Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Pulmonary Disease (COPD)

Copyright © 2010 Wild Iris Medical Education, Inc. All Rights Reserved.

By Michael Jay Katz, MD, PhD

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).

LEARNING OBJECTIVESUpon completion of this course, you will be able to:

Discuss airway obstruction and describe the two major forms of COPD.

Explain the damage to the lungs caused by COPD.

Identify the causes of COPD.

Describe characteristic findings in the history, physical exam, and lab values of a

patient with COPD.

Summarize the components of a long-term treatment plan for COPD.

Understand the goals and techniques of pulmonary rehabilitation.

Discuss acute exacerbations of COPD and their treatment.

Respond to telephoned questions from lay people about COPD and smoking.

WHAT IS COPD?

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 Two Major Forms of COPD

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).

EMPHYSEMA

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).

CHRONIC BRONCHITIS

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).

Airflow Obstruction: The Essence of COPD

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.

Prevention

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 INCIDENCE

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).

Age of Onset

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).

Gender

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.)

Race

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).

Mortality Rates

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)

PATHOPHYSIOLOGY OF COPD

COPD and Lung Tissue

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.

NORMAL LUNGS

Before exploring the details of COPD’s inflammatory damage, here is a review of

the structure and function of normal lungs.

Structure

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).

Function

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).

LUNGS WITH COPD

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.

Development of COPD

Smoke inhalation, sometimes compounded by certain genetic factors, is the

primary cause of COPD.

SMOKE: THE MAIN CAUSE

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).

Airway Sensitivity

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).

AAT Deficiency

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).

THE LUNG’S INFLAMMATORY RESPONSE TO SMOKING

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.

Enzymatic Destruction of Terminal Airways

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:

Destruction of alveoli

Loss of lung elasticity

Loss of lung supporting tissue

The collapse of small airways

Fibrosis and the Narrowing of Small Airways

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:

Mucus cells proliferate and become larger; this generates excess

mucus.

The smooth muscle in the airway walls thickens.

The airway walls bulge with invading inflammatory cells.

Functional Effects of COPD

REDUCED FEV1

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.

HYPERINFLATION OF THE LUNGS

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.

HYPOXEMIA AND HYPERCAPNIA

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).

PULMONARY HYPERTENSION

COPD also affects the blood vessels in the lung. COPD:

Destroys lung capillaries

Thickens the walls of small pulmonary blood vessels

Constricts lung arteries due to chronic hypoxia and acidemia

Constricts lung arteries due to the physical pressure of hyperinflated

lungs

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).

DAMAGE BEYOND THE LUNGS

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.

DYSPNEA AND ITS SPIRALING EFFECTS

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:

The urge to breathe. This sensation is triggered by exercise or by the

metabolic results of exercise—hypoxemia, hypercapnia, and metabolic

acidosis.

Difficulty breathing. This sensation is produced by excess chest

movement and by unusual effort required by the muscles of respiration

during breathing.

Anxiety. This sensation can be caused by a fear of suffocating or by a

memory of past discomfort with breathlessness. (The anxiety of dyspnea

can also come from entirely different sources of stress that are

happening at the time.) (Stulbarg & Adams, 2005)

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).

CLINICAL APPEARANCE OF STABLE COPD

The “Typical” COPD Patient

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:

If this person is on the emphysematous end of the spectrum, he will tend

to be thin and have a wide, barrel-shaped chest. He will always feel out

of breath. When he coughs, he will not produce much sputum. On chest

examination, this person’s breath sounds will be distant and relatively

clear.

If this person is on the chronic bronchitis end of the spectrum, he will

tend to be of normal weight or overweight. He will cough frequently and

will bring up sputum. On chest examination, his breath sounds will

include rales (dry crackles), rhonchi (wet crackles), and wheezes. A

COPD patient with chronic bronchitis will get more respiratory infections

than normal (Punturieri et al., 2009).

Chief Complaints

Patients with COPD usually present with the complaints of dyspnea and coughing.

DYSPNEA

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:

The urge to breathe. COPD patients have airway obstruction, and they

cannot fully empty their lungs before they need to take another breath.

The residual air, which keeps the lungs hyperinflated, dilutes the oxygen

content of the newly inhaled air. Thus, these people feel hypoxemic.

Difficulty breathing. COPD patients have hyperinflated lungs. Their

chests remain overly expanded in the resting state (i.e., after exhaling).

It is difficult for the respiratory muscles to expand their chest farther

when attempting to take a new breath. Thus, these people put an

unusual effort into breathing.

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).

COUGH

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.

Medical History

HISTORY OF THE CHIEF COMPLAINT

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).

SMOKING

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.

OTHER IMPORTANT INFORMATION

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:

Allergy history. Asthma and other allergic syndromes that affect the

respiratory system can worsen (or mimic) COPD.

Symptoms of GERD. Gastroesophageal reflux disease (GERD) can

cause chronic cough and can sometimes be confused with chronic

bronchitis.

Symptoms of clinical depression. Depression is more common in

people with chronic illnesses such as COPD (Anthonisen, 2008).

Physical Exam

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).

GENERAL APPEARANCE

Patients with emphysematous COPD are typically thin but barrel-

chested. They tend to breathe through pursed lips, and they sit leaning

forward in a “tripod position”; this posture widens the chest as much as

possible by supporting the upper body on the elbows or the extended

arms.

The tripod position. Patient leans forward, resting on elbows

or hands, in an effort to expand the chest and ease breathing.

(Source: Jason M. McAlexander, MFA. © 2007, Wild Iris

Medical Education.)

Patients with chronic bronchitis COPD are typically of normal weight or

overweight. They have a productive cough and may be cyanotic. At rest,

their rate of respiration is high, often more than 20 breaths per minute.

Patients may present as dull and irritable because their state of

consciousness can be clouded by hypoxemia.

WEIGHT

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.

CHEST

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.

LUNGS

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.

HEART

COPD can injure the heart in two major ways:

The chronic inflammatory state of COPD predisposes a person to

develop coronary artery disease. Therefore, the history and physical

examination of a patient with COPD should look for evidence of

ischemic heart problems.

COPD can cause pulmonary hypertension, which strains the right

ventricle of the heart. Pulmonary hypertension will intensify the

pulmonary component of the second heart sound. In addition, pulmonary

hypertension can cause tricuspid valve insufficiency, which can be heard

as a holosystolic murmur loudest along the left sternal border. When

pulmonary hypertension causes right-sided heart failure (cor pulmonale),

the patient will have jugular venous distension and edema of the legs

and ankles.

Laboratory Findings

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.

BLOOD OXYGEN LEVELS

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).

Arterial Blood Gases

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.

Pulse Oximetry

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%.

HEMATOCRIT

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%).

ALPHA1-ANTITRYPSIN LEVELS

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.

Imaging Studies

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

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:

When COPD includes significant emphysema, the chest is widened, the

diaphragm is flattened, and the lung fields have fainter and fewer

vascular markings. Emphysema can make the heart look long, narrow,

and vertical, and the airspace behind the heart can be enlarged.

When COPD includes significant chronic bronchitis, chest x-rays have a

“dirty” look. There are more vascular markings and more nonspecific

bronchial markings, and the walls of the bronchi look thicker than normal

when viewed end-on. Often, the heart appears enlarged (Swadron &

Mandavia, 2009).

COMPUTED TOMOGRAPHY (CT) SCANS

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).

Lung Function Tests

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.

LUNG VOLUME

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).

AIRFLOW RATES

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).

Ranking the Severity of COPD

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).

STAGING OF COPD

Stage Severity FEV1/FVC

*Pred ic ted FEV1 va lues ad jus ted for a person’s age , gender , he igh t , and weight can be ca lcu la ted f rom publ i shed equa t ions (Pe l legr ino e t a l . , 2005) .Sources : Modi f ied f rom Rabe e t a l . , 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

Differential Diagnosis, including Asthma

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:

The patient has never smoked.

The patient reports no wheezing.

No wheezing is heard on physical examination.

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):

Asthma usually appears in people <30 years of age, while COPD

typically appears in people >40 years of age.

Asthmatic attacks are reversed quickly and completely by medications,

while the symptoms of COPD are reversed only modestly and

temporarily by medications.

Asthma often runs in families, while COPD usually does not.

Only 20% to 30% of asthmatic patients have been smokers, and those

who smoke have less than a 20 pack-year history. On the other hand,

90% to 95% of COPD patients have been smokers, and most have

greater than a 20 pack-year history of smoking.

LONG-TERM TREATMENT OF COPD

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:

Slow the progression of the disease

Ease the symptoms

Increase the patient’s ability to be mobile and to do activities of daily

living

Prevent acute exacerbations

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:

Mild COPD is usually treated with short-acting bronchodilators, which

are used as needed for dyspnea.

Moderate COPD requires regular treatments with bronchodilators,

sometimes with the addition of inhaled corticosteroids. At this stage,

patients are often enrolled in a pulmonary rehabilitation program.

Severe COPD typically requires two or more bronchodilators regularly.

Inhaled corticosteroids are added to the regimen to prevent repeated

acute exacerbations.

Very severe COPD usually needs the addition of long-term oxygen

therapy. Surgical treatments can be appropriate at this stage.

(Source: National Institutes of Health.)

Therapeutic Lifestyle Changes

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).

PATIENT EDUCATION

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:

Don’t push yourself. Slow the speed at which you do things, and stop

and rest when you are tired.

Pace your activities and plan strenuous activities for times when you

have the most energy. For example, you will feel best soon after you

take your bronchodilator medicines. On the other hand, wait an hour

after meals before you do activities.

Sit on a chair or stool in the shower—don’t stand. Likewise, sit while you

shave, comb your hair, and brush your teeth.

Don’t use products that are hard on the lungs, such as hair sprays,

spray-on deodorants, or strong perfumes.

Use the exhaust fan in your kitchen to make it less likely that you will

breathe smoke and cooking vapors.

Wear slip-on shoes so you don’t have to bend over to tie laces.

Make sure your occupation does not require more physical exercise

than you can actually do. Consider setting smaller goals at work and

allow more time to finish tasks.

Find out how to get a daily air pollution report, and don’t go outside on

days with moderate or severe pollution.

Ask people not to smoke in your home or work area.

SMOKING CESSATION

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.

Counseling Patients

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.

1. Ask. Ask the patient if they smoke.

2. Advise. Strongly advise quitting.

3. Assess. Ask the patient whether they are ready to quit.

4. Assist. Help to formulate a workable smoking cessation plan, including

medications and regular interactions with a counselor.

5. Arrange. Take steps to put the plan into action: organize the necessary

medications, counseling, and follow-up visits.

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).

Pharmacologic Therapy

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

Nicotine replacements. To lessen withdrawal symptoms, nicotine can

be taken without smoking. Nicotine replacements are available as

gum, lozenges, transdermal patches, inhalers, and nasal sprays.

These should be used on a regular schedule and PRN (as needed for

cigarette cravings) for about two weeks, and then the doses should be

tapered. Nicotine patches are marketed as Habitrol and NicoDerm CQ;

nicotine gum includes Nicorette.

Antidepressants. One antidepressant, bupropion SR (sustained-

release) or Zyban, is approved by the FDA to help patients for whom

nicotine replacement therapy has not worked.

Nicotine agonists. In 2006, varenicline (Chantix), a nicotine agonist,

was approved by the FDA for anti-smoking therapy. Varenicline binds

to nicotine receptors and prevents nicotine from activating the

receptors while producing a smaller stimulant effect than nicotine.

Sources: Goodfel low & 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.

KEEPING AIRWAYS CLEAR

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.

NUTRITIONAL THERAPY

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

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

o Target muscles: muscles of ambulation and

upper-body muscles (specific training of breathing

muscles is not essential)

o 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).

Typical Programs

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:

Exercises for reconditioning the upper body and exercises aimed at

strengthening respiratory muscles.

Breathing instruction that teaches patients how to slow their rate of

breathing by pursing their lips. Also, instruction on how to rest the upper

respiratory muscles by using abdominal breathing instead of chest

breathing.

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).

Neuromuscular Stimulation

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).

Medications

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.

COMMONLY PRESCRIBED COPD MEDICINES

Sources : Gold , 2009; Kamangar e t a l . , 2009; and Res t repo , 2009 .

Bronchodilators

Anticholinergic Short-acting ipratropium (Atrovent)

Long-acting tiotropium (Spiriva)

Beta-agonist Short-acting albuterol (Accuneb, ProAir, Proventil, Ventolin,

VoSpire)

fenoterol (Berotec)

levalbuterol (Xopenex)

metaproterenol ( Alupent)

pirbuterol (Maxair)

salbutamol (albuterol)

terbutaline (Brethaire, Brethine)

Long-acting arformoterol (Brovana)

formoterol (Oxis, Foradil)

salmeterol (Serevent)

Premixed Combination Inhalers ipratropium & albuterol (DuoNeb, Combivent)

ipratropium & fenoterol (DuoVent)

Phosphodiesterase Inhibitor theophylline (Aminophylline, Theo-24, Slo-bid, 

Theo-Dur)

Anti-Inflammatory Agents

Corticosteroids beclomethasone (Beclovent, Qvar)

budesonide (Pulmicort)

fluticasone (Flovent)

prednisone (Sterapred)

triamcinolone (Azmacort)

Premixed Combination Inhalers (long-acting) formoterol & budesonide (Symbicort)

salmeterol & fluticasone (Advair)

BRONCHODILATORS

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.

Parasympathetic Bronchodilators

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).

Sympathetic Bronchodilators: Beta2 Adrenergic Agonists

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: Westfal l & Westfal l , 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.

Sympathetic Bronchodilators: Phosphodiesterase Inhibitors

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.

Bronchodilator Regimens

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

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.

OTHER MEDICATIONS

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:

Studies show that mucolytic agents (e.g., carbocisteine) appear to be

effective adjuncts to long-term drug regimens in place of inhaled

corticosteroids (Hurst & Wedzicha, 2009).

In some studies, the addition of erythromycin to the long-term drug

regimen have reduced the frequency of acute exacerbations (Hurst &

Wedzicha, 2009).

Fast-onset, ultra-long-acting (>24 hrs.) inhaled beta2 agonists, such as

indacaterol and carmoterol, are now in phase III clinical testing

(Restrepo, 2009).

Initial studies suggest that the regular oral administration of statins might

lessen mortality and morbidity of COPD patients (Dobler et al., 2009).

Oral n-acetylcysteine, which is used as an antidote for acetaminophen

overdose, may prevent or reduce the frequency of acute exacerbations

of COPD (Millea, 2009).

VACCINATIONS

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).

Oxygen Therapy

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).

CONTINUOUS OXYGEN

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 DELIVERY SYSTEMS

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.

HAZARDS

Medical. There is a small risk that too high a concentration of inspired

oxygen will suppress the respiratory drive of COPD patients. Long-term

low-flow oxygen therapy is probably safest when the amount of oxygen

delivered gives the patient a PaO2 of 60–65 mm Hg, which is toward the

low end of the acceptable range of inspired oxygen (Kamangar et al.,

2009).

Physical. Concentrated oxygen is flammable and poses a fire hazard.

Patients and their families cannot smoke or use open flames near the

oxygen equipment.

AIR TRAVEL

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 for COPD

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).

LUNG TRANSPLANTATION

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:

1. Body mass index (BMI)

2. Degree of airflow obstruction (FEV1)

3. Amount of dyspnea (MMRC dyspnea scale)

4. Exercise capacity (distance walked in 6 minutes)

Four years after a BODE assessment is made, estimated survival rates are

approximately:

82% for group 1

68% for group 2

57% for group 3

18% for group 4

Source: Cell i et al. , 2004.

LUNG VOLUME REDUCTION

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.

BULLECTOMY

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.

ACUTE EXACERBATION OF COPD

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).

Causes of Acute Exacerbations

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).

Signs and Symptoms of an Acute Exacerbation

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.

Treatment of an Acute Exacerbation

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.

RESCUE MEDICATIONS

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).

EMERGENCY EVALUATION

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).

MEDICAL MANAGEMENT

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:

cefuroxime (Zinacef)

azithromycin (Zithromax)

clarithromycin (Biaxin)

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.

END-STAGE CARE

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).

PROGNOSIS

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).

Chronic Obstructive Pulmonary Disorder (COPD) Case StudyPosted by: Lhynnelli, RN

August 10, 2009 · Comments (8) 

34

INTRODUCTION:

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow

limitation that is not fully reversible. This newest definition COPD, provided by the Global

Initiative for Chrnonic Obstructive Lung Disease (GOLD), is a broad description that better

explains this disorder and its signs and symptoms (GOLD, World Health Organization [WHO] &

National Heart, Lung and Blood Institute [NHLBI], 2004). Although previous definitions have

include emphysema and chronic bronchitis under the umbrella classification of COPD, this was

often confusing because most patient with COPD present with over lapping signs and

symptoms of these two distinct disease processes.

COPD may include diseases that cause airflow obstruction (e.g., Emphysema, chronic

bronchitis) or any combination of these disorders. Other diseases as cystic fibrosis,

bronchiectasis, and asthma that were previously classified as types of chronic obstructive lung

disease are now classified as chronic pulmonary disorders. However, asthma is now considered

as a separate disorder and is classified as an abnormal airway condition characterized primarily

by reversible inflammation. COPD can co-exist with asthma. Both of these diseases have the

same major symptoms; however, symptoms are generally more variable in asthma than

in COPD.

Currently, COPD is the fourth leading cause of mortality and the 12th leading cause of disability.

However, by the year 2020 it is estimated that COPD will be the third leading cause of death

and the firth leading cause of disability (Sin, McAlister, Man. Et al., 2003). People

with COPDcommonly become symptomatic during the middle adult years, and the incidence of

the disease increases with age.

ANATOMY AND PHYSIOLOGY:

The respiratory system consists of all the organs involved in breathing. These include the nose,

pharynx, larynx, trachea, bronchi and lungs. The respiratory system does two very important

things: it brings oxygen into our bodies, which we need for our cells to live and function properly;

and it helps us get rid of carbon dioxide, which is a waste product of cellular function. The nose,

pharynx, larynx, trachea and bronchi all work like a system of pipes through which the air is

funneled down into our lungs. There, in very small air sacs called alveoli, oxygen is brought into

the bloodstream and carbon dioxide is pushed from the blood out into the air. When something

goes wrong with part of the respiratory system, such as an infection like pneumonia, chronic

obstructive pulmonary diseases, it makes it harder for us to get the oxygen we need and to get

rid of the waste product carbon dioxide. Common respiratory symptoms include breathlessness,

cough, and chest pain.

The Upper Airway and Trachea

When you breathe in, air enters your body through your nose or mouth. From there, it travels

down your throat through the larynx (or voicebox) and into the trachea (or windpipe) before

entering your lungs. All these structures act to funnel fresh air down from the outside world into

your body. The upper airway is important because it must always stay open for you to be able to

breathe. It also helps to moisten and warm the air before it reaches your lungs.

The Lungs

Structure

The lungs are paired, cone-shaped organs which take up most of the space in our chests, along

with the heart. Their role is to take oxygen into the body, which we need for our cells to live and

function properly, and to help us get rid of carbon dioxide, which is a waste product. We each

have two lungs, a left lung and a right lung. These are divided up into ‘lobes’, or big sections of

tissue separated by ‘fissures’ or dividers. The right lung has three lobes but the left lung has

only two, because the heart takes up some of the space in the left side of our chest. The lungs

can also be divided up into even smaller portions, called ‘bronchopulmonary segments’.

These are pyramidal-shaped areas which are also separated from each other by membranes.

There are about 10 of them in each lung. Each segment receives its own blood supply and air

supply.

COPD VERSUS HEALTHY LUNG

How they work

Air enters your lungs through a system of pipes called the bronchi. These pipes start from the

bottom of the trachea as the left and right bronchi and branch many times throughout the lungs,

until they eventually form little thin-walled air sacs or bubbles, known as the alveoli. The alveoli

are where the important work of gas exchange takes place between the air and your blood.

Covering each alveolus is a whole network of little blood vessel called capillaries, which are very

small branches of the pulmonary arteries. It is important that the air in the alveoli and the blood

in the capillaries are very close together, so that oxygen and carbon dioxide can move (or

diffuse) between them. So, when you breathe in, air comes down the trachea and through the

bronchi into the alveoli. This fresh air has lots of oxygen in it, and some of this oxygen will travel

across the walls of the alveoli into your bloodstream. Traveling in the opposite direction is

carbon dioxide, which crosses from the blood in the capillaries into the air in the alveoli and is

then breathed out. In this way, you bring in to your body the oxygen that you need to live, and

get rid of the waste product carbon dioxide.

Blood Supply

The lungs are very vascular organs, meaning they receive a very large blood supply. This is

because the pulmonary arteries, which supply the lungs, come directly from the right side of

your heart. They carry blood which is low in oxygen and high in carbon dioxide into your lungs

so that the carbon dioxide can be blown off, and more oxygen can be absorbed into the

bloodstream. The newly oxygen-rich blood then travels back through the paired pulmonary

veins into the left side of your heart. From there, it is pumped all around your body to supply

oxygen to cells and organs.

The Work of Breathing

The Pleurae

The lungs are covered by smooth membranes that we call pleurae. The pleurae have two

layers, a ‘visceral’ layer which sticks closely to the outside surface of your lungs, and a ‘parietal’

layer which lines the inside of your chest wall (ribcage). The pleurae are important because they

help you breathe in and out smoothly, without any friction. They also make sure that when your

ribcage expands on breathing in, your lungs expand as well to fill the extra space.

The Diaphragm and Intercostal Muscles

When you breathe in (inspiration), your muscles need to work to fill your lungs with air. The

diaphragm, a large, sheet-like muscle which stretches across your chest under the ribcage,

does much of this work. At rest, it is shaped like a dome curving up into your chest. When you

breathe in, the diaphragm contracts and flattens out, expanding the space in your chest and

drawing air into your lungs. Other muscles, including the muscles between your ribs (the

intercostal muscles) also help by moving your ribcage in and out. Breathing out (expiration)

does not normally require your muscles to work. This is because your lungs are very elastic,

and when your muscles relax at the end of inspiration your lungs simply recoil back into their

resting position, pushing the air out as they go.

The Respiratory System and Ageing

The normal process of ageing is associated with a number of changes in both the structure and

function of the respiratory system. These include:

Enlargement of the alveoli. The air spaces get bigger and lose their elasticity, meaning that

there is less area for gases to be exchanged across. This change is sometimes referred to

as ‘senile emphysema’.

The compliance (or springiness) of the chest wall decreases, so that it takes more effort to

breathe in and out.

The strength of the respiratory muscles (the diaphragm and intercostal muscles) decreases.

This change is closely connected to the general health of the person.

All of these changes mean that an older person might have more difficulty coping with increased

stress on their respiratory system, such as with an infection like pneumonia, than a younger

person would.

PREDISPOSING FACTORS

Risk factors for COPD include environmental exposures and host factors. The most important

risk factor for COPD is cigarette smoking. Other risk factors are pipe, cigar, and other types of

tobacco smoking. In addition, passive smoking contributes to respiratory symptoms and COPD.

Smoking depresses the activity of scavenger cells and affects the respiratory tract’s ciliary

cleansing mechanism, which keeps breathing passages free of inhaled irritants, bacteria, and

other foreign matter. When smoking damages this cleansing mechanism, airflow is obstructed

and air becomes trapped behind the obstruction. The alveoli greatly distend, diminished lung

capacity. Smoking also irritates the goblet cells and mucus glands, causing an increased

accumulation of mucus, which in turn produces more irritation, infection, and damage to the

lung. In addition, carbon monoxide (a by product of smoking) combines with hemoglobin to form

carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen

efficiently.

A host risk factor for COPD is a deficiency of alpha antitrypsin, an enzyme inhibitor that protects

the lung parenchyma from injury. This deficiency predisposes young people to rapid

development of lobular emphysema, even if they do not smoke. Genetically susceptible people

are sensitive to environmental factors (eg. Smoking, air pollution, infectious agents, allergens)

and eventually developed chronic obstructive symptoms. Carriers of this genetic defect must be

identified so that they can modify environmental risk factors to delay or prevent overt symptoms

of disease.

PATHOPHYSIOLOGY

In COPD, the airflow limitation is both progressive and associated with an abnormal

inflammatory response of the lungs to noxious particles or gases. The inflammatory response

occurs throughout the airways, parenchyma, and pulmonary vasculature. Because of the

chronic inflammation and the body’s attempts to repair it, narrowing occurs in the small

peripheral airways. Over time, this injury-and-repair process causes scar tissue formation and

narrowing of the airway lumen. Airflow obstruction may also be caused by parenchymal

destruction, as is seen with emphysema, a disease of the alveoli or gas exchange units.

In addition to inflammation, processes related to imbalances of proteinases and antiproteinases

in the lung may be responsible for airflow limitation. When activated by chronic inflammation,

proteiness and other substances may be released, damaging the parenchyma of the lung. The

parenchymal changes may occur as a consequence of inflammation or environmental or genetic

factors (eg. Alpha1-antitrypsin deficiency).

Early in the course of COPD, the inflammatory response causes pulmonary vasculature

changes that are characterized by thickening of the vessel wall. These changes may result from

exposure to cigarette smoke, use of tobacco products, and the release of inflammatory

medicators.

CHRONIC BRONCHITIS

Lung damage and inflammation in the large airways

results in chronic bronchitis. Chronic bronchitis is

defined in clinical terms as a cough with sputum

production on most days for 3 months of a year, for 2

consecutive years. In the airways of the lung, the

hallmark of chronic bronchitris is an increased

number (hyperplasia) and increased size

(hypertrophy) of the goblet cells and mucous glands

of the airway. As a result, there is more mucus than

usual in the airways, contributing to narrowing of the

airways and causing a cough with sputum.

Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is

followed by scarring and remodeling that thickens the walls and also results in narrowing of the

airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change

in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the

airway wall). The consequence of these changes is a limitation of airflow.

Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema

were commonly referred to as “blue bloaters” because of the bluish color of the skin and lips

(cyanosis) seen in them. The hypoxia and fluid retention leads to them being called “Blue

Bloaters.”

ACUTE BRONCHITIS

PHYSICAL MANIFESTATIONS

One of the most common symptoms of COPD is shortness of breath (dyspnea). People

withCOPD commonly describe this as: “My breathing requires effort”, “I feel out of breath”, or “I

can not get enough air in”. People with COPD typically first notice dyspnea during vigorous

exercise when the demands on the lungs are greatest. Over the years, dyspnea tends to get

gradually worse so that it can occur during milder, everyday activities such as housework. In the

advanced stages of COPD, dyspnea can become so bad that it occurs during rest and is

constantly present. Other symptoms of COPD are a persistent cough, sputum or mucus

production, wheezing, chest tightness, and tiredness. People with advanced (very

severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish

discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon

dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of

advanced COPD is cor pulmonale, a strain on the heart due to the extra work required by the

heart to pump blood through the affected lungs. Symptoms of cor pulmonale are peripheral

edema, seen as swelling of the ankles, and dyspnea.

There are a few signs of COPD that a healthcare worker may detect although they can be seen

in other diseases. Some people have COPD and have none of these signs. Common signs are:

tachypnea, a rapid breathing rate

wheezing sounds or crackles in the lungs heard through a stethoscope

breathing out taking a longer time than breathing in

enlargement of the chest, particularly the front-to-back distance (hyperinflation)

active use of muscles in the neck to help with breathing

breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i.e.

barrel chest).

EMPHYSEMA

Emphysema is a chronic obstructive pulmonary

disease (COPD, as it is otherwise known, formerly

termed a chronic obstructive lung disease). It is often

caused by exposure to toxic chemicals, including long-

term exposure to tobacco smoke. Emphysema is

characterized by loss of elasticity (increased pulmonary

compliance) of the lung tissue caused by destruction of structures feeding the alveoli, owing to

the action of alpha 1 antitrypsin deficiency. This causes the small airways to collapse during

forced exhalation, as alveolar collapsibility has decreased. As a result, airflow is impeded and

air becomes trapped in the lungs, in the same way as other obstructive lung diseases.

Symptoms include shortness of breath on exertion, and an expanded chest. However, the

constriction of air passages isn’t always immediately deadly, and treatment is available.

PHYSICAL MANIFESTATIONS

Signs of emphysema include pursed-lipped breathing, central cyanosis and finger clubbing. The

chest has hyper resonant percussion notes, particularly just above the liver, and a difficult to

palpate apex beat, both due to hyperinflation. There may be decreased breath sounds and

audible expiratory wheeze. In advanced disease, there are signs of fluid overload such as pitting

peripheral edema. The face has a ruddy complexion if there is a secondary polycythemia.

Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist.

DIAGNOSTIC EVALUATION

1. PFTs demonstrative airflow obstruction – reduced forced vital capacity (FVC), FEV1, FEV1

to FVC ration; increased residual volume to total lung capacity (TLC) ratio, possibly

increased TLC.

2. ABG levels- decreased PaO2, pH, and increased CO2.

3. Chest X-ray – in late stages, hyperinflation, flattened diaphragm, increased rettrosternal

space, decreased vascular markings, possible bullae.

4. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in

emphysema.

TREATMENT

The goals of COPD treatment are 1) to prevent further deterioration in lung function, 2) to

alleviate symptoms, 3) to improve performance of daily activities and quality of life. The

treatment strategies include 1) quitting cigarette smoking, 2) taking medications to dilate airways

(bronchodilators) and decrease airway inflammation, 3) vaccinating against flu influenza and

pneumonia and 4) regular oxygen supplementation and 5) pulmonary rehabilitation.

Quitting cigarette smoking

The most important treatment for COPD is quitting cigarette smoking. Patients who continue to

smoke have a more rapid deterioration in lung function when compared to others who quit.

Aging itself can cause a very slow decline in lung function. In susceptible individuals, cigarette

smoking can result in a much more dramatic loss of lung function. It is important to note that

when one stops smoking the decline in lung function eventually reverts to that of a non-smoker.

Nicotine in cigarettes is addictive, and, therefore, cessation of smoking can cause symptoms of

nicotine withdrawal including anxiety, irritability, anger, depression, fatigue, difficulty

concentrating or sleeping, and intense craving for cigarettes. Patients likely to develop

withdrawal symptoms typically smoke more than 20 cigarettes a day, need to smoke shortly

after waking up in the morning, and have difficulty refraining from smoking in non-smoking

areas. However, some 25% of smokers can stop smoking without developing these symptoms.

Even in those smokers who develop symptoms of withdrawal, the symptoms will decrease after

several weeks of abstinence.

Bronchodilators

Treating airway obstruction in COPD with bronchodilators is similar but not identical to treating

bronchospasm in asthma. Bronchodilators are medications that relax the muscles surrounding

the small airways thereby opening the airways. Bronchodilators can be inhaled, taken orally or

administered intravenously. Inhaled bronchodilators are popular because they go directly to the

airways where they work. As compared with bronchodilators given orally, less medication

reaches the rest of the body, and, therefore, there are fewer side effects.

Metered dose inhalers (MDIs) are used to deliver bronchodilators. An MDI is a pressurized

canister containing a medication that is released when the canister is compressed. A standard

amount of medication is released with each compression of the MDI. To maximize the delivery

of the medications to the airways, the patient has to learn to coordinate inhalation with each

compression. Incorrect use of the MDI can lead to deposition of much of the medication on the

tongue and the back of the throat instead of on the airways.

To decrease the deposition of medications on the throat and increase the amount reaching the

airways, spacers can be helpful. Spacers are tube-like chambers attached to the outlet of the

MDI canister. Spacer devices can hold the released medications long enough for patients to

inhale them slowly and deeply into the lungs. Proper use of spacer devices can greatly increase

the proportion of medication reaching the airways.

Oxygen Therapy

Other treatments

Pulmonary rehabilitation has become a cornerstone in the management of moderate to

severe COPD. Pulmonary rehabilitation is a program of education regarding lung function

and dysfunction, proper breathing techniques (diaphragmatic breathing, pursed lip

breathing), and proper use of respiratory equipment and medications. An essential

ingredient in this program is the use of increasing physical exercise to overcome the

reduced physical capacity that usually has developed over time. In addition, occupational

and physical therapy are used to teach optimal and efficient body mechanics.

Lung volume reduction surgery (LVRS) has received much fanfare in the lay press. LVRS is

a surgical procedure used to treat some patients with COPD. The premise behind this

surgery is that the over-inflated, poorly-functioning upper parts of the lung compress and

impair function of the better-functioning lung elsewhere. Thus, if the over-inflated portions of

lung are removed surgically, the compressed lung may expand and function better. In

addition, the diaphragm and the chest cavity achieve more optimal positioning following the

surgery, and this improves breathing further. The best criteria for choosing patients for

LVRS are still uncertain. A national study was completed in 2003. Patients primarily with

emphysema at the top of their lungs, whose exercise tolerance was low even after

pulmonary rehabilitation, seemed to do the best with this procedure. On average, lung

function and exercise capacity among surviving surgical patients improved significantly

following LVRS, but after two years returned to about the same levels as before the

procedure. Patients with forced expiratory volume in FEVI of less than 20% of predicted and

either diffuse disease on the CAT scan or lower than 20% diffusing capacity or elevated

carbon dioxide levels had higher mortality. The role of LVRS is at present is very limited.

PHARMACOLOGIC INTERVENTIONS

Beta-agonists

Beta-2 agonists have the bronchodilating effects of adrenaline without many of its

unwanted side effects. Beta-2 agonists can be administered by MDI inhalers or orally.

They are called “agonists” because they activate the beta-2 receptor on the muscles

surrounding the airways. Activation of beta-2 receptors relaxes the muscles surrounding

the airways and opens the airways. Dilating airways helps to relieve the symptoms of

dyspnea (shortness of breath). Beta-2 agonists have been shown to relieve dyspnea in

many COPD patients, even among those without demonstrable reversibility in airway

obstruction. The action of beta-2 agonists starts within minutes after inhalation and lasts

for about 4 hours. Because of their quick onset of action, beta-2 agonists are especially

helpful for patients who are acutely short of breath. Because of their short duration of

action, these medications should be used for symptoms as they develop rather than as

maintenance. Evidence suggests that when these drugs are used routinely, their

effectiveness is diminished. These are referred to as rescue inhalers. Examples of beta-

2 agonists include albuterol (Ventolin, Proventil), metaproterenol (Alupent), pirbuterol

(Maxair), terbutaline (Brethaire), and isoetharine (Bronkosol). Levalbuterol (Xopenex) is

a recently approved Beta-2 agonist.

In contrast, Beta-2 agonists with a slower onset of action but a longer period of activity,

such as salmeterol xinafoate (Serevent) and formoterol fumarate (Foradil) may be used

routinely as maintenance medications. These drugs last twelve hours and should be

taken twice daily and no more. Along with some of these inhalers to be mentioned, these

are often referred to as maintenance inhalers.

Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast heart rate,

and low blood potassium.

Anti-cholinergic Agents

Acetylcholine is a chemical released by nerves that attaches to receptors on the

muscles surrounding the airway causing the muscles to contract and the airways to

narrow. Anti-cholinergic drugs such as ipratropium bromide (Atrovent) dilate airways by

blocking the receptors for acetylcholine on the muscles of the airways and preventing

them from narrowing. Ipratropium bromide (Atrovent) usually is administered via a MDI.

In patients with COPD, ipratropium has been shown to alleviate dyspnea, improve

exercise tolerance and improve FEV1. Ipratropium has a slower onset of action but

longer duration of action than the shorter-acting beta-2 agonists. Ipratropium usually is

well tolerated with minimal side effects even when used in higher doses. Tiotropium

(SPIRIVA) is a long acting and more powerful version of Ipratropium and has been

shown to be more effective.

In comparing ipratropium with beta-2 agonists in the treatment of patients with COPD,

studies suggest that ipratropium may be more effective in dilating airways and improving

symptoms with fewer side effects. Ipratropium is especially suitable for use by elderly

patients who may have difficulty with fast heart rate and tremor from the beta-2 agonists.

In patients who respond poorly to either beta-2 agonists or ipratropium alone, a

combination of the two drugs sometimes results in a better response than to either drug

alone without additional side effects.

Methylxanthines

Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl, Theo-24) and aminophylline are

examples of methylxanthines. Methylxanthines are administered orally or intravenously.

Long acting theophylline preparations can be given orally once or twice a day.

Theophylline, like a beta agonist, relaxes the muscles surrounding the airways but also

prevents mast cells around the airways from releasing bronchoconstricting chemicals

such as histamine. Theophylline also can act as a mild diuretic and increase urination.

Theophylline also may increase the force of contraction of the heart and lower pressure

in the pulmonary arteries. Thus, theophylline can help patients with COPD who have

heart failure and pulmonary hypertension. Patients who have difficulty using inhaled

bronchodilators but no difficulty taking oral medications find theophylline particularly

useful.

The disadvantage of methylxanthines is their side effects. Dosage and blood levels of

theophylline or aminophylline have to be closely monitored. Excessively high levels in

the blood can lead to nausea, vomiting, heart rhythm problems, and even seizures. In

patients with heart failure or cirrhosis, dosages of methylxanthines are lowered to avoid

high blood levels. Interactions with other medications, such as cimetidine (Tagamet),

calcium channel blockers (Procardia), quinolones (Cipro), and allopurinol (Zyloprim) also

can alter blood levels of methylxanthines.

Corticosteroids

When airway inflammation (which causes swelling) contributes to airflow obstruction,

anti-inflammatory medications (more specifically, corticosteroids) may be beneficial.

Examples of corticosteroids include Prednisone and Prednisolone. Twenty to thirty

percent of patients with COPD show improvement in lung function when given

corticosteroids by mouth. Unfortunately, high doses of oral corticosteroids over

prolonged periods can have serious side effects, including osteoporosis, bone fractures,

diabetes mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia,

emotional changes, and weight gain. Therefore, many doctors use oral corticosteroids

as the treatment of last resort. When oral corticosteroids are used, they are prescribed

at the lowest possible doses for the shortest period of time to minimize side effects.

When it is necessary to use long term oral steroids, medications are often prescribed to

help reduce the development of the above side effects.

Corticosteroids also can be inhaled. Inhaled corticosteroids have many fewer side

effects than long term oral corticosteroids. Examples of inhaled corticosteroids include

beclomethasone dipropionate (Beclovent, Beconase, Vancenase, and Vanceril),

triamcinolone acetonide (Azmacort), fluticasone (Flovent), budesonide (Pulmicort),

mometasone furoate (Asmanex) and flunisolide (Aerobid). Inhaled corticosteroids have

been useful in treating patients with asthma, but in patients with COPD, it is not clear

whether inhaled corticosteroid have the same benefit as oral corticosteroids.

Nevertheless, doctors are less concerned about using inhaled corticosteroids because

of their safety. The side effects of inhaled corticosteroids include hoarseness, loss of

voice, and oral yeast infections. A spacing device placed between the mouth and the

MDI can improve medication delivery and reduce the side effects on the mouth and

throat. Rinsing out the mouth after use of a steroid inhaler also can decrease these side

effects.

Treatment of Alpha-1 antitrypsin deficiency

Emphysema can develop at a very young age in some patients with severe alpha-1

antitrypsin deficiency (AAT). Replacement of the missing or inactive AAT by injection

can help prevent progression of the associated emphysema. This therapy is of no

benefit in other types of COPD.

COMPLICATIONS

1. Respiratory failure

2. Pneumonia, overwhelming respiratory infection

3. Right-sided heart failure, dysrhythmias

4. Depression

5. Skeletal muscle dysfunction

NURSING INTERVENTIONS

Monitoring

1. Monitor for adverse effects of bronchodilators – tremulousness, tachycardia, cardiac

arrhythmias, central nervous system stimulation, hypertension.

2. Monitor condition after administration of aerosol bronchodilators to assess for improved

aeration, reduced adventitious sounds, reduced dyspnea.

3. Monitor serum theophylline level, as ordered, to ensure therapeutic level and prevent

toxicity.

4. Monitor oxygen saturation at rest and with activity.

Supportive Care

1. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually

reduces pulmonary irritation, sputum production, and cough. Keep the patient’s room as

dust-free as possible.

2. Use postural drainage positions to help clear secretions responsible for airway obstructions.

3. Teach controlled coughing.

4. Encourage high level of fluid intake ( 8 to 10 glasses; 2 to 2.5 liters daily) within level of

cardiac reserve.

5. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Add

moisture (humidifier, vaporizer) to indoor air.

6. Avoid dairy products if these increases sputum production.

7. Encourage the patient to assume comfortable position to decrease dyspnea.

8. Instruct and supervise patient’s breathing retraining exercises.

9. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and depth

of respiration and improve respiratory muscle coordination.

10. Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.

11. Maintain the patient’s nutritional status.

12. Reemphasize the importance of graded exercise and physical conditioning programs.

13. Encourage use of portable oxygen system for ambulation for patients with hypoxemia and

marked disability.

14. Train the patient in energy conservation technique.

15. Assess the patient for reactive-behaviors such as anger, depression and acceptance.

Education and health maintenance

1. Review with the patient the objectives of treatment and nursing management.

2. Advise the patient to avoid respiratory irritants. Suggest that high efficiency particulate air

filter may have some benefit.

3. Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial

obstruction and sputum obstruction.

4. Warn patient to avoid persons with respiratory infections, and to avoid crowds and areas

with poor ventilation.

5. Teach the patient how to recognize and report evidence of respiratory infection promptly

such as chest pain, changes in character of sputum (amount, color and consistency),

increasing difficulty in raising sputum, increasing coughing and wheezing, increasing of

shortness of breath.

Holistic assessment of patients with COPD before the use of non-invasive ventilation21 May, 2009

This article uses a case study to illustrate why patients with COPD require

holistic assessment and arterial blood gas analysis before non-invasive

ventilation is used  

 

AuthorSteve Hunter, BSc, RGN, is critical care outreach nurse at Princess Royal

Hospital, Haywards Heath, West Sussex.

 

ABSTRACT

Hunter, S. (2009) Holistic assessment of patients with COPD before the use of

non-invasive ventilation. Nursing Times; 105: 20, early online publication.

The use of non-invasive ventilation (NIV) to manage patients with exacerbations

of COPD has increased in the past 10 years. However, the intervention can be

counterproductive. This article highlights why holistic patient assessment as well

as arterial blood gas analysis are important before NIV is used.

Keywords: Arterial blood gases, COPD, Non-invasive ventilation, Respiratory

care

This article has been double-blind peer reviewed

 

Lung function tests and respiratory symptoms are used to diagnose COPD. Periodic

worsening of these symptoms indicates an exacerbation of COPD (Box 1).

 

Box1.  Exacerbation of COPD

This is a sustained worsening of the patient’s symptoms from her or his stable

state that is beyond normal day-to-day variations, and is acute in onset.

Commonly reported symptoms are worsening breathlessness, a cough, an

increase in sputum production and a change in sputum colour.

Source: NICE (2004)

 

Pharmaceutical management of an acute exacerbation of COPD includes:

Increased frequency of bronchodilators;

Antibiotics to treat signs of infection;

Corticosteroids;

Theophyllines and respiratory stimulants.

Many patients improve rapidly if oxygen therapy is used alongside pharmaceutical

management (British Thoracic Society Standards of Care Committee, 2002).

However, optimising oxygen therapy requires careful monitoring of both oxygen

and carbon dioxide levels in the blood using arterial blood gas analysis.

Interpreting arterial blood gas is complicated but analysis is used with increasing

regularity on general wards in the acute hospital (Lynes, 2003), and nurses need to

understand when and why blood gases are monitored.

Allen (2005) and Lynes (2003) provide a comprehensive examination of blood gas

monitoring and the procedure for collecting samples.

Types of respiratory failureType 1 respiratory failure describes an abnormally low concentration of oxygen in

the blood where the partial pressure of oxygen dissolved in arterial blood (PaO2) is

low (<8kPa), while the carbon dioxide level (PaCO2) is normal or low (4.5–5.8kPa or

<4.5kPa).

Type 2 respiratory failure occurs when a patient has low oxygen levels but carbon

dioxide levels are raised. Definitions are summarised in Box 2.

 

Box 2.  Definitions of respiratory failure

Type 1: A failure of oxygenation

PO2<8kpa

Normal or low PCO2

Type 2: A failure of ventilation

PO2<8kpa

PCO2>6kpa

 

In type 2 respiratory failure, blood gas analysis helps to clarify the speed at which

the failure has occurred.

If the deterioration is rapid (acute), the rising level of carbon dioxide in the blood

will affect the body’s ability to compensate for the increased acidity. The result is

that the pH of the blood becomes acidic. (It will move below the normal pH of 7.4.)  

If the deterioration is chronic, the body has time to compensate for the retention of

carbon dioxide by retaining bicarbonate ions (which are alkaline). The blood gas will

display an elevated PaCO2 and an elevated HCO3 (bicarbonate ion concentration)

but the pH will remain normal.

Acute-on-chronic type 2 respiratory failure will display a mixture of the above. An

acute exacerbation of COPD may result in an acidic pH (<7.4), depicting the acute

phase of the condition, but the patient will have raised carbon dioxide and

bicarbonate levels associated with the chronic disease.

Box 3 outlines the systematic approach that should be used to analyse arterial

blood gas. It is possible to adopt an inappropriate management plan if the final step

of interpreting the blood gas within the context of the patient’s presenting

symptoms is missed.

 

Box 3.  Systematic assessment of arterial gases

Interpret the pH (normal, acid or alkaline)

Find the cause (respiratory and/or metabolic)

Assess for compensation

Assess oxygenation

Interpret the results in the light of the patient’s history

Source: Pratt (2006)

 

Using non-invasive ventilationNon-invasive ventilation in the form of biphasic positive airway pressure (BIPAP)

may be appropriate if the patient has acute or acute-on-chronic type 2 respiratory

failure that fails to respond to standard medical therapy.

It can be used:

As a holding measure while the use of additional therapies is discussed;

As a trial, with a view to mechanical ventilation if the patient fails to improve;

As a ceiling of treatment (NICE, 2004).

Contraindications to its use are listed in Box 4.

 

 

Box 4. Contraindications to the application of BIPAP

Recent facial or upper airway surgery

Facial abnormalities, burns or trauma

Fixed upper airway obstruction

Vomiting

Recent upper gastrointestinal surgery

Copious respiratory secretions

Life-threatening hypoxaemia

Severe co-morbidity

Untreated pneumothorax

Source:RCP, 2008

 

Updated BTS guidelines (Royal College of Physicians et al, 2008) recommend that a

stratification system is used, whereby patients are classified according to the most

appropriate treatment depending on their co-morbidities.

These classifications are:

Immediate intubation and ventilation;

Suitable for non-invasive BIPAP and intubation if the non-invasive BIPAP fails;

For non-invasive BIPAP but not for intubation or intensive care if the non-invasive

BIPAP fails.

Not suitable for non-invasive or invasive ventilation but for active medical

treatment.

For palliative care only.

The indications and contraindications do not highlight the real consequences of

using BIPAP inappropriately. The following case study identifies how it is possible to

use BIPAP in an acute situation to resolve an immediate clinical problem but how

this can also lead to mismanagement of a patient’s condition.

Case studyThe following blood gas reading was taken when Mr Smith was breathing 28%

oxygen from a venturi mask, after admission from a GP to the respiratory ward of a

general hospital (the patient’s name has been changed). He has been diagnosed

with an exacerbation of COPD.

pH            7.19kPa

PCO2         11.6kPa

PO2           6.2kPa

HCO3         26mEq/L (the nationally accepted units for HCO3levels on arterial blood

gases). See Box 5 for normal levels.

 

 

Box 5. Normal arterial blood gases

pH            7.35-7.45

PaCO2                4.5-5.8kPa

PaO2         10-13kPa

HCO3         22-26mEq/L

Base         2/+2mEq/L

(May vary with patient age and history)

 

These arterial blood gas results depict an acute respiratory acidosis (an acidic pH of

<7.4, a low PaO2 and a raised PaCO2 or carbon dioxide retention), and conform to

the classic definition of type 2 respiratory failure (Box 2).

However, the appropriate management plan for this patient will vary considerably,

depending on his presenting signs and symptoms, as well as the acute or chronic

nature of his disease.

Management options include:

Option 1

BIPAP, a form of non-invasive ventilation, could be administered with the key aims

of increasing the patient’s depth of breathing (tidal volume) and so reducing his

respiratory rate and work of breathing (Tully, 2002).

By optimising the patient’s BIPAP settings in accordance with RCP et al (2008)

guidelines, you would expect an improvement/reduction in the acidosis on the next

blood gas (pH moving towards 7.4 as a result of the reduction in retained levels of

CO2).

Non-invasive BIPAP can be performed on a general hospital ward (Elliott et al, 2002)

and, despite its slightly claustrophobic nature, it is generally well tolerated and can

offer a lifeline to some patients.

Once the decision to use BIPAP has been made, it is necessary to address the

question of whether this form of intervention represents the ceiling of the patient’s

therapy or whether mechanical ventilation would be considered if Mr Smith

continued to deteriorate.

Making the decision at this point means that further interventions can be started in

a controlled manner rather than in haste during an emergency.

Option 2

If the patient’s consciousness level is deteriorating rapidly, this key symptom will

influence the decision to adopt option 2. With no other information available, the

appropriate management would be immediate intubation and mechanical

ventilation.

Non-invasive ventilation relies on an awake and compliant patient (NICE, 2004) and

will assist respiratory effort when spontaneous breathing is present and the patient

can maintain an open airway.

Delaying intubation with a trial of BIPAP on a patient whose consciousness level is

deteriorating increases the risk of a respiratory arrest.

Option 3

This is used if auscultation of the patient’s lungs identifies that there are copious

upper airway secretions, but the patient is exhausted and is unable to clear them.

An increase in both volume and viscosity of secretions is a common symptom of

exacerbations of COPD. The application of BIPAP at this stage may inhibit the

removal of these secretions, especially if BIPAP is administered without

humidification.

Removal of secretions by oral or deep suctioning (potentially involving the insertion

of a nasopharyngeal airway) will keep a patent airway open and may also relieve

the acute respiratory symptoms and negate the need for non-invasive ventilation.

Option 4

This describes the care of Mr Smith during a subsequent hospital admission.

Patients with COPD will go on to develop raised bicarbonate levels. This blood gas

result is included to highlight the evolving chronic ill health of the patient.

In option 4, the blood gas result is:

pH              7.19

PaCO2          1 1.6kPa

PaO2           6.2kPa

HCO3           38mEq/L

The raised bicarbonate level suggests that Mr Smith’s respiratory acidosis has a

chronic and an acute element.

The patient has had numerous exacerbations of COPD with the result that his

quality of life is severely limited and it may be appropriate to start a discussion

about the need for palliative care rather than active treatment of his chronic

disease.

While the application of non-invasive BIPAP can give Mr Smith and healthcare team

time to review this decision, it may be viewed as a means of extending the life and

cause distress to a patient at the terminal stage of a disease process (Prigmore,

2006).

Once the decision to provide palliative care has been made, taking subsequent

arterial blood gas samples would be inappropriate as the procedure can cause pain

and distress.

Observation of Mr Smith’s respiratory rate, level of consciousness and work of

breathing can be used by nurses to inform them of changes in his condition.

ConclusionNon-invasive BIPAP can be life-saving for some patients admitted with

exacerbations of COPD in type 2 respiratory failure.However, without thorough

nursing assessment, alongside accurate arterial blood gas interpretation,

suboptimal care may be administered.

Nurses need to be vigilant with their observations and be prepared to broach key

questions with their medical colleagues about ongoing management of these

patients.