Among people with COPD, significantly more have the chronic bronchitis form than the emphysematous form (ALA, 2011).
Over 85% of the people who get COPD have been long-time smokers (Bišanović, 2012). Therefore, the characteristics of the population of people with COPD are the same as the characteristics of the population of people who have been long-time smokers.
A person’s smoking intensity is measured in pack-years. “One pack-year” means that a person has smoked approximately 1 pack (20 cigarettes) per day for 1 year. Smoking 1/2 pack a day for 1 year is equivalent to 1/2 pack-year, and smoking 2 packs a day for 10 years is equivalent to 20 pack-years.
COPD is most common in older people because symptomatic COPD usually takes more than 20 pack-years of smoking to develop. The typical COPD patient has a smoking history of more than 40 pack-years. Today, 21% of adult Americans are smokers, and 1 of 5 high school students has smoked in the last month (CDC, 2011).
In the United States, 5.1% (11.8 million) of adults aged 18 and over have COPD—a rate that was stable from 1998 through 2009. COPD prevalence was highest among women aged 65–74 (10.4%) and 75–84 (9.7%) and among men aged 75–84 (11.2%). The current generation of older adults has done a record-breaking amount of cigarette smoking. Although many elderly Americans have stopped smoking, even those who quit can develop symptoms of COPD and suffer a greater-than-normal decline in their breathing ability late in life (CDC, 2011).
COPD occurrence is higher among women in all age groups except the two highest age groups (75–84 and 85 and over), for which the difference was not statistically significant (CDC, 2011). The increased level of smoking by women over the past 30 years is causing the women’s death rate from COPD to rise. Today, more American women than men die from COPD, and more than 170,000 women die each year from smoking-related diseases (ALA, 2010). Women were diagnosed with COPD with lower pack-years, fewer comorbidities, and less bronchial obstruction, but worse diffusion capacity impairment (Laitenen, 2009).
The prevalence of COPD follows the history of the level of smoking in a population. In the United States, higher rates of COPD are found among those who have had the highest levels of smoking: white people, blue-collar workers, and people with less formal education. More Caucasians in the United States die from COPD than people of other races (CDC, 2009b).
COPD is the fourth leading cause of death in the United States (ALA, 2010). Approximately one half of COPD patients die within 10 years of their initial diagnosis (ALA, 2011).
COPD is a reactive disease: it is a disease in which the body is turned against itself. In COPD, the body’s reaction to inhaled pollutants (mainly smoke) results in chronic inflammation of the bronchial tree. Inflammation is a natural protective reaction, but it is useless against air pollutants. Instead of helping, the persistent inflammatory reactions damage the lungs.
Before exploring the details of COPD’s inflammatory damage, here is a review of the structure and function of normal lungs.
The two lungs comprise millions of microscopic alveoli clustered at the ends of tiny air tubes. The lung tubes begin at the trachea and branch into successively narrower, shorter, and more numerous tubules. The central tubes are the bronchi and bronchioles. The most peripheral tubes are the respiratory bronchioles, which are lined with alveoli. It is through the walls of the alveoli that gases are exchanged between the inspired air and the blood in the surrounding capillaries.
Figure A: Locations of the respiratory structures in the body.
Figure B: Enlarged image of airways, alveoli, and their capillaries.
Figure C: Location of gas exchange between the capillaries and alveoli.
(Source: National Institutes of Health.)
The medium and large bronchi are wrapped with smooth muscle, which tightens to narrow the airways and relaxes to widen the airways. The walls of all the airways are lined by ciliated epithelial cells with interspersed secretory cells, which coat the inner walls of the airways with mucus. All the cilia of the epithelial cells beat in the direction of the trachea and throat, so mucus and trapped particles are continuously moved up and out of the lungs.
Healthy lungs are lightweight, soft, spongy, and elastic. Normally, the chest walls stretch the lungs and keep them expanded to three times their relaxed size. When the chest is surgically opened, however, the lungs recoil, as the innate elasticity of the lungs pulls them back to their resting size.
When an adult takes a full breath, the volume of air in the lungs is about six liters. During life, the lung is never completely airless: even after a complete exhalation, there are about 2.5 liters of air left (Albertine et al., 2005).
Lungs are the organs through which oxygen is absorbed into and carbon dioxide is expelled from the bloodstream. These gas exchanges occur through the walls of the alveoli and the terminal respiratory airways, which make up the distal-most air spaces inside the lungs.
Maintaining healthy levels of blood gases are the lungs’ primary function, and the lungs contain an extensive capillary system to provide more than the necessary surface for gas exchange. The lung tissue itself is very thin and delicate, and most of the volume inside a normal lung is taken up by air. Since lung tissue is thin and air is light, most of the weight of a lung can be attributed to the blood circulating in it.
People with healthy lungs rarely use all the gas-exchange potential of their lungs. During the most strenuous activity, a healthy person will use only 60% to 70% of their maximal ventilatory capacity. Strenuous exercise does cause temporary dyspnea (shortness of breath), but the 30% to 40% ventilatory reserve quickly relieves the dyspnea of a healthy person after a short rest. Even the dyspnea caused by strenuous exercise in a healthy person is not as debilitating as the dyspnea in a person with severe COPD.
Healthy lungs function less efficiently as they age. As people get older their chest walls stiffen and their respiratory muscles weaken. Both changes make breathing almost twice as much work for a 70-year-old as for a 20-year-old. The forced vital capacity (VC or FVC) and the amount of air that can be exhaled in a second (1-second forced expiratory volume, or FEV1) gradually and progressively decline during a person’s lifetime. In a healthy person, none of these natural lung changes approaches the dramatic declines caused by COPD. The natural decline in lung function worsens the already compromised breathing of those elderly people who have COPD (Barnett, 2012a).
COPD slowly destroys the lung and makes it increasingly difficult for a patient to breathe. The most serious effect of COPD is a progressive obstruction of airflow.
In COPD the airways leading into the alveoli become narrowed and less flexible and they are often clogged with mucus. Eventually, many alveoli coalesce into larger, useless airspaces because the walls separating the alveoli become damaged or destroyed.
Upper right: Healthy alveoli.
Lower right: Alveoli with COPD.
(Source: National Institutes of Health.)
Smoke inhalation, sometimes compounded by certain genetic factors, is the primary cause of COPD.
In the industrialized world, cigarette smoking is the main cause of COPD. In underdeveloped countries, smoke from plant products that are burned for indoor cooking or heating is as much a cause of COPD as is cigarette smoking. Other causes of or contributors to COPD include air pollution, second-hand smoke, and occupational exposure to dust and chemicals (ALA, 2009; Engelke, 2012).
In the United States, chronic lung disease accounts for 73% of smoking-related conditions. Even among smokers who have quit, chronic lung disease accounts for 50% of smoking-related conditions (ALA, 2012a). Other smoking-related diseases or conditions include amputations from Buerger’s disease, throat cancer, stroke, heart attack, and asthma (ALA, 2012c). The longer and more intensely people smoke, the more likely they are to develop COPD.
Many long-term smokers eventually develop COPD, but the severity of the disease varies from person to person, even among heavy smokers. People living in the same environment and smoking the same amount can differ in their propensity for developing COPD. Two factors have been suggested as the basis for this difference: airway sensitivity and other specific genetic factors (Swadron & Mandavia, 2009).
Cigarette smoking causes COPD by inciting a chronic inflammatory response to the pollutants in the smoke. Eventually, this persistent inflammation is caused by the release of proteases in the lungs that lead to destruction of lung tissue, accumulation of mucus, and thickening of small airways. Smoke also flattens the cilia in the airways and prevents them from removing mucus and fluid (Ignatavicius & Workman, 2010).
In COPD, inflammation begins with the activation of local macrophages in the lung tissue. The gradual and progressive accumulation of macrophages throughout the lungs is a characteristic feature of COPD. Activated macrophages also attract neutrophils (polymorphonuclear leukocytes) from the bloodstream. The greater the number of neutrophils that invade the lung tissue, the faster lung function declines.
When responding to irritants, both macrophages and neutrophils secrete proteases. Normally, the destructive action of proteases is held in check by a sufficient concentration of antiproteases, such as alpha1-antitrypsin (AAT), which circulate in the bloodstream and which are also released by neighboring epithelial cells. Antiproteases limit the damage that short-term inflammation inflicts on local tissues (Ignatavicius & Workman, 2010).
In COPD, there is an imbalance between proteases and antiproteases. Cigarette smoke is a strong and continuous stimulant of inflammation, and in the lungs of a chronic smoker proteases are constantly being released. Meanwhile, the normal protective function of the local antiproteases is hampered because smoke in the lungs leads to an accumulation of free radicals, superoxide anions, and hydrogen peroxide, all of which reduce the effectiveness of antiproteases.
The resulting imbalance of proteases and antiproteases frees at least some of the proteases to damage local tissues by degrading elastin and other structural molecules in the walls of the airways and the alveoli. At first, holes appear in the walls, and later the weakened walls are ripped apart by the force of breathing. Alveoli, which were formerly small chambers with capillary-coated walls, merge into large wall-less air spaces. When these spaces become >1 cm in diameter, they are called “bullae,” and a lung filled with bullae is said to be emphysematous.
The progressive destruction of lung tissue leads to the emphysematous form of COPD, which is characterized by:
People differ in their airway sensitivities, that is, in how readily their airways constrict when exposed to a variety of irritants such as pollen, dust, and chemicals. Asthma is the most common disease of people who have abnormally sensitive airways. People with COPD also tend to have sensitive and reactive airways. Although asthma and COPD are different diseases, smokers with asthma or with the tendency to develop asthma are more likely to develop COPD and are more likely to have COPD that worsens quickly (Ignatavicius & Workman, 2010).
Besides airway sensitivity, certain families carry other genetic factors that make them especially susceptible to developing COPD. One of these genetic propensities is alpha1-antitrypsin (AAT) deficiency. AAT is a protein that slows or stops the action of elastase. Elastase is an inflammatory enzyme that chews up elastin, an extracellular protein used to build supporting tissues. The gene for AAT is recessive. Therefore, someone with one normal and one faulty allele for the deficiency would be a carrier but not more susceptible to COPD. According to the American Association for Clinical Chemistry (2012), the deficiency is diagnosed by a blood level of the protein or ATT phenotype, or genetic testing.
An inflammatory reaction in the lung, such as is caused by COPD, produces elastase. Normally, AAT circulating in the blood reduces the damage done by inflammatory elastase. However, a person with an AAT deficiency has little or no protection against inflammatory elastase. AAT deficiency allows the chronic inflammation caused by inhaled smoke to do considerable damage to the lungs; specifically, AAT deficiency fosters the destruction that causes emphysema.
Long-time smokers typically develop COPD when they are 50 to 60 years old. Smokers who are born with AAT deficiency, however, develop symptomatic COPD 10 to 20 years earlier, at an average age of 40 years. Elastase is so destructive that emphysema can even develop in nonsmokers if they have a severe AAT deficiency. In the United States, AAT deficiency is the primary cause of only 1% to 2% of cases of COPD because fewer than 1 in 3,000 people are born with severe AAT deficiency (Fairman & Malhotra, 2009).
The hallmark of COPD is the increased resistance it causes for airflow in the lungs. In the chronic bronchitis form of COPD, much of the airflow obstruction comes from a progressive thickening and stiffening of the small airways. The pathologic process underlying the narrowing of airways is fibrosis. With fibrosis, excess collagen accumulates in and around the airways, making them fatter and more rigid. Extra collagen is secreted as a natural repair response to tissue damage.
The chronic bronchitis form of COPD includes other changes in the small airways. These changes reduce airway volume still further. Specifically:
When inhaling, a person stretches his or her chest and lung tissues. During exhalation, the elastic recoil of the chest and lungs is a major contributor to the force that pushes air out of the lungs.
In COPD, fibrosis reduces lung elasticity. Therefore, a patient with COPD needs to replace the lost elastic force with extra muscular effort, and the extra effort must be sustained for a longer time. The narrowed airways in lungs with COPD carry smaller volumes of air, and people with COPD take longer to empty their lungs.
The extent of airway obstruction can be quantified for COPD patients. One standard assessment measures the patient’s 1-second forced expiratory volume (FEV1), the volume of air that can be pushed out of the lungs during the first second after a full inhalation. (See “Lung Function Tests” below.) A persistent, irreversible low FEV1 is the most characteristic objective finding in COPD.
In COPD, the difficulty of breathing is worsened by excessively expanded (hyperinflated) lungs. Most people with COPD have some degree of emphysema, and part of each breath flows into nonfunctioning spaces, where it is unusable. To get sufficient oxygen into their system, people with COPD need to take larger breaths.
People with COPD also take longer exhaling, and after taking a large breath, there is not enough time to fully exhale the air. Excess air remains in their lungs during each breathing cycle.
Wasted air space and excess residual air lead to hyperinflated lungs. Hyperinflated lungs change the shape of the chest and diaphragm, making the mechanics of breathing more difficult. With hyperinflated lungs, breathing can be exhausting.
Together, the obstructed airflow and the hyperinflated lungs of COPD make breathing hard work. When COPD is severe, just the breathing required for slow walking could use one third of the body’s total oxygen intake.
In COPD, patients may not have enough energy to pull in all the oxygen they need or to expel all the carbon dioxide they produce. Compounding the problem of maintaining adequate gas exchange, COPD destroys alveoli and the small capillaries that surround them, making each breath even less effective. As a result, people with severe COPD become chronically hypoxemic (too little circulating oxygen) and hypercapnic (too much circulating carbon dioxide). People with moderate COPD become hypoxemic during modest exercise, and as the disease worsens, they can become unable to exercise at all (Tarrega et al., 2011).
COPD also affects the blood vessels in the lung. COPD:
These changes increase the arterial resistance inside the lungs. More force is needed to push blood through the lungs, and the person develops pulmonary hypertension. In a normal adult lung, the mean pulmonary artery pressure is <16 mm Hg. In a lung with pulmonary hypertension, the mean pulmonary artery pressure is >20 mm Hg.
Pulmonary hypertension is especially hard on the right ventricle of the heart, which hypertrophies in response. As the strain on the right ventricle persists, the heart can fail. Heart failure secondary to lung problems is called “cor pulmonale,” and COPD is the leading cause of cor pulmonale (Weitzenblum & Chaouat, 2009).
Patients with COPD have problems with organ systems other than their lungs. COPD leads to chronic hypoxemia, it drains energy reserves, and it is a source of chronic inflammation. These problems cause total body muscle weakness and weight loss.
Chronic hypoxemia strains the heart and reduces the ability of the heart’s ventricles to respond to the demands of exercise.
Chronic inflammation initiates a generalized prothrombotic condition in the circulation. This makes blood clots more likely to form, and patients with COPD are at increased risk for developing myocardial infarctions, strokes, deep-vein thromboses (DVTs), and pulmonary emboli.
In addition, people with COPD have a high incidence of clinical depression. The depression is not only a psychological reaction to their increasingly restricted lifestyles. The metabolic and inflammatory changes of COPD make depression more likely biochemically.
Andy Portal is a 68-year-old retired construction worker with a 12-year history of COPD after a 35-pack-year history of smoking. He has not smoked in 9 years. He presents in the emergency department complaining of a sharp pain and redness at his posterior left calf, which is also hot and tender to the touch. The medical diagnosis of deep-vein thrombosis (DVT) is made by contrast venography. The nursing diagnosis is ineffective tissue perfusion: peripheral related to decreased venous circulation in the right leg.
When Andy’s wife asks, “What happens now?”, the nurse explains to them both that the goal is to prevent further clot formation and preventing the clot traveling as in pulmonary emboli. This is accomplished by anticoagulants, anti-embolitic stockings, and warm compresses. The nurse discusses the possible pharmacological treatments and side effects. When Andy’s wife asks, “Why did this happen?”, the nurse explains to them that COPD is one of the risk factors for DVT (Vesa et al., 2009).
Over the years, patients with COPD become less and less able to do even modest exercise without developing dyspnea. Dyspnea, the feeling of breathlessness, is a common symptom. It comes from a mix of three sensations:
Breathlessness is upsetting. It stops people from exercising, and it is the main reason that people with COPD limit their activities. Dyspnea with exercise gets worse as COPD progresses. Patients begin to spend all their time either sitting in a chair or lying in bed, and after months of inactivity, COPD patients become deconditioned as their muscles and circulatory system settle into sedentary states.
It is a spiraling problem: dyspnea causes lack of exercise, lack of exercise causes deconditioning, and deconditioning makes it harder to exercise. When they have become deconditioned, COPD patients get severe leg tiredness and leg discomfort when they try to exercise. Leg problems become yet another limiting factor when deconditioned people with COPD attempt to exercise.
To break this cycle, people with COPD must exercise. Pulmonary rehabilitation, which includes gradually increasing, supervised training regimens, can reverse muscle weakness, reduce leg pain, and increase exercise tolerance (see “Pulmonary Rehabilitation” below).
The “typical” American patient with moderate to severe COPD is an elderly non-Hispanic white female living below the poverty line in the east south-central United States (CDC, 2011) with a history of smoking at least one pack of cigarettes a day for more than 40 years. She complains of general tiredness and becomes short of breath when exercising. Her legs bother her when walking, so she spends most of her time sitting. If you ask her to exhale quickly, it takes her an unnaturally long time.
Other aspects of the “typical” picture range along a spectrum:
Roy Evans presents to the urgent care clinic with a fever of 102.5°, tympanic diaphoresis, severe dyspnea with a respiratory rate of 28/m, a heart rate of 122/m, blood pressure of 158/92, and an oxygen saturation of 89% on room air. He is moderately obese. Upon assessment, the nurse auscultates his lungs and finds diminished bases and expiratory wheezes throughout all fields. He is sitting on the examination table bent forward, audibly wheezing, and using accessory chest muscles to breathe. He displays equilateral expansion of his chest. He states he is coughing up more secretions than usual and that it is yellower and thicker.
Mr. Evans is known to have chronic bronchitis-type COPD. He takes Valarest to thin secretions to make them easier to bring up and the antibiotic Zithromax every day to prevent infections, in addition to his daily inhalers. He is diagnosed with a community-acquired pneumonia on top of his chronic COPD and given an Albuterol/Atrovent nebulizer treatment and has the antibiotic Avelox added to his medications.
The nurse demonstrates the nebulizer machine to Mr. Evans and his wife, as they will have one delivered to their home for self-administered treatments until his condition improves. The nurse discusses the current medication regime and the new additions, and questions the patient for compliancy with taking the meds correctly.
Patients with COPD usually present with the complaints of dyspnea and coughing.
Dyspnea during mild exercise is the most common reason that people with COPD first seek out a doctor. This dyspnea will have appeared gradually over a period of years. The dyspnea of COPD reflects at least two sensations:
Sometimes a COPD patient will come to the healthcare provider reporting that a recent illness has triggered dyspnea. Illnesses, especially respiratory illnesses, worsen dyspnea. If the patient actually has COPD, a careful review of the history of the patient’s exercise tolerance usually turns up evidence of increasing dyspnea before the illness (Victorson et al., 2009).
While dyspnea is the symptom that most often brings COPD patients to visit a healthcare provider, coughing is the most common symptom found in patients with early COPD. The cough of COPD is usually worse in the mornings. Early in the disease, the cough produces only a small amount of colorless sputum (i.e., mucus and lung secretions that are expelled into the throat by coughing). Coughing typically begins earlier in the development of COPD than dyspnea, but unlike dyspnea, coughing may or may not limit the patient’s daily activities; it depends on what the patient needs to do in a day. (For example, if they teach or preach, coughing may interfere with their work.)
Coughing is stimulated by irritation of the bronchial tree. The sudden onset of new coughing is usually caused by irritation from a respiratory infection and is accompanied by fever, tachycardia, and tachypnea. This type of cough typically lasts less than three weeks, although in some people coughs can hang on as long as two months after a respiratory illness. The coughing of COPD, however, occurs intermittently for years.
Shelley Bradley made an appointment with her family nurse practitioner (FNP) because of increased dyspnea (difficulty breathing) after a viral respiratory infection she came down with in spite of getting her annual flu shot. She told the FNP that she has had a persistent cough for three weeks after the first flu-like symptoms appeared.
Shelley was diagnosed with COPD four years ago. She quit smoking at that time and has a 32-pack-year history of smoking. She has no signs of infection and receives a chest x-ray, which shows no infection and no change in her airway. She is given a prescription for an Atrovent inhaler to use in addition to her longer-acting Serevent inhaler.
Shelley’s FNP discusses the importance of protecting herself from contracting a respiratory infection in the future. She discusses the availability of flu and pneumonia vaccines, the value of frequent handwashing, and avoiding proximity to people with signs of respiratory infections. The FNP discusses Shelley’s medication regimes and makes sure she understands how to use her inhalers.
Almost as a rule, the health system first sees COPD patients when they are in their late forties to mid-fifties and with chief complaints of dyspnea and excessive coughing. In retrospect, their symptoms have been going on for at least a decade, with coughing having shown up first. At one time the dyspnea had only been noticed during heavy exertion, but eventually it began to interfere with even mild activities.
Many COPD patients will report that typical respiratory infections are now occurring more frequently, lasting longer, and seeming more severe: colds bring on breathlessness, wheezing, coughing, and sometimes the production of colored (yellow, green, or blood-tinged) sputum (Kamangar et al., 2009).
The key element in taking the history of a COPD patient is inquiring about smoking. The first symptoms of COPD appear after about 20 pack-years of smoking, and the disease usually becomes clinically significant after 40 pack-years of smoking.
Besides asking about chronic diseases and heart conditions, a few other specific problems should be explicitly investigated when taking the history of a patient with COPD:
A patient with mild COPD may have no signs of the disease when sitting quietly, and their physical exam may be normal. In contrast, the physical exam of a person with severe COPD can be diagnostic (Swadron & Mandavia, 2009).
Patients with emphysematous COPD are typically thin but barrel-chested. They tend to breathe through pursed lips, and they sit leaning forward in a “tripod position.” This posture widens the chest as much as possible by supporting the upper body on the elbows or the extended arms.
The tripod position. Patient leans forward, resting on elbows or hands, in an effort to expand the chest and ease breathing. (Source: Jason M. Alexander, MFA. © 2007, Wild Iris Medical Education.)
Patients with chronic bronchitis COPD are typically of normal weight or overweight. They have a productive cough and may be cyanotic. At rest their rate of respiration is high, often more than 20 breaths per minute. Patients may present as dull and irritable because their state of consciousness can be clouded by hypoxemia.
The patient’s weight will influence the treatment recommendations. Obesity worsens the symptoms of COPD. On the other hand, many COPD patients, especially patients with the emphysematous form of COPD, are cachectic and underweight and have wasted muscles. In these cases, nutritional therapy will be important.
A COPD patient with chronic bronchitis but little emphysema may have a normal-sized chest. Significant emphysema, however, leads to a wide, barrel-shaped chest with a flattened diaphragm. In a patient with emphysema, the chest remains perpetually in the position of inhalation. To take a new breath, emphysematous patients must expand their chests beyond the normal position of inhalation. This requires using accessory respiratory muscles of the shoulder, neck, and back.
The chest of an emphysematous patient is unusually resonant to percussion, and the breath sounds are distant. At the other end of the spectrum, the chest of a chronic bronchitis patient can have dull spots when percussed, and their lungs will be noisy with rales, rhonchi, and wheezing.
The common feature of all forms of COPD is airway obstruction that worsens as the disease becomes more severe. A simple, direct measure of airway obstruction is the time it takes a patient to exhale an entire lungful of air. A normal person has a forced expiratory time (FET) of <3 seconds. An FET of >4 seconds suggests obstruction. An FET of >6 seconds indicates considerable airway obstruction, at the level of moderate-to-severe COPD.
COPD can injure the heart in two major ways:
Carl Messenger is a 72-year-old in the intensive care unit following a myocardial infarction. He has a history of diabetes mellitus II, hypertension, coronary artery disease, hypercholesterolemia, cor pulmonale, and COPD. He presently lies comfortably in bed without pain or difficulty breathing on 2 lpm of oxygen by nasal cannula. His cardiac monitor shows sinus tachycardia with a heart rate of 110/m and occasional premature ventricular contractions (PVCs).
Upon physical exam by the critical care nurse, Mr. Messenger displays clear but diminished breath sounds, a systolic heart murmur, 2+ radial pulses, 1+ pedal pulses, 3+ pitting edema half-way to the knees, jugular vein distension while upright, and clubbing of the fingertips. As his condition is stable, he will be transferred to the step-down unit as soon as a monitored bed is available.
The key chemistry values in a person with COPD are the levels of blood gases—oxygen and carbon dioxide—and the pH of the blood.
The severity of a patient’s COPD can be estimated by the degree that the blood gases deviate from normal. In the early stages of the disease, the amount of oxygen in arterial blood is usually within normal limits. Oxygen concentration in arterial blood is measured as its partial pressure (PaO2), and a normal oxygen partial pressure (or oxygen tension) is 80 to 100 mm Hg.
As COPD worsens, the PaO2 can drop below 60 mm Hg. This level signals respiratory distress to the brain and it strongly activates the respiratory centers. When the PaO2 is below 60 mm Hg, a person hyperventilates in an attempt to reverse the hypoxemia by breathing in more air. Unfortunately, hyperventilation due to hypoxemia expels too much carbon dioxide from the bloodstream and causes respiratory alkalosis, a pH imbalance in the blood. Hypoxemia with alkalosis is found in the middle phase of the course of COPD.
In later stages of COPD, the patient does not have the energy to hyperventilate, so carbon dioxide builds up in the blood. Now the hypoxemia is accompanied by hypercapnia (excess blood carbon dioxide), and the patient develops chronic respiratory acidosis, an ominous sign. Hypoxemia with acidosis is found in the late phase of the course of COPD (Kamangar et al., 2009; Swadron & Mandavia, 2009).
Early in the course of COPD, arterial blood gases (ABGs) do not need to be checked regularly. However, an early set of baselines values should be taken because they can be used as a comparison to evaluate the degree of change brought by an acute exacerbation.
|Base excess (BE)||-2 to +2|
|O2 saturation (sat)||94%–100%|
Accurately measuring a person’s blood oxygen tension requires drawing arterial blood and testing it in a laboratory. Pulse oximetry is a quicker, noninvasive way to test blood oxygenation. A pulse oximeter has a small probe that can be clipped onto a patient’s finger or earlobe. Using measurements of transmitted light, the oximeter determines the percent of the patient’s hemoglobin (Hgb) that is saturated with oxygen.
Pulse oximeters are not as accurate as direct oxygen tension measurements from arterial blood gases, and the percent of hemoglobin saturation measured by an oximeter is not the same as a person’s PaO2. Nonetheless, the two values are related. A person with a normal PaO2 (80–100 mm Hg as determined from blood gases) will have a hemoglobin saturation of 94% to 100% (as determined by pulse oximetry). A person with hypoxemia of 60 mm Hg will have a hemoglobin saturation of approximately 86%. Normal range of oxygen saturation is 94% to 100%, but a person with moderate to severe COPD may run lower than normal saturation levels when breathing room air.
Routine blood analyses are not needed to manage most cases of COPD. Some people with severe COPD produce excess red blood cells (polycythemia) in response to their chronic hypoxia. This leads to hematocrit readings of >52% in men (normal is 43%–52%) and >48% in women (normal is 37%–48%).
Patients who develop emphysema at an early age (under 40 years old) and nonsmokers of any age who develop emphysema are usually tested for their blood levels of the enzyme AAT. Deficiency of this enzyme makes a person unusually susceptible to emphysematous COPD. AAT deficiency is not common. When it is found, the patient and family should be educated about the genetics of this disease. It is sometimes possible to treat AAT deficiency with replacement doses of the enzyme.
COPD is a disease that is defined functionally: COPD causes progressively worsened airflow obstruction in the lungs. Therefore, breathing measurements are better diagnostic indicators of the disease than are static pictures of the lung. Nonetheless, imaging studies play a role in evaluating COPD patients.
The most commonly used images for evaluating and managing COPD are chest x-rays and computed tomography (CT) scans. Other modalities that are sometimes used include magnetic resonance imaging (MRI) and optical coherence tomography (OCT) (Coxson et al., 2009).
Chest x-rays are used to rule out other causes of airway obstruction, such as mechanical obstruction, tumors, infections, effusions, or interstitial lung diseases. In acute exacerbations of COPD, chest x-rays are used to look for pneumothorax, pneumonia, and atelectasis (collapse of part of a lung) (Ignatavicius & Workman, 2010).
In its later phases, COPD produces a number of changes that can be seen in chest x-rays:
CT scans are now the imaging technique of choice for lung evaluations (Coxson et al., 2009). CT scans, especially high-resolution scans, are better than chest x-rays at resolving the details of the lung abnormalities caused by COPD. Specifically, CT scans can help define which areas of a patient’s lungs are predominately emphysematous and which are predominately bronchiolitic. CT scans are also better than chest x-rays at identifying other diseases, such as tumors or infections, that may be complicating a patient’s COPD. Late in the disease, CT scans are used to evaluate COPD patients who are to be treated surgically.
In developed countries, medical imaging is the source of most of the radiation to which the average person is exposed, other than the natural background radiation of the environment. Of the common medical imaging techniques, CT scans give the highest dose of radiation.
Cancers caused by radiation tend to take many years to develop, and radiation damage is often cumulative. Therefore, CT scans pose the most danger to young people. “Based on radiation exposure issues, CT uses should be strongly constrained in children, used cautiously in young adults, and used prudently in older adults…. [I]n all cases, it is recommended that CT radiation dose be adjusted on the basis of the size of the patient to be as low as necessary to answer the clinical question posed” (Coxson et al., 2009).
Pulmonary function tests are used to assess the extent of a patient’s airway obstruction. When COPD is diagnosed, baseline pulmonary function values should be recorded. Later tests can be used to measure the progression of the disease and to evaluate the effectiveness of treatments. For COPD, the two general classes of breathing tests are measurements of lung volumes and measurements of airflow rates/volumes.
In COPD, airway obstruction makes it difficult to fully empty the lungs. The air that remains keeps the lungs inflated even after a complete exhalation. This makes it more difficult for a patient to pull in sufficient air during the next breath. As a result, the total air volume contained by the lungs increases, but the effective volume of air, the amount of air actually breathed in and out, decreases.
The effective volume of air is called the vital capacity (VC). VC denotes the largest volume of air that can be exhaled after a full inhalation. Usually, this volume is measured by having a patient take as large a breath as possible and then exhaling as quickly and forcefully as possible. With these testing instructions, the result is more accurately called the forced vital capacity (FVC) (Ignatavicius & Workman, 2010).
Besides limiting the effective volume of air in the lungs, COPD also slows the movement of air inside the lungs. This slowing can be measured directly. Measurements of the rate of air movement during breathing are called “spirometric measurements”; more specifically, spirometry measures the volume of air exhaled in a defined period of time (Lefebvre et al., 2012).
A small, handheld spirometry device can be used for quick office or clinic tests. (Source: National Institutes of Health.)
The most common spirometric measurement used for COPD is the 1-second forced expiratory volume (FEV1). This is the maximum amount of air that a patient can breathe out in the first second of a forced exhalation after having taken a full breath.
Spirometry is helpful in evaluating the severity of airflow obstruction in patients with symptomatic COPD. On the other hand, spirometry does not add much to the evaluation of asymptomatic patients with COPD because treatments (other than smoking cessation) are not typically begun until after a patient becomes symptomatic (Lefebvre et al., 2012).
People with normal lungs can expel most of the air in their lungs within 1 to 2 seconds. The amount of air forcefully exhaled in the first second (FEV1) is about 3/4 of a healthy person’s FVC.
In COPD, airway obstruction restricts the rate of exhaling, and people with COPD cannot get a normal amount of air out of their lungs in one second. People with COPD have FEV1/FVC <0.70. When a person has an FEV1/FVC <0.70 and a history of more than 20 pack-years of smoking, they can be given a presumptive diagnosis of COPD (Ignatavicius & Workman, 2010). That is, a person who has a history of >20 pack-years of smoking and an FEV1/FVC <0.70 is almost certain to have COPD.
The four basic stages of COPD are mild, moderate, severe, and very severe. COPD is staged by the degree to which the FEV1/FVC is below 0.70 when corrected for the person’s age, gender, and body build (Swadron & Mandavia, 2009).
|Source: Ignatavicius & Workman, 2010.|
|I||Mild||FEV1/FVC <0.70 and FEV1 ≥80% predicted value*|
|II||Moderate||FEV1/FVC <0.70 and 50%≤ FEV1 <80% predicted value*|
|III||Severe||FEV1/FVC <0.70 and 30%≤ FEV1 <50% predicted value*|
|IV||Very Severe||FEV1/FVC <0.70 and FEV1 <30% predicted value*
or FEV1 <50% predicted value plus chronic respiratory or heart failure
|* Predicted FEV1 values adjusted for a person’s age, gender, height, and weight can be calculated from published equations.|
Dyspnea and chronic cough are the presenting symptoms of a number of conditions other than COPD (Gonzales & Nadler, 2010). These conditions include pneumothorax, pulmonary emboli, pneumonia, lung infections, atelectasis, interstitial lung disease, sarcoidosis, effusions, lung masses, upper-airway or foreign-body obstructions, and congestive heart failure. Most of these conditions can be identified using imaging studies, such as chest x-rays, and clinical signs. Anemia or metabolic acidosis can also cause chronic dyspnea, and both of these can be identified by blood studies.
Asthma, which is another common obstructive airway disease, is high on the list of differential diagnoses for conditions presenting with both dyspnea and cough. Asthma usually cannot be distinguished from COPD by chest x-rays, clinical signs, or blood studies.
Patients with asthma have hypersensitive airways that are always slightly inflamed, edematous, and filled with immune cells, characteristically eosinophils. Certain inhaled allergens and a variety of stresses can trigger these primed immune cells, causing a flare of the disease, an asthmatic attack, that brings on edema, mucus, and narrowed airways. Like COPD, asthmatic attacks will obstruct airways and impede airflow; but unlike COPD, the airway restrictions of an asthmatic attack can be, at least in young people, quickly and almost entirely reversed by bronchodilators.
As people with asthma age, however, their airway obstruction sometimes becomes more fixed and less reversible. Clinically, these people’s disease begins to share more features with COPD, and the two diseases may be hard to distinguish. Determining which disease is present can be important for a patient’s treatment. For example, the dyspnea of asthmatic patients tends to improve markedly when the patient is given steroids, but the chronic dyspnea of most COPD patients does not improve following steroids (Ignatavicius & Workman, 2010).
Some useful distinctions between asthma and COPD include:
|Respiratory Disorder||Symptoms||Treatment||Smoking a Factor?|
|Source: Ignatavicius & Workman, 2010.|
|COPD||Dyspnea, cough with sputum production, exercise intolerance||Bronchodilators, steroids, oxygen, pulmonary rehabilitation||80% with emphysema|
|Asthma||Dyspnea, chest tightness, cough with mucus production, wheezing||Preventive and rescue drugs (bronchodilators, anti-inflammatories, steroids, NSAIDs), oxygen||20%–30%|
|Pneumothorax||Pain on affected side at end of inspiration and expiration, tachycardia, rapid shallow breathing, air hunger, akinetic chest wall on affected side||Oxygen, pain medication, thoracentesis||No|
|Pulmonary emboli||Sudden onset of dyspnea, stabbing chest pain, crackles, dry cough, hemoptysis, apprehension||Anti-coagulants (heparin, enoxaparin, warfarin), fibrinolytics (Alteplase), oxygen, embolectomy||No|
|Lung masses||Hoarseness, hemoptysis, dyspnea, cough, chest pain or tightness, fever, weight loss, clubbing||Oxygen, surgical removal, chemotherapy or radiation therapy (cancer)||85%|
|Foreign body obstruction||Choking, inability to swallow, wheezing||Remove object manually or surgically, cool mist humidification||No|
|Atelectasis||Dyspnea, diminished breath sounds||Oxygen, treatment of cause||No|
|Interstitial lung diseases||Dyspnea||Steroids, oxygen||No|
|Pulmonary hypertension||Dyspnea, fatigue, chest pain, elevated pulmonary artery pressure||Calcium channel blockers, warfarin, endothelin-receptor agonists (bosentan)||No|
|Effusions||Dyspnea, hypoxia, tachypnea, pain with inspiration||Bronchodilators, percussion, thoracentesis, oxygen||Possibly|
|Congestive heart failure||Dyspnea, edema, jugular vein distention, reduced ejection fraction, orthopnea, hypertension, gallop||ACE inhibitors, diuretics, nitrates, inotropics, beta-adrenergic blockers, oxygen, fluid- and sodium-restricted diet||Possibly|
|Pneumonia||Dyspnea, chest pain with inspiration, hypoxemia, cough, sputum production, fever||Oxygen, antibiotics (if bacterial or fungal), anti-pyretics, anti-tussives, fluids||Possibly|
COPD is a life-long disease. It requires special medical treatment during acute exacerbations, and after the disease reaches the “moderate” level, it requires daily medications and permanent adjustments to a patient’s lifestyle. GOLD (2009) guidelines offer a comprehensive framework for the management of COPD.
The goals of long-term COPD treatments are:
Education is important. All COPD patients should learn about their disease and understand that smoking and air pollution will further damage their lungs. Patients need to make a special effort to avoid respiratory infections and to get yearly influenza vaccinations (Engelke, 2012).
At each stage of the disease, there are some characteristic medical therapies:
(Source: National Institutes of Health.)
Medications are the fundamental day-to-day tools for controlling the symptoms of COPD, but there are also five effective nonpharmaceutical techniques for treating COPD: patient education, smoking cessation, keeping airways clear, nutritional therapy, and pulmonary rehabilitation (Engelke, 2012).
Teach your COPD patients about their disease. Explain that the disease causes irreversible and progressive problems. Warn patients that they will have episodes in which the symptoms—difficulty breathing, wheezing, productive cough, and tiredness—get worse for days or even weeks.
Assure patients that they will be helped by medications that make breathing easier. Tell them there are several things that they can do to slow the progression of the disease and to lessen the number of acute exacerbations. The most important thing is to stop smoking. Although smoking has already damaged their lungs, continued smoking will increase the damage and will make their COPD worsen more quickly.
Let patients with COPD know that they should make every effort to stay active while recognizing the need to monitor and time their efforts throughout the day. In addition, give them practical suggestions that will help them to cope with the inevitable limitations posed by COPD. For example, tell them:
Most patients with COPD have a long smoking history and many will still be smoking when they are under medical care. From day one, strongly urge your patients to stop smoking.
Quitting can be difficult, since the nicotine in tobacco smoke is powerfully addictive. In addition, the rituals of smoking fill basic psychological needs. Therefore, when caregivers merely tell patients to stop smoking, their patients succeed over the long term only 5% of the time. Smoking cessation programs significantly improve the odds. Long-term success rates of greater than 20% to 40% can be achieved by comprehensive programs that include behavioral therapy and medications.
Begin by saying to your patients, “COPD cannot be cured, but if you continue smoking, the disease will worsen much more quickly. Have you thought about quitting smoking?” Regardless of the answer, follow it with the offer, “When you’re ready to stop smoking, I’ll be happy to work with you to set up as effective a program as possible.”
Successful smoking intervention programs begin by asking the patient to set a specific quitting date. The programs then maintain continued contact with the patient to provide medication, counseling, support, advice, and a modicum of social pressure. The report “Treating Tobacco Use and Dependence: Clinical Practice Guidelines” from the U.S. Surgeon General’s website offers specific recommendations (see “Resources” at the end of this course).
Healthcare workers use the Five As when counseling their patients who smoke. Taking even one step is constructive.
The pharmacologic aspect of smoking cessation programs attempts to ease the effects of nicotine withdrawal. Smokers who need their first cigarette within a half-hour of getting up in the morning are likely to be highly addicted to nicotine. When these people stop smoking, they become anxious, irritable, easily angered, easily tired, and depressed. Their sleep is disrupted. They have difficulty concentrating. These withdrawal effects are common during the first 2 to 3 weeks after quitting (Goodfellow & Waugh, 2009).
Nicotine replacements. To lessen withdrawal symptoms, nicotine can be taken without smoking. Nicotine replacements are available as gum, lozenges, transdermal patches, inhalers, and nasal sprays. These should be used on a regular schedule and PRN (as needed for cigarette cravings) for about two weeks, and then the doses should be tapered. Nicotine patches are marketed as Habitrol and NicoDerm CQ; nicotine gum includes Nicorette. As nicotine is a vasoconstrictor, people with coronary artery disease are advised not to use any nicotine replacement therapy.
Antidepressants. One antidepressant, bupropion SR (sustained-release) or Zyban, is approved by the FDA to help patients for whom nicotine replacement therapy has not worked.
Nicotine agonists. In 2006, varenicline (Chantix), a nicotine agonist, was approved by the FDA for anti-smoking therapy. Varenicline binds to nicotine receptors and prevents nicotine from activating the receptors while producing a smaller stimulant effect than nicotine.
Sources: Goodfellow & Waugh, 2009; Kamangar et al., 2009.
On July 1, 2009, the U.S. Food and Drug Administration (FDA) announced that it would require manufacturers to put a Boxed Warning on the prescribing information for the smoking cessation drugs Chantix (varenicline) and Zyban (bupropion). The warning highlights the risk of serious mental health events—including changes in behavior, depressed mood, hostility, and suicidal thoughts—when taking these drugs.
“The risk of serious adverse events while taking these products must be weighed against the significant health benefits of quitting smoking,” said Janet Woodcock, M.D., director of FDA’s Center for Drug Evaluation and Research. “Smoking is the leading cause of preventable disease, disability, and death in the United States, and we know these products are effective aids in helping people quit.”
Source: FDA, 2009.
Nurse Jeffries has a patient in her unit, Mrs. Hunter, who struggles with quitting smoking in spite of being diagnosed with moderate COPD. She has tried nicotine patches and gum, the nicotine agonist Chantix, hypnotherapy, acupuncture, and counseling. Each method has been temporarily successful, and then Mrs. Hunter started smoking again. Mrs. Hunter states that the patches caused skin irritation and scarring, the gum didn’t work, Chantix caused severe nausea, and the hypnotherapist couldn’t put her under.
At present, the patient’s doctor has ordered the anti-depressant Zyban to reduce nicotine cravings. Although Mrs. Hunter understands the dangers of smoking and the effects on her health, she returns to smoking in times of stress. Nurse Jeffries sits with Mrs. Hunter to discuss the types of stressors that trigger her addiction and some strategies to avoid them or handle them in other ways.
COPD patients with significant chronic bronchitis must keep their airways clear. They should be encouraged to cough up sputum, and they should not get in the habit of using cough suppressants or sedatives. Postural drainage can help patients who cannot clear their secretions by coughing (Ignatavicius & Workman, 2010).
Most people’s lungs secrete extra mucus in response to inhaled irritants. To avoid stimulating excess secretions, COPD patients need to stay out of smoke-filled rooms, and they should stay indoors during air pollution alerts. Home air conditioners and air filters are effective at keeping indoor air clear of particulates.
The symptoms of COPD improve when overweight patients lose weight. Some COPD patients, however, have the opposite problem: they have become thin and malnourished. In part, this cachexia results from the high energy cost of breathing with COPD. In addition, the chronic inflammatory state underlying COPD tends to put the body’s metabolism into a catabolic state. To help them maintain a healthy body weight, thin COPD patients should be given dietary counseling that includes specific recommendations for meals that are nutritionally balanced and that contain sufficient calories to make up for the work of breathing (Engelke, 2012; ADA, 2009). (For more information on nutrition, see “Resources” at the end of this course.)
Pulmonary rehabilitation (PR) is the term for a group of techniques used to improve patients’ conditioning and to ease their exercising difficulties. Pulmonary rehabilitation is done as outpatient therapy. Some rehabilitation programs continue for an extended time, but most run for a few weeks and then give patients individualized instructions for continuing at home. Education sessions are important parts of rehabilitation programs; in these sessions, patients and their families learn details about COPD and its treatment (Chesnutt et al., 2010).
The primary objective of an evidence-based, multidisciplinary, comprehensive PR program is to restore individual patients to as independent a level of function as possible with an improved health-related quality of life. It is evidence-based that dyspnea symptoms improve in COPD patients who undergo a PR regime. PR is proven to be a cost-effective treatment model and reduces the number of hospital admissions, but it cannot be substantiated that PR extends the life of COPD patients (Reis et al., 2007).
The various disciplines that comprise the PR team include some combination of doctors, nurses, physical therapists, occupational therapists, respiratory therapists, nutritionists, and exercise specialists.
Patient and family education is central to all PR programs, although it has been demonstrated that education alone does not improve outcomes. Education should inform the patient and family how to self-manage the disease in collaboration with the various PR disciplines. Prevention and treatment of disease exacerbations are the essence of education in PR.
Comprehensive pulmonary rehabilitation improves the quality of patients’ lives. However, only one aspect of it, individually tailored exercise training, has been shown to reverse the muscle deconditioning caused by COPD (Man et al., 2009). Exercise training does not improve lung functioning but it can reduce COPD symptoms and increase the amount of exercise that the patients can do without being stopped by dyspnea. It can also reduce the number of hospitalizations for acute exacerbations (AACVPR, 2011).
Physical inactivity is the greatest source of the muscle weakness that plagues COPD patients. Although people with COPD have irreversible breathing difficulties, exercise training can significantly increase a patient’s strength and endurance and reduce their fatigability. These improvements result from increased muscle size (specifically, cross-sectional area), increased blood flow to muscles, increased oxidative enzyme capacity, and reduction of lactic acid production during exercise (Man et al., 2009).
Lower extremity exercises at high intensity focusing on the muscles of ambulation are the central core of every PR program. Endurance training in the form of walking and cycling retards the progression of activity intolerance in patients with COPD, as does unsupported upper extremity exercises. Inspiration muscle training (IMT) has not proven to be of benefit for COPD patients (Reis et al., 2007).
Pulmonary rehabilitation programs are tailored to the needs of each individual. Typically, the programs include graded aerobic exercises, such as regular sessions of walking or stationary bicycling three times weekly. The walking exercise program, for example, might begin with slow treadmill walking for only a few minutes. Gradually, the length and speed of the walking is increased over 4 to 6 weeks. The goal would be for the patient to walk for 20 to 30 minutes without needing to stop because of shortness of breath. At that point, the patient would be assigned a maintenance exercise program to be done at home.
Rehabilitation sessions also include:
Supplemental oxygen is recommended during exercise for patients who experience severe exercise-induced hypoxemia. This may improve exercise endurance during a high-intensity exercise program (Reis et al., 2007).
Some COPD patients have such poor lung function or such weak musculature that they cannot take part in the usual aerobic exercise training programs. Small studies suggest that electrical stimulation of the patients’ lower limbs can improve their muscle strength and exercise tolerance. This has worked even for bedridden patients. Neuromuscular stimulation routines are safe and inexpensive, and they can be done at home (Man et al., 2009).
Stuart Moody is being discharged from the hospital with a new diagnosis of mild to moderate emphysema-type COPD. His doctor has ordered that Mr. Moody start a pulmonary rehabilitation (PR) program with a follow-up visit to the doctor’s office in six weeks. The nurse explains to Mr. Moody that a PR program consists of education about medications, the use of inhalers, the use and care of a nebulizer machine, how to self-measure peak flows, breathing training, panic control, and airway control. Mr. Moody will see a registered dietician in consultation before discharge to help him maintain or achieve his correct weight. He will also work with a physical therapist to learn progressive aerobic exercise.
Mr. Moody is fortunate to be started on PR at this time. Previously, PR was only ordered for moderately severe COPD. He is also fortunate that PR is now covered by Medicare.
The medicines currently available for COPD focus on long-term therapy with prevention of symptoms. Stepped therapy, the process by which additional medications are added as symptoms progress, is the standard in treating COPD (Ignatavicius & Workman, 2010). Inhaled and systemic drugs for COPD patients include beta-adrenergic agents, cholinergic antagonists, methylxanthines, corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and mucolytic agents.
Drug therapy is used to reduce the extent to which dyspnea restricts a patient’s activities. Most COPD drugs work by keeping airways as wide open as possible. Medications (bronchodilators) used to reduce airflow obstruction are not typically given to asymptomatic COPD patients (Ignatavicius & Workman, 2010).
Bronchodilators are the workhorses of the COPD medications. Although spirometry shows that bronchodilators only modestly reduce airway obstruction in most COPD patients, regular doses of bronchodilators relieve dyspnea sufficiently for COPD patients to increase their levels of activity.
Bronchodilators work by relaxing the muscles in the walls of the lungs’ airways; this widens the airways and allows air to move through them more easily. Short- and fast-acting bronchodilators are used as “rescue” medicines to relieve sudden bouts of dyspnea and coughing. Long-acting bronchodilators are used in daily, regularly scheduled drug regimens (Ignatavicius & Workman, 2010).
Airway muscles are smooth muscles controlled by the autonomic nervous system. The autonomic nervous system has two divisions: parasympathetic and sympathetic. The major parasympathetic neurotransmitter is acetylcholine. The major sympathetic neurotransmitter is norepinephrine. Stimulation of the parasympathetic division of the autonomic nervous system tightens airway muscles and narrows the airways, while stimulation of the sympathetic division of the autonomic nervous system relaxes airway muscles and widens the airways. Bronchodilators are available to work at either parasympathetic receptors or sympathetic receptors.
All symptomatic patients are prescribed a short-acting rescue bronchodilator that they can use to recover from a bout of suddenly worsening dyspnea (Restrepo, 2009). Either short-acting parasympatholytic or short-acting sympathomimetic bronchodilators can be used as fast-relief medications.
The parasympatholytic bronchodilators are anticholinergic drugs, which relax the smooth muscles in the airway by blocking the effect of acetylcholine, produced by the parasympathetic nervous system (Ignatavicius & Workman, 2010).
The most commonly prescribed short-acting anticholinergic bronchodilator is ipratropium (Atrovent). Ipratropium is relatively inexpensive and widely available. It is usually administered via a metered-dose inhaler (MDI), although there are other formulations. It can be used as a PRN medication. It takes effect in 15 to 30 minutes, has its peak action in 1 to 2 hours, and lasts 4 to 6 hours.
Traditionally, ipratropium has also been used as the main anticholinergic in long-term drug regimens. However, studies have shown that tiotropium (Spiriva) is a more effective drug. Tiotropium is a longer-acting anticholinergic bronchodilator. It is more expensive than ipratropium, but a typical dose lasts an entire day. Tiotropium is helpful when used alone and is even more effective in combination with a long-acting beta agonist (Keating, 2012). Tiotropium is inhaled as a powder via a dry powder inhaler (DPI).
When used correctly, MDIs and DPIs deliver the medication directly to the airway. MDIs work best when connected to a “spacer” to guide the medication down the patient’s airway (Ignatavicius & Workman, 2010).
How to Use an Inhaler Correctly with a Spacer
How to Use a Dry Powder Inhaler (DPI)
(For inhalers requiring loading)
(After loading the device and for inhalers that do not require drug loading)
Source: Ignatavicius & Workman, 2010.
One class of sympathomimetic bronchodilators, the beta2 agonists, acts by mimicking the effect of norepinephrine on airway muscles. Beta2 agonists stimulate the beta2-adrenergic neuroreceptors and cause smooth muscles to relax, widening the airways. These are also known as adrenergics or catecholamines. Muscle tremors and heart palpitations are the most common side effects of beta2 agonists, but when the medicines are inhaled (as opposed to taken in oral formulations), the side effects are usually mild.
The short-acting beta2 agonists, which include albuterol (Accuneb, ProAir, Proventil, and Ventolin) and metaproterenol (Alupent), are the most commonly prescribed sympathomimetic bronchodilators. These drugs are usually administered via either MDI or DPI. Short-acting beta2 agonists such as albuterol and metaproterenol take effect in 5 to 15 minutes and last for 2 to 4 hours.
Short-acting beta2 agonists are used as rescue medicines when a patient needs immediate relief from sudden episodes of increased dyspnea. A short-acting beta2 agonist can also be added to an anticholinergic drug as part of a regular drug regimen.
The long-acting beta2 agonist bronchodilators include formoterol (Foradil) and salmeterol (Serevent). These drugs are more expensive than albuterol or metaproterenol, but a typical dose lasts for at least 12 hours. Inhalation is the recommended route for administering the long-acting beta2 agonists.
Another class of sympathomimetic bronchodilators, the phosphodiesterase inhibitors or xanthines, acts by stimulating the release of norepinephrine, which then relaxes smooth muscles in the airways of the lung. For COPD, the phosphodiesterase inhibitor theophylline (Elixophyllin, Theo-Dur) is used to dilate airways, stimulate the respiratory centers of the brain, and improve the function of respiratory muscles.
Theophylline is usually used as a systemic drug. It is taken orally and side effects are common; among them are sleeplessness and gastrointestinal upset, including nausea and vomiting. Occasionally, theophylline causes serious cardiac arrhythmias or seizures, especially when liver disease has decreased the body’s ability to metabolize the drug. Older people are more likely to get theophylline toxicity. Two newer phosphodiesterase inhibitors, cilomilast (Ariflo) and roflumilast (Daxas), appear to be safer than theophylline.
|Sources: Ignatavicius & Workman, 2010; Everyday Health, 2012.|
|Short-acting beta agonists: relax bronchiolar smooth muscle||
||Tachycardia, palpitations, anxiety, muscle tremors||Fast-acting rescue drug; take 5 minutes before other inhalers; used for treatment|
|Long-acting beta agonists: relax bronchiolar smooth muscle||
||(see above)||Do not use for acute onset of symptoms; shake inhaler, since drug separates; used for prevention|
|Anticholinergic agents: inhibit parasympathetic nervous system||
||Cough, dry mouth||May exacerbate cardiac symptoms; shake inhaler, since drug separates; used for prevention; must carry at all times if this is to be used as a rescue drug|
|Phosphodiesterase inhibitors: methylxanthines (similar to caffeine)||
||Stomach upset, heartburn, insomnia, headache, nervousness or irritability, tachycardia, tachypnea||Do not use caffeine; monitor blood levels|
Patients vary in their response to bronchodilators, so the most effective drug regimens are those that have been individually tailored. Finding the right drug or set of drugs is empirical. Patients may try many different inhalers until finding a combination that works best for them. When drug combinations are being tried, it is best to introduce the drugs one at a time to learn the patient’s response to that drug only.
For patients with chronic stable COPD, short-acting bronchodilators will eventually be insufficient to control their symptoms. Currently, the long-acting anticholinergic drug tiotropium is usually recommended as the first drug to try in a regular daily medication regimen. It is taken once daily and it does not have the side effects of sympathomimetic drugs, but it is generally not as effective as the beta agonists and is only recommended if the COPD patient cannot tolerate the beta agonist side effects (Ignatavicius & Workman, 2010).
Concurrently, a short-acting beta2 agonist, such as albuterol, is usually prescribed as a rescue drug. If this initial regimen is insufficient, the short-acting beta2 agonist is added to the regularly scheduled drug regimen rather than being used only when needed. The combination of ipratropium and albuterol is available commercially (DuoNeb) as an inhalant.
As COPD progresses, most patients do better with combinations of two or three bronchodilators. In American and Western European medicine, theophylline (or another phosphodiesterase inhibitor) is usually the last bronchodilator to be added.
If they are to be followed faithfully, drug regimens must be realistic. Bronchodilator therapy with two or three drugs is expensive. In addition, using inhalers can be physically difficult for some people, especially the elderly, and physicians may need to modify an optimal pharmacologic therapy to make it practical for a particular patient.
Corticosteroids are two-edged swords. On the one hand, they are effective anti-inflammatory medicines and can be used to tone down the inflammatory response that underlies or exacerbates many diseases. On the other hand, the continued use of corticosteroids causes Cushing’s syndrome, glaucoma, cataracts, myopathy, ulcers, osteoporosis, hyperglycemia, poor wound healing, and the inability to overcome infections.
In stable COPD, the problems that come from the long-term use of oral or systemic corticosteroids usually outweigh the drugs’ benefits. Inhaled steroids—such as fluticasone (Flovent), beclomethasone (Beclovent, Beconase), and budesonide (Pulmicort Turbuhaler)—have fewer adverse effects than oral formulations, and approximately 10% of people with COPD find that regularly inhaled steroids reduce their airway obstruction. For this population of patients, inhaled steroids can be a useful addition to the other regularly scheduled bronchodilators.
The regular use of inhaled corticosteroids is usually reserved for patients with severe COPD. In people with severe COPD, steroids will reduce the number of exacerbations and the rate of mortality. For people with severe COPD, inhaled corticosteroids are typically combined with a long-acting beta2 agonist in a regular treatment regimen (Ignatavicius & Workman, 2010). Regular use of inhaled corticosteroids for COPD does, however, increase a patient’s risk of developing pneumonia (Restrepo, 2009).
The usefulness of corticosteroid therapy cannot be predicted in advance for any one patient. At the moment, spirometrically testing a patient’s response to the medication is the only way to identify in advance those COPD patients who will be helped by adding inhaled steroids to their regular regimen of bronchodilators.
|Sources: Ignatavicius & Workman, 2010; Everyday Health, 2012.|
|Corticosteroids: disrupt inflammatory pathways||Inhaled:
|Inhaled: coughing, hoarseness, dry mouth, sore throat||Must be taken every day, even if there are no symptoms; do not stop taking suddenly; take with food; reduces local immunity, may increase risk for local infections like candida (yeast)|
|Oral: glaucoma, edema, hypertension, mood swings, weight gain, cataracts, hyperglycemia, infections, osteoporosis and fractures, menstrual irregularities, suppressed adrenal gland hormone production, thin skin, easy bruising and slower wound healing|
|Non-steroidal anti-inflammatory drugs (NSAIDs): stabilize mast cell membranes to prevent inflammation||Nedocrimil (Tiladel)||Dyspepsia, nausea, hyperacidity
In higher doses: MI, CVA, rash, GI bleeding
|Must be taken by inhaler every day for prophylaxis, even if there are no symptoms|
|Sources: Ignatavicius & Workman, 2010; Everyday Health, 2012.|
|Combine the effects of bronchodilators and corticosteroids||Short-acting:
||(see tables above)||(see tables above)|
Patients with COPD often have thick, tenacious mucus that is very difficult to expectorate, particularly during an acute exacerbation. Mucolytic agents can be given by respiratory nebulizer treatments, sometimes mixed with normal saline to thin secretions. They can also be given orally to produce a systemic effect. Acetylcysteine (Mucomyst) or dornase alfa (Pulmozyme) are commonly given by inhaled nebulizer treatment, and guaifenesin (Robitussin) is given by mouth to promote expectoration (Ignatavicius & Workman, 2010).
|Sources: Ignatavicius & Workman, 2010; Everyday Health, 2012.|
|Thin secretions to promote expectoration||Inhaled:
||Foul smell, sticky nebulizer mask, white patches or sores inside mouth or on lips, nausea, fever, nasal drainage, sore throat, drowsiness, rash, or clammy skin.||Must be instructed in home nebulizer use; may interact with some vitamins, minerals, and herbs|
COPD is a continually worsening condition. Researchers have been searching for additional medications that can slow the inevitable decrease in lung function suffered by COPD patients. Examples of ongoing investigations include:
As protection against serious respiratory illnesses, people with COPD should get an influenza vaccination each year. During outbreaks of strains of flu not covered by the annual vaccination, people with COPD should probably receive prophylactic antiviral treatment such as amantadine (Symmetrel), rimantadine (Flumadine), oseltamivir (Tamiflu), or zanamivir (Relenza).
Pneumococcal vaccinations are also recommended. A second dose is recommended for people 65 years and older who got their ﬁrst dose when they were younger than 65 and it has been 5 or more years since the ﬁrst dose. A second dose is also recommended for people 2 through 64 years of age who:
When a second dose is given, it should be given 5 years after the first dose.
Source: CDC, 2009d.
Supplemental oxygen improves levels of blood oxygenation and reduces the rate at which patients need to breathe. For people with COPD, supplemental oxygen also slows the rate at which muscles fatigue. These effects make it easier for patients to breathe more deeply and to exercise for longer periods. For patients with advanced COPD, supplemental oxygen reduces mortality rates.
Oxygen therapy is expensive and involves special equipment. Therefore, when people with COPD can maintain a blood oxygenation level of PaO2 >55–60 mm Hg (an oxygenation saturation of more than ~89%), supplemental oxygen therapy is not routinely prescribed (Chesnutt et al., 2010).
Eventually, however, supplemental oxygen will be necessary. For some COPD patients, oxygen is needed to participate in regular exercise programs. For other patients, oxygen is needed to carry out the typical activities of daily living.
If they live long enough, all patients with COPD lose sufficient lung function to the point that they will become hypoxemic at rest, even on an optimal regimen of regular bronchodilator treatments. For these people, continuous oxygen therapy can prolong their lives and reduce hospitalizations. When a patient’s blood PaO2 is <55–60 mm Hg (an oxygen saturation of less than ~85%–89%) at rest, it is recommended that supplemental oxygen be given continuously—which means, in practical terms, more than 19 hours per day (Tarrega et al., 2011).
Low-flow (2–3 liter/min) oxygen inhaled through nasal cannulas is usually sufficient to raise a COPD patient’s blood PaO2 to 65–80 mm Hg (an oxygen saturation of 89%–94%). In addition to increasing survival rates by about 50%, this level of supplemental oxygen lowers the person’s hematocrit toward a normal range, makes sleep easier, and improves exercise tolerance.
Home oxygen therapy is also recommended for COPD patients with heart failure, pulmonary hypertension, or erythrocytosis (i.e., a hematocrit >56%), even when their PaO2 is >55 mm Hg. Some patients who maintain a higher level of arterial oxygen during the day drop to a PaO2 <55 mm Hg when they sleep. For people whose hemoglobin desaturates at night, nocturnal oxygen therapy is helpful.
Home oxygen can be purchased as liquid O2 or as compressed gas; it can also be “manufactured” directly by home oxygen concentrators. The cost of continuous home oxygen therapy can be $500 or more per month. In many cases, Medicare will cover 80% of the cost.
Patients usually breathe supplemental oxygen via a continuous-flow nasal cannula. Devices that “conserve oxygen”—reservoir cannulas, demand pulse delivery devices, transtracheal oxygen delivery—are especially efficient because they provide all the supplemental oxygen early in each inhalation. Some patients who have trouble keeping low blood-levels of carbon dioxide can be fitted with facemasks from machines that deliver supplemental oxygen at continuous positive-pressure; these systems provide noninvasive positive-pressure ventilation (NIPPV) (Kamangar et al., 2009).
A home system is usually adjusted to deliver 2 to 3 liters of oxygen per minute, and in most cases this will maintain a patient’s oxygen saturation at >89%. For patients who continue to have dyspnea at night, the flow rate is raised by 1 liter/min during sleep.
One goal of oxygen therapy is to allow patients to remain active. Inside the home, long tubes can connect the nasal cannulas to stationary oxygen delivery units so patients that can move around. For more freedom and to go outdoors, patients can carry portable tanks of compressed oxygen or liquid oxygen.
Medical. There is a small risk that too high a concentration of inspired oxygen will suppress the respiratory drive of COPD patients. Long-term low-flow oxygen therapy is probably safest when the amount of oxygen delivered gives the patient a PaO2 of 60–65 mm Hg, which is toward the low end of the acceptable range of inspired oxygen (Kamangar et al., 2009).
Physical. Concentrated oxygen is flammable and poses a fire hazard. Patients and their families cannot smoke or use open flames near the oxygen equipment. The long oxygen tubing may constitute a fall risk.
Commercial planes maintain an internal air pressure equivalent to 5,000–8,000 feet above sea level. For those COPD patients whose resting arterial blood oxygen concentration is low (PaO2 <69 mm Hg) even at sea level, the cabin concentration of oxygen will usually not be high enough to avoid hypoxemia. Airlines can provide supplemental oxygen, and some airlines will allow patients to bring small oxygen delivery systems with them, although patients must make arrangements with the airline in advance.
Surgery is risky in people with severe COPD. Postoperatively, many normal patients temporarily have reduced lung volumes, rapid shallow breathing, and an impaired ability to take in oxygen and expel carbon dioxide. These routine postoperative problems add additional stress to the already compromised respiratory systems of patients with COPD. One result is that patients with severe COPD develop postoperative pneumonia 13 times more often than patients with normal lung function. (Preoperative antibiotics can reduce the high rate of postoperative pneumonia.)
The lack of alternative treatments for severe COPD has led to the development of three surgical procedures that attempt to improve and prolong the lives of COPD patients. The techniques are lung transplantation, lung volume reduction surgery, and bullectomy (Ignatavicius & Workman, 2010).
People with severe COPD are the most common recipients of lung transplants. Candidates for lung transplantation are patients with severe COPD who have exhausted medical therapies and have life expectancies of ≤2 years. (The BODE Index is usually used to estimate a COPD patient’s life expectancy [Kamangar et al., 2009]. See box below.) Typically, patients should also be younger than 65 years. Three quarters of COPD patients who receive lung transplants live for ≥2 years after the operation and many of the survivors have substantially improved abilities to exercise.
The updated Bronchial Obstruction, Dyspnea, Exercise (BODE) Index uses four measurements to assign COPD patients to 1 of 15 groups, each with a different estimated survival rate. The measurements are:
Three years after a BODE assessment is made, estimated mortality rates for long-standing COPD patients are approximately:
Source: McDonald, 2010.
As noted earlier, the lungs of an emphysematous patient become hyperinflated with air spaces that contribute little to gas exchange. The widened chest caused by hyperinflated lungs is difficult for the patient to expand farther when attempting to inhale. By removing lung tissue that contains dead air space, surgery can sometimes reduce the patient’s work of breathing.
In lung volume reduction surgery, 20% to 30% of the lung volume is removed from both sides of the chest. As a result, survivors can usually exercise more than they could before the surgery. Those patients who have mainly upper-lung emphysema also have an increased lifespan after this surgery. For other COPD patients, however, longevity is not increased and it may even be shortened.
The major postoperative complication of lung volume reduction surgery is continuing air leakage from the lungs into the chest. Operative mortality rates are from 4% to 10% in hospitals providing the procedure.
In some cases, individual large empty air spaces (bullae) can be surgically removed. Typical bullae in a patient with emphysema are a few centimeters in diameter. Occasionally, however, bullae can be huge, taking up as much as a third of the chest space. These giant bullae squeeze the healthier lung tissue and compress the adjacent blood vessels. By removing giant bullae, the remaining lung tissue can reexpand and some of the circulation will be restored. As with lung volume reduction surgery, a major postsurgical complication of bullectomy is persistent air leakage.
According to the National Institutes of Health (2012), the average hospital stay after most lung surgeries without complications is 5 to 7 days.
Patients with COPD have little or no ventilatory reserve, and a further compromise of their respiratory system can send them into hypoxemia. The normal wear and tear of daily life puts respiratory compromises in everyone’s path periodically. People with COPD respond poorly to these respiratory problems and often experience an increase in dyspnea, cough, and sputum production. Such episodes of suddenly worsening symptoms are called “acute exacerbations” (Hurst & Wedzicha, 2009).
Acute exacerbations of COPD can be brought on by a variety of factors. Infections, especially respiratory infections from colds to pneumonias, are common triggers. Acute exacerbations occur more often in the winter, the season with the most viral infections. Increases in air pollution can also trigger an acute exacerbation.
Acute exacerbations can be triggered by other medical conditions, especially when these conditions impinge on the cardiovascular or respiratory systems. Pneumothorax, pulmonary emboli, congestive heart failure, heart arrhythmias, chest trauma, lung atelectasis, and pleural effusions will all worsen a patient’s COPD.
Inappropriate drugs can also trigger an acute exacerbation of COPD. For example, beta-blockers and cholinergic drugs prescribed for other reasons can produce bronchospasms, or sedatives can reduce a person’s respiratory drive, which may bring on hypoxemia in COPD patients (Braithwaite & Perina, 2009).
At the same time, however, many acute exacerbations cannot be easily explained. No cause can be identified in approximately one third of the episodes of suddenly worsening COPD (Punturieri et al., 2009).
During an acute exacerbation, patients become more breathless than usual. They have chest tightness, they may begin to wheeze or to cough, and they can find it difficult to talk. In addition, their airways can become clogged with sputum, which may be yellowish or greenish and filled with white cells.
A sudden decrease in the ability to breath efficiently makes patients tachycardic and sweaty, and their percent of oxygenated hemoglobin (measured by pulse oximetry) decreases. In serious cases, patients become hypercapnic because they cannot get rid of sufficient carbon dioxide, making them acidotic and lethargic.
A patient’s regularly scheduled medications will not reverse an acute exacerbation. Instead, extra rescue medicines (short-acting bronchodilator) are needed. To prevent ventilatory decompensation from worsening, further medical assistance, including hospitalization, can be needed to treat an acute exacerbation and its cause.
Unlike attacks of asthma, which can usually be reversed quickly, acute exacerbations of COPD improve slowly even when the patient gets prompt medical help. On average, it will take a week for a person to recover from an exacerbation of COPD, and recovery from 1 out of 4 acute exacerbations takes more than a month. For patients with severe COPD, an acute exacerbation can be fatal.
As a first step in counteracting the sudden worsening of their lung functions, patients are usually advised to take a predetermined “rescue dose” of a short-acting bronchodilator. Typically, it is a beta2 agonist (albuterol, pirbuterol, or terbutaline), ipratropium, or the combination of albuterol and ipratropium. Patients should be advised to always keep their quick-relief inhaler with them (Hurst & Wedzicha, 2009).
When a sudden worsening of the ability to breathe is not improved by rescue therapy, the patient needs to be seen quickly by a doctor. Besides COPD, the patient could be experiencing a medical emergency such as pneumothorax, pulmonary embolism, anaphylaxis, airway obstruction, or myocardial infarction. When the person with COPD does not improve with the usual rescue medications or home oxygen, if available, the patient or family should call the physician or 911, depending on the severity of symptoms.
Anyone with the sudden onset of severe dyspnea should be evaluated as a medical emergency. First, it must be ascertained that the patient has a clear airway. The patient should then be checked for trauma, bleeding, shock, cardiac failure, and the inability to move air autonomously into and out of the lungs. Any of these problems require immediate treatment.
At the same time, an intravenous (IV) line should be established and a cardiac monitor connected. If the patient’s pulse oximetry shows an oxygen saturation of <98%, supplemental oxygen should be given. Blood chemistries, blood gases, and chest x-rays (both PA and lateral) should be obtained. The cardiac status should be assessed with an ECG. The possibility of a pulmonary embolus should always be considered when there is a sudden increase in dyspnea and hypoxia (Gold, 2009).
The patient should be medically stabilized. Patients with a serious instability or decompensation are admitted to an intensive care unit and the workup continues there. Mental confusion, cyanosis, lethargy, extreme muscle fatigue, worsening hypoxemia, respiratory acidosis, or the need for mechanical ventilation are all conditions best treated in intensive care (Gold, 2009).
For patients experiencing an acute exacerbation of COPD, the immediate goals are to maintain an adequate level of blood oxygen and an appropriate blood pH in the patient.
For some COPD patients, their exacerbation will be sufficiently mild that bronchodilators, steroids, and oxygen will lead to a rapid improvement. If no treatable trigger is found for this episode, the patients can often be sent home and followed outside the hospital.
Other patients’ lung functioning will have deteriorated sufficiently that these persons need to be supported in a hospital. COPD leads to chronic respiratory failure, and acute exacerbations can lead to the superposition of acute respiratory failure. The result has been called “acute-on-chronic respiratory failure.” In acute-on-chronic respiratory failure, patients have increasing dyspnea and may eventually develop an altered mental state or even respiratory arrest. Acute-on-chronic respiratory failure typically produces an acidosis, with pH <7.35 (normal is pH = 7.38–7.44) (Goldring & Wedzicha, 2008).
For acute-on-chronic respiratory failure patients, hospital therapy includes bronchodilator treatments, systemic steroids, controlled oxygen, and often, intravenous antibiotics. When necessary, steps must be taken to maintain the patient’s ventilation and circulation. Supplemental oxygen is given to keep blood oxygenation levels of 88%–92%. Meanwhile, attempts are made to identify and reverse the precipitating factors; if a specific infection has not been identified, antibiotics are sometimes given prophylactically (Goldring & Wedzicha, 2008).
Respiratory infections are frequent causes of acute exacerbations of COPD. When an acute exacerbation includes signs of infection (e.g., fever, elevated white blood-cell count, purulent sputum, or a suggestive chest x-ray), the empirical administration of antibiotics is usually recommended. When COPD patients are hospitalized for acute exacerbations, the early use of antibiotics will reduce mortality and treatment failures (Mathew et al., 2012). Likely microbes include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Pseudomonas aeruginosa, and appropriate antibiotics include:
Source: Kamangar et al., 2009.
The patient’s blood gases and blood chemistries should be watched, and supplemental oxygen given to maintain the PaO2 >60 mm Hg (oxygen saturation >~89%). In severe cases, noninvasive positive pressure mechanical ventilation (also called noninvasive ventilatory support or NIVS) with a facemask or nasal cannulas will often improve gas exchange without having to intubate the patient. Noninvasive ventilation leads to fewer secondary pneumonias and is easier to wean than endotracheal intubation (Goldring & Wedzicha, 2008).
Recovery from an acute exacerbation can take weeks to months. For those COPD patients who need to be hospitalized during an acute exacerbation, there is a 10% mortality rate.
The American Thoracic Society recommends that COPD patients be given a balance of palliative and restorative care from the very outset of the patient’s symptoms (Barnett, 2012a). This means that maintaining and, when possible, improving a patient’s quality of life should always be a prime motivator of therapy.
Early palliative care also means that patients and their families should be encouraged to consider end-of-life options early in the disease process, before the patient becomes mentally compromised or the family becomes emotionally worn out. Decisions that patients and their families will face include whether to participate in drug trials, what type of ventilation to use and for how long, whether to consider lung transplantation, whether to take advantage of hospice, and what type of end-of-life palliation is desired (Barnett, 2012a). Counseling may be provided by specially trained hospice nurses or in-hospital palliative care nurses (Iley, 2012).
Severe difficulty in breathing is an uncomfortable and upsetting problem to both patients and their families. Near the end of a COPD patient’s life, dyspnea must be eased (Barnett, 2012a):
Although patients with chronic lung disease are normally encouraged to exercise to maintain their state of fitness, there comes a time when a different approach is required and the focus shifts from prolongation of life to relief of distress. When dyspnea with exertion is extreme, it may be more appropriate to restrict activity and to focus on modifying treatments such as oxygen, opiates, and anxiolytics. Palliative treatment may include partial ventilatory support or, under rare circumstances, a tracheostomy with mechanical ventilation. Such dramatic steps to relieve dyspnea must be taken with full understanding of the ramifications and complications. Some patients may choose a morphine drip to allow a comfortable death, whereas others might choose an aggressive approach focused on prolongation of life as well as relief of discomfort. It is up to the healthcare provider to help the individual patient understand these choices (Stulbarg & Adams, 2005).
COPD develops quietly. Early in their disease, patients have measurable declines in their lung function before they develop symptoms. The first symptoms are usually an intermittent cough and some shortness of breath during exercise. Patients often dismiss these as temporary lung irritations or as a lack of physical conditioning.
After many years, the cough becomes chronic or the spells of breathlessness become more frequent. Typically, this is the stage at which people first seek medical help. As time progresses, even with bronchodilator therapy, the patient’s lung function continues to gradually decline. Occasional episodes of debilitating exacerbations become more frequent. Patients admitted to intensive care units with acute exacerbations of COPD have a mortality rate of >20%, and when the patient is older than 65 years, the mortality rate doubles. Forty percent of the COPD deaths in an ICU are from pulmonary emboli.
Eventually, dyspnea limits a COPD patient to only minimal activity. Patients are continually fatigued, they lose weight, and at some point they succumb to a respiratory illness, pulmonary embolism, heart failure, acute respiratory failure, or lung cancer. When the patient’s FEV1 has dropped to <0.75 liters/sec (very severe COPD), there is a 30% chance that they will die within a year and a 95% chance that they will die within 10 years (Roizen & Fleisher, 2009).
Health professionals who advise patients over the telephone should know straightforward answers to basic questions. Here are a few important questions and answers about COPD and smoking.
Q:What is COPD?
A:The full name for COPD is “chronic obstructive pulmonary disease.” This disease is caused by inflammation of the lungs from many years of breathing in cigarette smoke or other types of pollution. The airways in the lungs become narrowed, and in some people, the airways become clogged with mucus. These problems make it harder and harder to move air into and out of your lungs.
A person with COPD frequently feels short of breath. COPD makes normal breathing tiring, and it can make it so difficult to breathe that exercise becomes too tiring to do. COPD continues to worsen over time, especially if the person is still smoking.
Q:What causes COPD?
A:Smoking is the most common cause of COPD. Cigarette, cigar, and pipe tobacco can all cause COPD when the smoke is inhaled. Other kinds of air pollution can be just as bad as smoke if the pollution is inhaled for many years.
Anyone can get COPD from smoking, although it usually takes many years of smoking for the disease to be noticeable. A small number of people have an inherited genetic defect called alpha1-antitrypsin deficiency that makes them more likely to get the disease after only a few years of smoking or sometimes without having ever smoked at all.
Q:Is COPD contagious?
Q:Do children inherit COPD?
A:Most types of COPD are not inherited. COPD is usually caused by cigarette smoking. Teaching children not to smoke will protect them from getting COPD.
A small number of people inherit a genetic defect called alpha1-antitrypsin deficiency, which makes them unusually susceptible to developing COPD. When these people get COPD, it is the emphysema type of COPD, and it usually shows up early, in people younger than 40 years old. If you think you may have this problem, your doctor can test you to find out.
Q:Can COPD be cured?
A:There is no cure for COPD, and it is a major cause of illness and death.
Q:What is a good way to get trustworthy information about COPD?
A:The American Lung Association has a COPD center online that is full of useful information. Another good source is the COPD website of the National Heart, Lung, and Blood Institute. (See also “Resources” at the end of this course.)
Q:How do I know if I have COPD?
A:The signs and symptoms of COPD are different for each person, but common symptoms are cough, coughing up mucus, shortness of breath, wheezing, and chest tightness. COPD usually occurs in people who are at least 40 years old and who have smoked for many years. To make the diagnosis, a doctor or nurse practitioner will give you a physical exam and a set of breathing tests.
Q:What is spirometry?
A:Spirometry measures how much air you breathe and how quickly you can get air into and out of your lungs. Spirometry tests are easy and painless. You breathe forcefully into a tube, and the machine at the other end measures how much air you are moving. Spirometry can detect COPD even before you have many symptoms.
Q:I have COPD—so what do I do to fix it?
A:COPD cannot be cured, but it can be treated to make your life more comfortable. See your doctor or NP and get set up with a treatment plan tailored specifically for you. Meanwhile, quitting smoking is the single most important thing you can do to slow the progress of the disease.
Q:I have COPD. What should I do if I am having more trouble than usual catching my breath or if I am coughing more than usual?
A:If you have a set of rescue medicines that you have been told to take, go ahead and use them. Then call your doctor or NP right away.
Q:I have COPD. What do I do when I’m getting sick, like with a fever or a cold?
A:Call your doctor or NP right away.
Q:How often do I have to get flu shots for my COPD?
A:Flu can cause serious problems in people with COPD, and flu shots can reduce your chances of getting the flu. You should get a flu shot every year. In addition, you should have a pneumococcal vaccination, usually every five years.
Q:I have COPD. How do I know when I need emergency help?
A:People with COPD will have episodes called “acute exacerbations.” During these times, you will have a much harder time catching your breath. You may also have chest tightness, more coughing, a change in your sputum, or a fever. It is important to call your doctor or NP if you have any of those signs or symptoms. Specifically, you should get emergency help or advice if:
Because it is likely that you will have an acute exacerbation at some time, be prepared. Plan now and have these things easily available:
Q:I have COPD. Can I still use my fireplace at home?
A:Unless your fireplace is the only way for you to heat your home, you should not burn wood or kerosene in your home. It is important to keep the air in your house clean. Keep your windows closed and stay indoors when there is a lot of pollution or dust outside. When you cook, keep smoke and cooking vapors out of the air with an exhaust fan or open a winow or a door. Don’t let anyone smoke in your house. Avoid using any aerosol (spray) products. Don’t use strong perfumes. When your house is being painted or is being sprayed for insects, stay away from the house for as long as possible until the fumes settle.
Q:What can be done for my COPD?
A:Treatment for COPD helps prevent complications, prolong life, and improve a person’s quality of life. Quitting smoking, staying away from people who are smoking, and avoiding exposure to other lung irritants are the most important ways to reduce your risk of developing COPD or to slow the progress of the disease if you have it.
Treatment for COPD includes medicines such as bronchodilators, steroids, flu shots, and pneumococcal vaccine to avoid or to reduce further complications.
As the symptoms of COPD get worse over time, a person may have more difficulty walking and exercising. You should talk to your doctor or NP about exercise programs. Ask whether you will benefit from a pulmonary rehab (PR) program—a coordinated program of exercise, physical therapy, disease management training, advice on diet, and counseling.
Oxygen treatment and surgery (to remove part of a lung or even to transplant a lung) may be recommended for patients with severe COPD.
Q:Exactly what is pulmonary rehab?
A:Pulmonary rehabilitation (pulmonary rehab or PR) is a program that includes regular exercise, training in how to manage your disease, and practical advice, all of which help you to stay active and to remain able to carry out your day-to-day activities. After some medical breathing evaluations, you meet with a pulmonary rehab team and make a plan that is best for your disease and your lifestyle. Usually, there are meetings, exercise classes, suggestions for long-term improvements in your lifestyle, and an advisor whom you can always contact for advice.
Q: Why should I quit smoking?
A: People who stop smoking live longer. If you quit smoking before you are 35, you will live about six years longer. Even if you quit at age 55, you can still add two years to your life. By quitting smoking, you reduce your chances of getting lung disease, heart disease, and cancer. You will feel better and healthier. Smoking injures your senses of taste and smell, and quitting smoking will even make food taste better.
Q:Frankly, I like to smoke, and I know people who have lived a long time even though they were smokers. Why should I go through the agony of stopping something I enjoy? Besides, I may not even be able to quit.
A:Cigarettes are legal addictive drugs, and they are easier to buy and less expensive than illegal drugs—but smoking is gambling, with bad odds. As a smoker, you have a 1-in-3 chance of dying earlier than you would if you quit. When you do die, it will most likely be of heart disease, stroke, cancer, or COPD. Smoking is responsible for about 1 out of every 5 deaths in the United States, and almost a half million Americans die each year from diseases caused by smoking.
Your smoking can hurt the people around you. Just breathing in another person’s smoke can cause lung problems in children and can cause cancer and heart disease in adults. Pregnant women and new mothers and fathers can protect their baby’s health by stopping smoking now.
Sure, it is tough to quit smoking. Staying healthy and protecting the health of the people around you is difficult. But don’t hide behind the excuse that you can’t stop smoking. Studies suggest that everyone can quit smoking.
Q:What is the first thing I need to do once I’ve decided to quit?
A:You should set a quit date. Then make an appointment to see a doctor before the quit date. Your doctor or NP will help you devise a plan that will make quitting easier. There are a variety of anti-smoking medicines and a doctor or NP can suggest the best one for you.
Also, plan to join a support group or a stop-smoking program. The American Lung Association has an online stop-smoking program called “Freedom from Smoking Online”. Another helpful organization is Nicotine Anonymous, which runs 12-step programs with group support. Information can be found at nicotine-anonymous.org.
Here are some other general tips:
Q:What medicines should I take when I’m trying to stop smoking?
A:Nicotine is an addictive drug. For many people, nicotine replacements help to keep withdrawal symptoms to a minimum. Nicotine replacements come as patches, gums, lozenges, and an inhaler. Get your doctor to advise you when choosing which to take. Your doctor or NP can also prescribe a nicotine-free tablet called Chantix, which reduces withdrawal symptoms. Some people get help from an antidepressant called bupropion, which is a prescription medicine.
Q:Will I gain weight if I quit smoking?
A:Many smokers gain weight when they quit, but it is usually less than 10 pounds. Eat a healthy diet, stay active, and try not to let weight gain distract you from your main goal—quitting smoking. Some of the medications that help you quit may also help to delay weight gain. Remember, smoking will hurt your health much more than a few extra pounds of weight.
Q:Aren’t nicotine replacement products just as bad as smoking?
A:No, nicotine replacements do not have all the tars and poisonous gases that are found in cigarettes. Furthermore, these medicines give you less nicotine than a smoker gets from cigarettes. Nicotine replacement products (patches, gums, lozenges, or inhalers) should not be used by pregnant or nursing women. People with other medical conditions should check with their doctor before using any nicotine replacement product. It is important that smokers quit smoking completely before starting to use nicotine replacements.
Nutritional guidelines for people with COPD (Cleveland Clinic)
California Smokers Helpline
Treating Tobacco Use and Dependence (PDF) (U.S. Surgeon General)
Albertine KH, Williams MC, Hyde DM. (2005). Anatomy of the lungs. In RJ Mason, JF Murray, VC Broaddus, & JA Nadel (Eds.), Murray and Nadel’s textbook of respiratory medicine (4th ed.) (chapter 1). Philadelphia: Elsevier Saunders.
American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR). (2011). Guidelines for pulmonary rehabilitation programs (eBook) (4th ed.). Retrieved August 2012 from http://www.humankinetics.com
American Association for Clinical Chemistry (AACC). (2012). Lab tests online. Retrieved October 2012 from http://labtestsonline.org
American Dietetic Association (ADA). (2009). Chronic obstructive pulmonary disease (COPD): evidence-based nutrition practice guideline. Retrieved December 2009 from http://www.adaevidencelibrary.com
American Lung Association (ALA). (2012a). Living with COPD: a life change. Retrieved August 2012 from http://www.lung.org
American Lung Association (ALA). (2012b). Learning more about asthma. Retrieved August 2012 from http://www.lung.org
American Lung Association (ALA). (2012c). Fighting fire with fire to reduce smoking. Retrieved October 2012 from http://www.lung.org
American Lung Association (ALA). (2011). Trends in COPD (chronic bronchitis and emphysema): morbidity and mortality. Retrieved August 2012 from http://www.lung.org
American Lung Association (ALA). (2010). American Lung Association commemorates World No Tobacco Day by urging women to quit smoking. Retrieved October 2012 from http://www.lung.org
American Lung Association (ALA). (2009). Chronic obstructive pulmonary disease (COPD) fact sheet. Retrieved December 2009 from http://www.lungusa.org
Barnett M. (2012a). End of life issues in the management of COPD. Journal of Community Nursing, 26(3), 4–6.
Barnett M. (2012b). How to effectively manage COPD in care home residents. Nursing and Residential Care, 13(12), 578–581.
Bišanović S. (2012). The length of cigarette smoking is the principal risk factor in developing COPD. International Journal of Collaborative Research on Internal Medicine & Public Health (IJCRIMPH), 4(1), 45–54.
Braithwaite S & Perina D. (2009). Dyspnea. In J A Marx, et al. (Eds.), Rosen’s emergency medicine: concepts and clinical practice (7th ed.) (chapter 17). Philadelphia: Mosby.
Cazzola M, Calzetta L, & Matera MG. (2011). B2-adrenoceptor agonists: current and future direction. British Journal of Pharmacology, 163(1), 4–17. Doi: 10.1111/j.1476-5381.2011.01216.x.
Centers for Disease Control and Prevention (CDC). (2012). Smoking cessation. Retrieved August 2012 from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2011). Chronic obstructive pulmonary disease among adults aged 18 and over in the United States, 1998–2009. Retrieved August 2012 from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2009a). Faststats: Smoking. Retrieved December 2009 from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2009b). Cigarette smoking among adults and trends in smoking cessation—United States, 2008. MMWR Weekly Reports, 58(44), 1227–1232. Retrieved December 2009 from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2009c). Smoking and tobacco use. Retrieved August 2012 from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2009d). Pneumococcal polysaccharide vaccine: what you need to know. Retrieved August 2012 from http://www.cdc.gov
Chesnutt MS, Gifford AH, Prendergast TJ. (2010). Pulmonary disorders. In SJ McPhee & MA Papadakis Jr. (Eds.), Current medical diagnosis & treatment 2010 (49th ed.) (chapter 9). New York: McGraw-Hill.
Coxson HO, et al. (2009). New and current clinical imaging techniques to study chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine, 180, 588–597.
Dobler CC, Wong KK, Marks GB. (2009). Associations between statins and COPD: a systematic review. BMC Pulmonary Medicine, 9, 32–44. Retrieved from http://www.biomedcentral.com
Engelke Z. (2012). Patient education: teaching the patient with chronic obstructive pulmonary disease (COPD). Cinahl Information Systems, April, 1–5.
Everyday Health. (2012). Medications for COPD. Retrieved October 2012 from http://www.everydayhealth.com
Fairman P & Malhotra R. (2009). Alpha1-antitrypsin deficiency. Retrieved December 2009 from http://emedicine.medscape.com
Food and Drug Administration (FDA). (2009). Chantix and Zyban to get boxed warning on serious mental health events. Retrieved December 2009 from http://www.fda.gov
Gold PM. (2009). The 2007 GOLD guidelines: a comprehensive care framework. Respiratory Care, 54(8), 1040–1049.
Goldring JJP & Wedzicha JA. (2008). Managing acute on chronic respiratory failure: a guide to non-invasive ventilation. British Journal of Hospital Medicine, 69(8), 444–449.
Gonzales R & Nadler PL. (2010). Common symptoms. In SJ McPhee & MA Papadakis Jr. (Eds.), Current medical diagnosis & treatment 2010 (49th ed.) (chapter 2). New York: McGraw-Hill.
Goodfellow LT & Waugh JB. (2009). Tobacco treatment and prevention: what works and why. Respiratory Care, 54(8), 1082–1090.
Hurst JR & Wedzicha JA. (2009). Management and prevention of chronic obstructive pulmonary disease exacerbations: a state of the art review. BMC Medicine, 7, 40–46. Retrieved from http://www.biomedcentral.com
Ignatavicius DD & Workman LM. (2010). Medical-surgical nursing: patient-centered collaborative care. St. Louis: Saunders Elsevier.
Iley K. (2012). Improving palliative care for patients with COPD. Nursing Standard, 26(37), 40–46.
Kamangar N, Nikhanj NS, Sharma S. (2009). Chronic obstructive pulmonary disease. Retrieved December 2009 from http://emedicine.medscape.com
Keating GM. (2012). Tiotropium bromide inhalation powder. Drugs, 72(2), 273–300.
Laitenen T, et al. (2009). Real-world clinical data identiﬁes gender-related proﬁles in chronic obstructive pulmonary disease. COPD: Journal of Chronic Obstructive Pulmonary Disease, 6, 256–262. Doi: 10.1080/15412550903051799.
Lefebvre Q, Vandergoten T, Derom E, Marchandise E, & Liistro G. (2012). Technical aspects of spirometers connected in series. Respiratory Care, 57(8), 1273–7.
Man WD-C, Kemp P, Moxham J, Polkey MI. (2009). Exercise and muscle dysfunction in COPD. Clinical Science, 117, 281–291.
Mathew S, Zeitlin D, & Rickett K. (2012). Clinical inquiry: do antibiotics improve outcomes in COPD patients hospitalized with exacerbations? Journal of Family Practice, 61(9), 561–73.
McDonald CF. (2010). ACP journal club. An updated BODE index and a simplified ADO index predicted three-year mortality in COPD better than the original BODE index. Ann Intern Med, 152(2), JC1–12.
Millea PJ. (2009). N-acetylcysteine: multiple clinical applications. American Family Physician, 80(3), 265–269.
Motiani B, Haidri FR, & Rizvi N. (2011). Frequency of depression in chronic obstructive pulmonary disease (COPD) patients. Pakistan Journal of Medical Sciences, 27(5), 1112–1115.
National Institutes of Health (NIH). (2012). Lung surgery. Retrieved December 2012 from http://www.nlm.nih.gov
Punturieri A, Weinmann GG, Reynolds HY. (2009). Chronic obstructive pulmonary disease and acute exacerbations. In GL Mandell, JE Bennett, & R Dolin (Eds.), Principles and practice of infectious diseases (7th ed.) (chapter 62). Philadelphia: Churchill Livingstone.
Reis AL, et al. (2007). Pulmonary rehabilitation: Joint ACCP/AACVPR evidence-based clinical practice guidelines. Chest, 131(5), 4s–42s. Retrieved October 2012 from http://journal.publications.chestnet.org. Doi: 10.1378/chest.06-2418.
Restrepo RD. (2009). A stepwise approach to management of stable COPD with inhaled pharmacotherapy: a review. Respiratory Care, 54(8), 1058–1081.
Roizen MF & Fleisher LA. (2009). Anesthetic implications of concurrent diseases. In RD Miller (Ed.), Anesthesia (7th ed.) (chapter 35). Philadelphia: Churchill Livingstone.
Stulbarg MS & Adams L. (2005). Dyspnea. In RJ Mason, JF Murray, VC Broaddus, & JA Nadel (Eds.), Murray and Nadel’s textbook of respiratory medicine (4th ed.) (chapter 28). Philadelphia: Elsevier Saunders.
Swadron SP & Mandavia DP. (2009). Chronic obstructive pulmonary disease. In JA Marx et al. (Eds.), Rosen’s emergency medicine: concepts and clinical practice (7th ed.) (chapter 72). Philadelphia: Mosby.
Tarrega J, Anton A, Guell R, Mayos M, Samolski D, Marti S, Farrero E, Prats E, & Sanchis J. (2011). Predicting nocturnal hyperventilation in hypercapnic chronic obstructive pulmonary disease patients undergoing long-term oxygen therapy. Respiration, 82(1), 4–9.
Vesa ŞC, Crişan S, Macarie A, Teodorescu M, & Ghidrai O. (2009). Deep vein thrombosis: risk factors and location of thrombus. Human & Veterinary Medicine, 1(2), 03–113.
Victorson DE, Anton S, Hamilton A, Yount S, & Cella D. (2009). A conceptual model of the experience of dyspnea and functional limitations in chronic obstructive pulmonary disease. Value Health, 12(6), 1018–25.
Weitzenblum E & Chaouat A. (2009). Cor pulmonale. Chronic Respiratory Disease, 6, 177–185.