Wild Iris Medical Education
COURSE PRICE: $35.00
CONTACT HOURS: 5
This course is available until February 1, 2013.
ACCREDITATION / APPROVAL
This course is approved by Wild Iris Medical Education. Wild Iris Medical Education, Inc. is a Continuing Competency Approval Agency recognized by the Physical Therapy Board of California.
Approval of physical therapy continuing education credit varies by state. Confirm approval with your state's licensing agency before you take the course for CE credit. See Physical Therapy CE Approval for more information.
The planners and authors of this CE activity have disclosed no relevant financial relationships with any commercial companies pertaining to this activity.
Copyright © 2010 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,” and COPD is characterized by a progressively increasing airflow obstruction that cannot be fully reversed, although it can sometimes be temporarily improved by medications (Wise, 2007). In almost all cases, COPD has been caused by the long-term inhalation of pollutants, especially cigarette smoke (Punturieri et al., 2009).
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, i.e., difficulty breathing. The dyspnea of COPD feels like shortness of breath. Early on, shortness of breath occurs only during vigorous exercise. Over the years, however, the dyspnea begins to happen with mild exercise. Later, normal activities of living cause dyspnea. Finally, a person with COPD is short of breath even when sitting quietly. 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 (Reilly et al., 2008).
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 (Shapiro et al., 2005).
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. Besides reducing the lung area available for gas exchange, emphysema leads to hyperinflated lungs and obstructed airflow (Anthonisen, 2008).
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, 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 (Lokke et al., 2007).
COPD is the most common serious lung disease in the United States. Over the last few decades, there has been an increase in the percent of Americans with COPD. Currently, between 10 and 14 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 (Shapiro et al., 2005; ALA, 2009).
Eighty to ninety percent of the people who get COPD have been long-time smokers (ALA, 2009). 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 (Wise, 2007).
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 1 year is equivalent to 2 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, 2009a).
In the United States, 1 of every 7 people between the ages of 55 and 64 has moderate COPD, and 1 of every 4 people older than 75 years has moderate COPD. This is the highest rate of COPD in history because 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 (Hall & Ahmed, 2007).
More men than women have COPD. Among white Americans, for example, approximately 5% of all men have COPD, while approximately 2% of all women have the disease (Swadron & Mandavia, 2009). The difference between men and women reflects the historical tendency for men to have smoked more heavily than women.
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 (Anthonisen, 2008; ALA, 2009).
Women are twice as likely to be diagnosed with the chronic bronchitis form of COPD, while men are 1.25 times more likely to be diagnosed with the emphysematous form of COPD (ALA, 2009).
COPD Mortality by Gender: United States 2000–2005
In the twentieth century, COPD caused the deaths of more men than women. Since 2000, however, the statistics have reversed. Currently, COPD kills more women than men each year in the United States.
(Source: Drawn from data in CDC, 2008.)
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 (Wise, 2007; CDC, 2009b).
COPD is the fourth leading cause of death in the United States. Between the years 2000 and 2004, there was an average of 120,000 deaths from COPD a year, a frequency of 42 deaths per 100,000 people. Approximately 1/2 of COPD patients die within 10 years of their initial diagnosis (ALA, 2009).
The ten leading causes of death in the U.S. in 2006. (Black column indicates the subset of all heart-related deaths caused specifically by CAD, coronary artery disease.) (Source: National Heart, Lung, and Blood Institute, 2008)
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.
Lung Anatomy
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 3 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 6 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 vital capacity (VC or FVC) and the amount of air that can be exhaled in a second (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 does, however, worsen the already compromised breathing of those elderly people who have COPD (Prendergast & Russo, 2006).
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.
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 (Shapiro et al., 2005). Other causes of or contributors to COPD include air pollution, second-hand smoke, and occupational exposure to dust and chemicals (ALA, 2009).
In the United States, more than a quarter of all people who have smoked for 25 years or more develop COPD, while another 10% to 20% of smokers have measurably decreased lung function for their age (Lokke et al., 2007). 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).
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 (Reilly et al., 2008).
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.
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).
Cigarette smoking causes COPD by inciting a chronic inflammatory response to the pollutants in the smoke. Over time, this persistent inflammation leads to destruction of lung tissue, accumulation of mucus, and thickening of small airways (Reilly et al., 2008).
In COPD, inflammation begins with the activation of local macrophages in the lung tissue; in fact, 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.
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:
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. Again, chronic inflammation is at the root of the problem. Extra collagen is secreted as a natural repair response to tissue damage. In COPD, the lung is continuously damaged by chronic inflammation, and this damage is met by continuing fibrosis in an attempt to fix the damaged tissue.
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. Moreover, 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 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 can use a 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 (Gold, 2005b).
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, 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.
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 on 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” patient with moderate to severe COPD is an elderly white male with a history of smoking at least one pack of cigarettes a day for more than 40 years. He complains of general tiredness and becomes short of breath when exercising. His legs bother him when walking, so he spends most of his time sitting. If you ask him to exhale quickly, it takes him an unnaturally long time.
Other aspects of the “typical” picture range along a spectrum:
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 doctor 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 (Reilly et al., 2008).
While dyspnea is the symptom that most often brings COPD patients to a doctor, 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 does not limit the patient’s daily activities.
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 3 weeks, although in some people, coughs can hang on as long as 2 months after a respiratory illness. The coughing of COPD, however, occurs intermittently for years.
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, 2009).
The key element in the history of a COPD patient is 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 (Shapiro et al., 2005; Swadron & Mandavia, 2009).
The tripod position. Patient leans forward, resting on elbows or hands, in an effort to expand the chest and ease breathing. (Source: Jason M. McAlexander, MFA. © 2007, Wild Iris Medical Education.)
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, which 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:
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 this 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 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.
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 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 ≥96% (as determined by pulse oximetry); a person with hypoxemia of 60 mm Hg will have a hemoglobin saturation of approximately 86%.
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 alpha1-antitrypsin (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) (Wise, 2007).
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.
CT SCANS AND RADIATION EXPOSURE
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 (Gold, 2005a). For COPD, the two general classes of breathing tests are (1) measurements of lung volumes, and (2) measurements of airflow rates and 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, although 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); specifically, 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 exhale as quickly and forcefully as possible. With these testing instructions, the result is more accurately called the forced vital capacity (FVC) (Wanger & West, 2005).
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 (Miller et al., 2005).
A small, handheld spirometry device can be used for quick office or clinic tests. (Source, National Institutes of Health.)
Office spirometers come in a variety of forms. (Source: Dougherty, n.d.)
The most common spirometric measurement used for COPD is the one-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 (Qaseem et al., 2007).
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 (the FEV1) is about 3/4 of a healthy person’s vital capacity (the FVC).
If someone could exhale the lungs’ entire vital capacity in 1 second, their FEV1/FVC ratio would be 1.00. A normal person has an FEV1/FVC ration between 0.70 and 0.80; in other words, a person with normal lungs can exhale between 70% and 80% of their vital capacity in the first second. This ratio, FEV1/FVC (the percent of the vital capacity that can be exhaled in one second), declines as a person ages, but even elderly people will have FEV1/FVC >0.70 if their lungs are normal.
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 (Wagner & West, 2005).
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. Patients with COPD have an abnormally low one-second exhaled percent of vital capacity (i.e., FEV1/FVC <0.70). 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 (Wise, 2007; Swadron & Mandavia, 2009).
| Stage | Severity | FEV1/FVC |
|---|---|---|
| *Predicted FEV1 values adjusted for a person’s age, gender, height, and weight can be calculated from published equations (Pellegrino et al., 2005). Sources: Modified from Rabe et al., 2007; Ries, 2008; and Gold, 2009. |
||
| 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 |
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.
UNLIKELY TO HAVE COPD
As a quick diagnostic rule, a combination of three negative findings gives a high likelihood that the patient does not have COPD. The triad is:
Source: Qaseem et al., 2007.
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 (Jeffery, 2008).
Some useful distinctions between asthma and COPD include (Barnes, 2008):
COPD is a life-long disease. It requires special medical treatment during acute exacerbations, and after the disease reaches the level called “moderate COPD,” it requires daily medications and permanent adjustments to a patient’s lifestyle. Gross (2008) and Gold (2009) are guides to the management of COPD.
The goals of long-term COPD treatments are:
Education is important. All COPD patients should learn about their disease and should 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 (Rich & McLaughlin, 2007; Shapiro et al., 2005).
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 (Shapiro et al., 2005; Stulbarg & Adams, 2005).
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 you will help them by ordering medications that make breathing easier. Tell them there are several things that they themselves 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.
Explain to patients the importance of staying active. In addition, give them practical suggestions that will help them to cope with the inevitable limitations posed by COPD. For example, tell them:
In the United States, smoking is the major cause of COPD (CDC, 2009b). Americans start smoking in their teenage years: 90% of adult smokers began smoking before the age of 18. More than 1/4 of high school students and 1 in 10 middle school students smoke (Ranney et al., 2006).
Most patients with COPD have a long smoking history, and many will still be smoking when they are under medical care. Currently, the only way to change the course of COPD is for the patient to stop smoking. No matter how old they are and no matter how long they have been smoking, COPD patients will benefit from quitting. Workplace and public smoking bans help, and they have been shown to reduce both the use of tobacco and second-hand smoke exposure (Goodfellow & Waugh, 2009).
COPD is an insidious disease; it develops long before its effects cause people to seek medical care. The disease has become irreversibly destructive by the time that it is diagnosed, so treatment should be aggressive from the beginning. From day one, strongly urge your patients to stop smoking.
Quitting can be difficult. The nicotine in tobacco smoke is powerfully addictive. In addition, the rituals of smoking fill basic psychological needs. Therefore, when doctors 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.
Although simply advising smokers to quit is rarely effective, healthcare professionals often forget to offer help along with their advice (CDC, 2007). Many patients are not eager to quit smoking, so healthcare workers are encouraged to use a step-by-step approach, as outlined in the box below.
THE FIVE A’S FOR COUNSELING SMOKERS
Healthcare workers should use five steps—the five A’s—when counseling their patients who smoke. Taking even one step is constructive.
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. For specific recommendations, 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 the course).
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).
PHARMACOLOGIC THERAPY FOR SMOKING CESSATION
Sources: Goodfellow & Waugh, 2009; Kamangar et al., 2009.
CHANTIX AND ZYBAN HAVE FDA WARNINGS
On July 1, 2009, the U.S. Food and Drug Administration (FDA) announced that it is requiring manufacturers to put a Boxed Warning on the prescribing information for the smoking cessation drugs Chantix (varenicline) and Zyban (bupropion). The warning will highlight 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,” says 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.
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 (Stulbarg & Adams, 2005).
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 (Stulbarg & Adams, 2005; Wise, 2007; ADA, 2009). (For more information, see “Resources” at the end of the course.)
Pulmonary rehabilitation 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).
2008 ACCP/AACVPR GUIDELINES FOR PULMONARY REHABILITATION
The updated American College of Chest Physicians/American Association of Cardiovascular and Pulmonary Rehabilitation guidelines on pulmonary rehabilitation (PR) for patients with COPD includes these key statements:
Appropriate PR lessens dyspnea and improves the quality of life
Required elements of PR include:
- Education on self-care and on prevention and management of acute exacerbations
- A regular, individually tailored exercise program
- Target muscles: muscles of ambulation and upper-body muscles (specific training of breathing muscles is not essential)
- Types of training:
- Both low- and high-intensity aerobic training (for lower limbs, high-intensity training is most beneficial)
- Endurance training of upper extremities
- Strength training to increase muscle mass and strength
- Length of program: minimum of 6–12 weeks
- Oxygen: supplemental oxygen should be used for patients with severe hypoxemia on exercise
Source: Ries, 2008.
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).
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:
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 (Stulbarg & Adams, 2005).
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).
The medicines currently available for COPD do not significantly change the progressive decline in lung function that is caused by the disease (Gross, 2008). Instead, 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 (Hall & Ahmed, 2007). Medications (bronchodilators) used to reduce airflow obstruction are not typically given to asymptomatic COPD patients (Qaseem et al., 2009). Restrepo (2009) presents a detailed discussion of the management of stable COPD using inhaled medications.
| Sources: Gold, 2009; Kamangar et al., 2009; and Restrepo, 2009. | ||
| Bronchodilators | ||
|---|---|---|
| Anticholinergic | Short-acting |
|
| Long-acting |
|
|
| Beta-agonist | Short-acting |
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| Long-acting |
|
|
| Premixed Combination Inhalers |
|
|
| Phosphodiesterase Inhibitor |
|
|
| Anti-Inflammatory Agents | ||
| Corticosteroids |
|
|
| Premixed Combination Inhalers (long-acting) |
|
|
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 lung’s 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 (Gross, 2008; Qaseem et al., 2009).
Airway muscles are smooth muscles, which are 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 bronchodilator that they can use to recover from a bout of suddenly worsening dyspnea (Restrepo, 2009). Either short-acting parasympathetic or short-acting sympathetic bronchodilators can be used as fast-relief medications.
The parasympathetic bronchodilators are anticholinergic drugs, which relax airway muscles by blocking the effect of acetylcholine. The classic anticholinergic drug is atropine, but atropine has unwanted side effects because it gets through the blood-brain barrier and into the central nervous system (CNS). The anticholinergic drugs used for COPD do not get into the CNS, and their side effects are in the periphery, causing, for example, pupillary dilation, blurred vision, and dry mouth (Hall & Ahmed, 2007).
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, recent studies show that tiotropium (Spiriva) is a more effective drug (Qaseem et al., 2007; Gross, 2008). 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 (Gross, 2008). Tiotropium is inhaled as a powder via a dry powder inhaler (DPI).
One class of sympathetic 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; this widens airways. 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.
WHAT ARE BETA2 ADRENERGIC AGONISTS?
When the sympathetic nervous system is activated, we get a “fight or flight” response—the heart beats faster and harder, the lungs’ airways widen, sugar is released into the bloodstream, and peripheral blood vessels narrow, sending more blood to central organs and muscles. To produce this response, epinephrine and norepinephrine are secreted by sympathetic nerve endings, and the neurotransmitters then activate adrenergic receptors.
Adrenergic agonists are chemicals like epinephrine and norepinephrine that can cause sympathetic responses. There are two main types of adrenergic receptors, alpha and beta. Lung airways have mainly beta2 receptors, while the heart has mainly beta1 receptors. To limit the side effects on other organs, COPD is treated using beta2 agonists, such as albuterol.
Source: Westfall & Westfall, 2006.
The short-acting beta2 agonists, which include albuterol (Accuneb, ProAir, Proventil, and Ventolin) and metaproterenol (Alupent), are the most commonly prescribed sympathetic 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 sympathetic bronchodilators, the phosphodiesterase inhibitors, 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.
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. 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 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, it does not have the side effects of sympathetic drugs, and it is generally more effective than the comparable twice-daily beta agonists. 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 schedule 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 2 or 3 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 (i.e., 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 (Hall & Ahmed, 2007). 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.
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 (Hall & Ahmed, 2007).
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 (Rich & McLaughlin, 2007; 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 that they will be 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 <55–60 mm Hg (an oxygen saturation of less than ~85–89%) at rest, it is recommended that supplemental oxygen should be given continuously—which means, in practical terms, more than 19 hours per day (Qaseem et al., 2007).
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 face masks 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.
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.)
Nonetheless, 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 (Gold, 2005a).
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.) 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.
BODE INDEX
The BODE Index uses four measurements to assign COPD patients to one of four groups, each with a different estimated survival rate. The measurements are:
Four years after a BODE assessment is made, estimated survival rates are approximately:
Source: Celli et al., 2004.
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.
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—typically, short-acting bronchodilators—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 even 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.
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 the person needs 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).
ANTIBIOTICS FOR ACUTE EXACERBATIONS OF COPD
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. 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 (Lanken et al., 2008). 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 (Lanken et al., 2008).
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 (Lanken et al., 2008).
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.
What Is COPD?
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.
What causes COPD?
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.
Is COPD contagious?
No.
Do children inherit COPD?
Most types of COPD are not inherited. COPD is usually caused by cigarette smoking. Teach 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.
Can COPD be cured?
There is no cure for COPD, and it is a major cause of illness and death.
What is a good way to get trustworthy information about COPD?
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.
How do I know if I have COPD?
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 will give you a physical exam and a set of breathing tests.
What is spirometry?
Spirometry measures how much air you breathe and how quickly you can get air into and out of your lungs. The 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.
I have COPD—so what do I do to fix it?
COPD cannot be cured, but it can be treated to make your life more comfortable. See your doctor 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.
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?
If you have a set of rescue medicines that you have been told to take, then go ahead and use them. Then call your doctor right away.
I have COPD. What do I do when I’m getting sick, like with a fever or a cold?
Call your doctor right away.
How often do I have to get flu shots for my COPD?
Flu (influenza) 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.
I have COPD. How do I know when I need emergency help?
People with chronic obstructive pulmonary disease (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 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:
I have COPD. Can I still use my fireplace at home?
Unless it 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 window 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.
What can be done for my COPD?
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 about exercise programs. Ask whether you will benefit from a pulmonary rehab 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.
Exactly what is pulmonary rehab?
Pulmonary rehabilitation (“pulmonary rehab”) 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.
Why should I quit smoking?
People who stop smoking live longer. If you quit smoking before you’re 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.
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.
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.
What’s more, your smoking hurts 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’s 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.
What is the first thing I need to do once I’ve decided to quit?
You should set a quit date. Then make an appointment to see a doctor before the quit date. Your doctor will help you devise a plan that will make quitting easier. There are a variety of anti-smoking medicines, and a doctor 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 http://www.nicotine-anonymous.org.
Here are some other general tips:
What medicines should I take when I’m trying to stop smoking?
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 can also prescribe a new nicotine-free tablet called Chantix, which reduces withdrawal symptoms. Some people get help from an antidepressant called bupropion, which is also a prescription medicine.
Will I gain weight if I quit smoking?
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.
Aren’t nicotine replacement products just as bad as smoking?
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.
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http://www.thoracic.org/sections/copd/
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Freedom From Smoking® Online (American Lung Association’s online smoking cessation program)
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Nicotine Anonymous (A 12-step program with group support)
http://www.nicotine-anonymous.org
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