Management of Patients With Chronic Obstructive Pulmonary ...nursing4all.weebly.com/uploads/9/5/4/8/9548528/ch24.pdf · Management of Patients With Chronic Obstructive Pulmonary

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24Management of PatientsWith Chronic ObstructivePulmonary Disease

LEARNING OBJECTIVESOn completion of this chapter, the learner will be able to:

1. Describe the pathophysiology of chronic obstructive pulmonarydisease (COPD).

2. Discuss the major risk factors for developing COPD and nursinginterventions to minimize or prevent these risk factors.

3. Use the nursing process as a framework for care of the patient withCOPD.

4. Develop a teaching plan for patients with COPD.5. Describe the pathophysiology of asthma.6. Discuss the medications used in asthma management.7. Describe asthma self-management strategies.8. Describe the pathophysiology of cystic fibrosis.

C hronic obstructive pulmonary disease (COPD) is a leadingcause of morbidity and mortality in the United States. Nursesare involved with COPD patients across the spectrum of care,from outpatient and home care to critical care and the hospicesetting. Patients with COPD or asthma need care from nurseswho not only have astute assessment and clinical managementskills, but who also understand how these disorders can affect pa-tients’ quality of life. Patient and family teaching is an importantnursing intervention to enhance self-management of COPD,asthma, and cystic fibrosis.

Chronic Obstructive Pulmonary DiseaseChronic obstructive pulmonary disease (COPD) is a diseasestate characterized by airflow limitation that is not fully reversible.This newest definition of COPD, provided by the Global Initia-tive for Chronic Obstructive Lung Disease, provides a broad de-scription that better explains this disorder and its signs andsymptoms (National Institutes of Health [NIH], 2001). Whileprevious definitions have included emphysema and chronic bron-chitis under the umbrella classification of COPD, this was oftenconfusing because most patients with COPD present with over-lapping signs and symptoms of these two distinct diseaseprocesses.

COPD may include diseases that cause airflow obstruction(eg, emphysema, chronic bronchitis) or a combination of thesedisorders. Other diseases such as cystic fibrosis, bronchiectasis,and asthma were previously classified as types of chronic ob-structive lung disease. However, asthma is now considered a sep-arate disorder and is classified as an abnormal airway conditioncharacterized primarily by reversible inflammation. COPD cancoexist with asthma. Both of these diseases have the same majorsymptoms; however, symptoms are generally more variable inasthma than in COPD. This chapter discusses COPD as a dis-ease and briefly describes chronic bronchitis and emphysema asdistinct disease states, providing a foundation for understandingthe pathophysiology of COPD. Bronchiectasis, asthma, and cys-tic fibrosis are discussed separately.

COPD is the fifth leading cause of death in the United Statesfor all ages and both genders; fifth for men and fourth for women(National Center for Health Statistics [NCHS], 2000). In 1998,more than 12,000 persons died of COPD. This represents a risein the mortality rate for this disorder at a time when death rates

from other serious illnesses, such as heart disease and cerebral vas-cular disease, were declining. Approximately 16 million people inthe United States have some form of COPD; it is responsible forover 13.4 million office visits per year and is the third most fre-quent justification for home care services (NCHS, 2000; Na-tional Heart, Lung and Blood Institute [NHLBI], 1998). Peoplewith COPD commonly become symptomatic during the middleadult years, and the incidence of COPD increases with age.Although certain aspects of lung function normally decrease withage (eg, vital capacity and forced expiratory volume in 1 second[FEV1]), COPD accentuates and accelerates these physiologicchanges.

PathophysiologyIn COPD, the airflow limitation is both progressive and associatedwith an abnormal inflammatory response of the lungs to noxiousparticles or gases. The inflammatory response occurs throughoutthe airways, parenchyma, and pulmonary vasculature (NIH,2001). Because of the chronic inflammation and the body’s at-tempts to repair it, narrowing occurs in the small peripheral air-ways. Over time, this injury-and-repair process causes scar tissueformation and narrowing of the airway lumen. Airflow obstruc-tion may also be due to parenchymal destruction as seen with em-physema, a disease of the alveoli or gas exchange units.

In addition to inflammation, processes relating to imbalancesof proteinases and antiproteinases in the lung may be responsiblefor airflow limitation. When activated by chronic inflammation,proteinases and other substances may be released, damaging theparenchyma of the lung. The parenchymal changes may also beconsequences of inflammation, environmental, or genetic factors(eg, alpha1 antitrypsin deficiency).

Early in the course of COPD, the inflammatory responsecauses pulmonary vasculature changes that are characterized bythickening of the vessel wall. These changes may occur as a resultof exposure to cigarette smoke or use of tobacco products or as aresult of the release of inflammatory mediators (NIH, 2001).

Chronic BronchitisChronic bronchitis, a disease of the airways, is defined as the pres-ence of cough and sputum production for at least 3 months in eachof 2 consecutive years. In many cases, smoke or other environ-mental pollutants irritate the airways, resulting in hypersecretion

Chapter 24 Management of Patients With Chronic Obstructive Pulmonary Disease 569

Glossaryair trapping: incomplete emptying of alveoli

during expiration due to loss of lung tis-sue elasticity (emphysema), bronchospasm(asthma), or airway obstruction

alpha1 antitrypsin deficiency: genetic dis-order resulting from deficiency of alpha1

antitrypsin, a protective agent for thelung; increases patient’s risk for develop-ing panacinar emphysema even in the ab-sence of smoking

asthma: a disease with multiple precipitatingmechanisms resulting in a common clinicaloutcome of reversible airflow obstruction;no longer considered a category of COPD

bronchiectasis: chronic dilation of abronchus or bronchi; the dilated airways

become saccular and are a medium forchronic infection. Is no longer considereda category of COPD.

bronchitis: a disease of the airways definedas the presence of cough and sputum pro-duction for at least a combined total of 3 months in each of 2 consecutive years; is a category of COPD

chronic obstructive pulmonary disease:disease state characterized by airflow limitation that is not fully reversible;sometimes referred to as chronic airwayobstruction or chronic obstructive lung disease

emphysema: a disease of the airways char-acterized by destruction of the walls of

overdistended alveoli; is a category ofCOPD

metered-dose inhaler (MDI): patient-activated medication canister that pro-vides aerosolized medication that thepatient inhales into the lungs

polycythemia: increase in the red blood cellconcentration in the blood; in COPD, thebody attempts to improve oxygen carryingcapacity by producing increasing amountsof red blood cells

spirometry: pulmonary function tests thatmeasure specific lung volumes (eg, FEV1,FVC) and rates (FEF25–75%); may be mea-sured before and after bronchodilatoradministration

of mucus and inflammation. This constant irritation causes themucus-secreting glands and goblet cells to increase in number,ciliary function is reduced, and more mucus is produced. Thebronchial walls become thickened, the bronchial lumen is nar-rowed, and mucus may plug the airway (Fig. 24-1). Alveoli adja-cent to the bronchioles may become damaged and fibrosed,resulting in altered function of the alveolar macrophages. This issignificant because the macrophages play an important role in de-stroying foreign particles, including bacteria. As a result, the pa-tient becomes more susceptible to respiratory infection. A widerange of viral, bacterial, and mycoplasmal infections can produceacute episodes of bronchitis. Exacerbations of chronic bronchitisare most likely to occur during the winter.

EmphysemaIn emphysema, impaired gas exchange (oxygen, carbon dioxide)results from destruction of the walls of overdistended alveoli.“Emphysema” is a pathological term that describes an abnormaldistention of the air spaces beyond the terminal bronchioles, withdestruction of the walls of the alveoli. It is the end stage of aprocess that has progressed slowly for many years. As the walls ofthe alveoli are destroyed (a process accelerated by recurrent in-fections), the alveolar surface area in direct contact with the pul-monary capillaries continually decreases, causing an increase indead space (lung area where no gas exchange can occur) and im-paired oxygen diffusion, which leads to hypoxemia. In the laterstages of the disease, carbon dioxide elimination is impaired,resulting in increased carbon dioxide tension in arterial blood(hypercapnia) and causing respiratory acidosis. As the alveolarwalls continue to break down, the pulmonary capillary bed is re-duced. Consequently, pulmonary blood flow is increased, forcingthe right ventricle to maintain a higher blood pressure in the pul-monary artery. Hypoxemia may futher increase pulmonary arterypressure. Thus, right-sided heart failure (cor pulmonale) is one ofthe complications of emphysema. Congestion, dependent edema,distended neck veins, or pain in the region of the liver suggeststhe development of cardiac failure.

There are two main types of emphysema, based on the changestaking place in the lung: panlobular (panacinar) and centrilobular(centroacinar) (Fig. 24-2). Both types may occur in the same pa-

570 Unit 5 GAS EXCHANGE AND RESPIRATORY FUNCTION

tient. In the panlobular (panacinar) type, there is destruction ofthe respiratory bronchiole, alveolar duct, and alveoli. All air spaceswithin the lobule are essentially enlarged, but there is little in-flammatory disease. The patient with this type of emphysematypically has a hyperinflated (hyperexpanded) chest (barrel cheston physical examination), marked dyspnea on exertion, andweight loss. To move air into and out of the lungs, negative pres-sure is required during inspiration, and an adequate level of pos-itive pressure must be attained and maintained during expiration.The resting position is one of inflation. Instead of being an in-voluntary passive act, expiration becomes active and requires mus-

Normalbronchus

Smoothmuscle

Open airway

Mucous gland

Chronic bronchitis

Excess mucuscausing chroniccough

Increased number ofmucous glands

Inflammation

FIGURE 24-1 Pathophysiology of chronic bronchitis as compared to a normal bronchus. The bronchus in chronicbronchitis is narrowed and has impaired air flow due to multiple mechanisms: inflammation, excess mucus production,and potential smooth muscle constriction (bronchospasm).

Panlobular emphysema (PLE)

Centrilobular emphysema (CLE)

Normal

FIGURE 24-2 Changes in alveolar structure in centrilobular and panlob-ular emphysema. In panlobular emphysema, the bronchioles, alveolar ducts,and alveoli are destroyed and the air spaces within the lobule are enlarged. Incentrilobular emphysema, the pathologic changes occur in the lobule, whilethe peripheral portions of the acinus are preserved.

cular effort. The patient becomes increasingly short of breath, thechest becomes rigid, and the ribs are fixed at their joints.

In the centrilobular (centroacinar) form, pathologic changestake place mainly in the center of the secondary lobule, preserv-ing the peripheral portions of the acinus. Frequently, there is aderangement of ventilation–perfusion ratios, producing chronichypoxemia, hypercapnia (increased CO2 in the arterial blood),polycythemia, and episodes of right-sided heart failure. Thisleads to central cyanosis, peripheral edema, and respiratory fail-ure. The patient may receive diuretic therapy for edema.

Risk FactorsRisk factors for COPD include environmental exposures andhost factors (Chart 24-1). The most important risk factor forCOPD is cigarette smoking. Pipe, cigar, and other types of to-bacco smoking are also risk factors. In addition, passive smok-ing contributes to respiratory symptoms and COPD (NIH,2001). Smoking depresses the activity of scavenger cells and af-fects the respiratory tract’s ciliary cleansing mechanism, whichkeeps breathing passages free of inhaled irritants, bacteria, andother foreign matter. When smoking damages this cleansingmechanism, airflow is obstructed and air becomes trapped be-hind the obstruction. The alveoli greatly distend, diminishinglung capacity. Smoking also irritates the goblet cells and mucusglands, causing an increased accumulation of mucus, which inturn produces more irritation, infection, and damage to the lung.In addition, carbon monoxide (a byproduct of smoking) com-bines with hemoglobin to form carboxyhemoglobin. Hemoglo-bin that is bound by carboxyhemoglobin cannot carry oxygenefficiently.

Smoking is not the only risk factor for COPD. Other factorsinclude prolonged and intense exposure to occupational dustsand chemicals, indoor air pollution, and outdoor air pollution,which adds to the total burden of inhaled particles on the lung(NIH, 2001).

A host risk factor for COPD is a deficiency of alpha1 anti-trypsin, an enzyme inhibitor that protects the lung parenchymafrom injury. This deficiency predisposes young patients to rapiddevelopment of lobular emphysema even in the absence of smok-ing. Alpha1 antitrypsin deficiency is one of the most commongenetically linked lethal diseases among Caucasians and affectsapproximately one in every 3,000 Americans or approximately80,000 to 100,000 cases (George, San Pedro & Stoller, 2000).The genetically susceptible person is sensitive to environmentalfactors (smoking, air pollution, infectious agents, allergens) andin time develops chronic obstructive symptoms. Carriers of thisgenetic defect must be identified so that they can modify envi-ronmental risk factors to delay or prevent overt symptoms of dis-

ease. Genetic counseling should also be offered. Alpha-proteaseinhibitor replacement therapy, which slows the progression of thedisease, is available for patients with this genetic defect and forthose with severe disease. This intermittent infusion therapy iscostly and is required on an ongoing basis.

Clinical ManifestationsCOPD is characterized by three primary symptoms: cough, spu-tum production, and dyspnea on exertion (NIH, 2001). Thesesymptoms often worsen over time. Chronic cough and sputumproduction often precede the development of airflow limitationby many years. However, not all individuals with cough and spu-tum production will develop COPD. Dyspnea may be severe andoften interferes with the patient’s activities. Weight loss is com-mon because dyspnea interferes with eating, and the work ofbreathing is energy-depleting. Often the patient cannot partici-pate in even mild exercise because of dyspnea; as COPD pro-gresses, dyspnea occurs even at rest. As the work of breathingincreases over time, the accessory muscles are recruited in an ef-fort to breathe. The patient with COPD is at risk for respiratoryinsufficiency and respiratory infections, which in turn increasethe risk for acute and chronic respiratory failure.

In COPD patients with a primary emphysematous compo-nent, chronic hyperinflation leads to the “barrel chest” thorax con-figuration. This results from fixation of the ribs in the inspiratoryposition (due to hyperinflation) and from loss of lung elasticity(Fig. 24-3). Retraction of the supraclavicular fossae occurs on in-spiration, causing the shoulders to heave upward (Fig. 24-4). Inadvanced emphysema, the abdominal muscles also contract oninspiration.

Assessment and Diagnostic FindingsThe nurse should obtain a thorough health history for a patientwith known or potential COPD. Chart 24-2 lists the key factorsto assess. Pulmonary function studies are used to help confirm thediagnosis of COPD, determine disease severity, and follow dis-ease progression. Spirometry is used to evaluate airflow obstruc-tion, which is determined by the ratio of FEV1 (volume of air thatthe patient can forcibly exhale in 1 second) to forced vital capac-ity (FVC). Spirometric results are expressed as an absolute vol-ume and as percent-predicted using appropriate normal values forgender, age, and height. With obstruction, the patient either hasdifficulty exhaling or cannot forcibly exhale air from the lungs,reducing the FEV1. Obstructive lung disease is defined as aFEV1/FVC ratio of less than 70%.

In addition, bronchodilator reversibility testing may be per-formed to rule out the diagnosis of asthma and to guide initialtreatment. With this type of testing, spirometry is first obtained,then the patient is given an inhaled bronchodilator per a proto-col, and finally spirometry is repeated. The patient demonstratesa degree of reversibility if the pulmonary function values improveafter administration of the bronchodilator.

Arterial blood gas measurements may also be obtained to as-sess baseline oxygenation and gas exchange. In addition, a chestx-ray may be obtained to exclude alternative diagnoses. Lastly,alpha1 antitrypsin deficiency screening may be performed for pa-tients under age 45 or for those with a strong family history ofCOPD.

The severity of COPD is classified into four stages (Table 24-1)(National Institutes of Health, 2001). Factors that determine theclinical course and survival of patients with COPD include history


Chart 24-1Risk Factors for COPD

Exposure to tobacco smoke accounts for an estimated 80% to90% of COPD cases (Rennard, 1998)

Passive smokingOccupational exposureAmbient air pollutionGenetic abnormalities, including a deficiency of alpha1-

antitrypsin, an enzyme inhibitor that normally counteracts the destruction of lung tissue by certain other enzymes

acteristics of asthma include onset often early in life, variation indaily symptoms and day-to-day occurrence or timing of symp-toms, family history of asthma, and a largely reversible airflow ob-struction. It may be difficult to differentiate between a patientwith COPD and one with chronic asthma. A key part of differ-entiation is the patient history, as well as the patient’s respon-


Physical Activity in Patients With COPD

PurposeFor patients with chronic obstructive pulmonary disease (COPD),physical activity is an important part of their quality of life. Yet lit-tle is known about the contributions of psychological and physio-logic variables to physical activity in this population. The purposeof this study was to determine the relationships among differingfunctional performance measures (physical activity, functional ca-pacity, symptom experience, and health-related quality of life) inthis population.

Study Sample and DesignThis cross-sectional, descriptive study evaluated 63 outpatients withCOPD prior to entry into a pulmonary rehabilitation program. Thesample was predominantly male (60 men and 3 women) with a meanage of 65.4 ± 8.0 years. None of the participants had been hospital-ized in the past 2 months for a respiratory problem, and none was en-gaged in a formalized exercise program. Functional performance wasmeasured by physical activity (evaluated by an accelerometer and self-report). Functional capacity was measured by three measures of im-pairment (pulmonary function tests [FEV1], 6-minute walk test, and

NURSING RESEARCH PROFILE 24-1

a self-efficacy questionnaire for walking). The symptom experiencesof dyspnea and fatigue as well as health-related quality of life weremeasured by widely used reliable and valid questionnaires.

FindingsSixty-nine subjects were initially enrolled in the study but six werewithdrawn due to missing data. Daily physical activity as measured bythe accelerometer was strongly associated with the maximal distancewalked in the 6-minute walk test, the level of airway obstruction asmeasured by pulmonary function tests, walking self-efficacy, andphysical health status. Physical activity was not correlated with thesubjects’ self-report of functional status. The 6-minute walk test wasthe only predictor of physical activity in this sample.

Nursing ImplicationsFunctional performance status is an important multidimensional out-come measure for both nursing and medicine. This study demon-strates that the multiple measures of functional performance status,which are frequently used in clinical practice and research, may differin their relationship to the actual physical activity level of the patient.

Belza, B., Steele, B. G., Hunziker, J., Lakshminaryan, S., Holt, L., & Buchner, D. M. (2001). Correlates of physical activity in chronic obstructive pulmonary disease. Nursing Research, 50(4), 195–202.

FIGURE 24-3 Characteristics of normal chest walland chest wall in emphysema. The normal chest walland its cross section are illustrated on the left (A). Thebarrel-shaped chest of emphysema and its cross sectionare illustrated on the right (B).

of cigarette smoking, passive smoking exposure, age, rate of declineof FEV1, hypoxemia, pulmonary artery pressure, resting heart rate,weight loss, and reversibility of airflow obstruction (George, SanPedro & Stoller, 2000).

In diagnosing COPD, several differential diagnoses must beruled out. The primary differential diagnosis is asthma. Key char-

A B

(with severe COPD) or acute (with severe bronchospasm orpneumonia in the patient with severe COPD). Acute respiratoryinsufficiency and failure may necessitate ventilatory support untilother acute complications, such as infection, can be treated. Man-agement of the patient requiring ventilatory support is discussedin Chapter 25. Other complications of COPD include pneumo-nia, atelectasis, pneumothorax, and cor pulmonale.

Medical ManagementRISK REDUCTIONSmoking cessation is the single most effective intervention toprevent COPD or slow its progression (NIH, 2001). Recent sur-veys indicate that 25% of all American adults smoke (USPHS,2000). Nurses play a key role in promoting smoking cessationand educating patients about ways to do so. Patients diagnosedwith COPD who continue to smoke must be encouraged and as-sisted to quit. Factors associated with continued smoking varyamong patients and may include the strength of nicotine addic-tion, continued exposure to smoking-associated stimuli (at workor in social settings), stress, depression, and habit. Continuedsmoking is also more prevalent among those with low incomes,a low level of education, and psychosocial problems (Pohl,2000).

Because there are multiple factors associated with continuedsmoking, successful cessation often requires multiple strategies.The health care provider should promote cessation by explainingthe risks of smoking and personalizing the “at-risk” message to thepatient. After giving a strong warning about smoking, the healthcare provider should work with the patient to set a definite “quitdate.” Referral to a smoking cessation program may be helpful.Follow-up within 3 to 5 days after the quit date to review progressand to address any problems is associated with an increased rateof success; this should be repeated as needed. Continued rein-forcement with telephone calls or clinic visits is extremely bene-ficial. Relapses should be analyzed, and the patient and healthcare provider should jointly identify possible solutions to preventfuture backsliding. It is important to emphasize successes rather


FIGURE 24-4 Typical posture of person with COPD—primarily em-physema. The person tends to lean forward and uses the accessory musclesof respiration to breathe, forcing the shoulder girdle upward and causing thesupraclavicular fossae to retract on inspiration.

Table 24-1 • Stages of COPD

STAGE CHARACTERISTICS

0 Normal spirometryChronic symptoms of cough, sputum pro-

duction

I (mild COPD) FEV1/FVC < 70%FEV1 ≥ 80% predictedMay or may not have chronic symptoms

of cough, sputum production

II (moderate COPD) FEV1/FVC < 70%FEV1 between 30% and 80% predictedMay or may not have chronic symptoms

of cough, sputum production

III (severe COPD) FEV1/FVC < 70%FEV1 < 30% predicted or FEV1 < 50%

predicted plus respiratory failure or clini-cal signs of right heart failure

National Institutes of Health (2001). Global initiative for chronic obstructive lung dis-ease: Global strategy for the diagnosis, management, and prevention of chronic obstructivepulmonary disease. U.S. Department of Health and Human Services, NIH PublicationNumber 2701B.

siveness to bronchodilators. Other diseases that must be consideredin the differential diagnosis include heart failure, bronchiectasis,and tuberculosis (NIH, 2001).

ComplicationsRespiratory insufficiency and failure are major life-threateningcomplications of COPD. The acuity of the onset and the sever-ity of respiratory failure depend on the patient’s baseline pul-monary function, pulse oximetry or arterial blood gas values,comorbid conditions, and the severity of other complications ofCOPD. Respiratory insufficiency and failure may be chronic

Chart 24-2 • ASSESSMENT

Key Factors to Assess in the COPDPatient’s Health History

Exposure to risk factors—types, intensity, durationPast medical history—respiratory diseases/problems, including

asthma, allergy, sinusitis, nasal polyps, history of respiratoryinfections

Family history of COPD or other chronic respiratory diseasesPattern of symptom developmentHistory of exacerbations or previous hospitalizations for

respiratory problemsPresence of comorbiditiesAppropriateness of current medical treatmentsImpact of the disease on quality of lifeAvailable social and family support for patientPotential for reducing risk factors (eg, smoking cessation)

than failures. First-line pharmacotherapies that reliably increaselong-term smoking abstinence rates are bupropion SR (Zyban,Wellbutrin), nicotine gum, nicotine inhaler, nicotine nasalspray, or nicotine patches. Second-line pharmacotherapiesinclude clonidine (Catapres) and nortriptyline (Aventyl) (USPHS,2000).

Smoking cessation can begin in a variety of health care settings—outpatient clinic, pulmonary rehabilitation, community, hospital,and the patient’s home. Regardless of the setting, the nurse hasthe opportunity to teach the patient about the risks of smokingand the benefits of smoking cessation. A variety of materials, re-sources, and programs are available to assist with this effort (eg,Agency for Healthcare Research and Quality [formerly Agencyfor Healthcare Policy and Research], United States Public HealthService, Centers for Disease Control and Prevention, NationalCancer Institute, American Lung Association, American CancerSociety).

PHARMACOLOGIC THERAPY

Bronchodilators. Bronchodilators relieve bronchospasm and re-duce airway obstruction by allowing increased oxygen distribu-tion throughout the lungs and improving alveolar ventilation.These medications, which are central in the management of COPD(NIH, 2001), are delivered through a metered-dose inhaler, bynebulization, or via the oral route in pill or liquid form. Bron-chodilators are often administered regularly throughout the dayas well as on an as-needed basis. They may also be used prophy-lactically to prevent breathlessness by having the patient use thembefore an activity, such as eating or walking.

A metered-dose inhaler (MDI) is a pressurized device con-taining an aerosolized powder of medication. A precise amountof medication is released with each activation of the canister(Dhand, 2000). Patients need to be instructed on the correct use

of the device. A spacer (holding chamber) may also be used to en-hance deposition of the medication in the lung and help the pa-tient coordinate activation of the MDI with inspiration. Spacerscome in several designs, but all are attached to the MDI and havea mouthpiece on the opposite end (Fig. 24-5). Once the canisteris activated, the spacer holds the aerosol in the chamber until thepatient inhales (Dhand, 2000). The patient should take a slow,3- to 5-second inhalation immediately following activation of theMDI (Expert Panel Report II, 1997).

Several classes of bronchodilators are used: beta-adrenergicagonists, anticholinergic agents, and methylxanthines. Thesemedications may be used in combination to optimize the bron-chodilation effect. Some of these medications are short-acting;others are long-acting. Long-acting bronchodilators are more con-venient for patient use. Examples of medications in these differ-ing classes are shown in Table 24-2. Nebulized medications(nebulization of medication via an air compressor) may also beeffective in patients who cannot use an MDI properly or who pre-fer this method of administration.

Corticosteroids. Inhaled and systemic corticosteroids (oral orintravenous) may also be used in COPD but are used more fre-quently in asthma. Although it has been shown that cortico-steroids do not slow the decline in lung function, these medicationsmay improve symptoms. A short trial course of oral cortico-steroids may be prescribed for patients with stage II or III COPDto see if pulmonary function improves and symptoms decrease.Inhaled corticosteroids via MDI may also be used. Examples ofcorticosteroids in the inhaled form are beclomethasone (Beclovent,Vanceril), budesonide (Pulmicort), flunisolide (AeroBid), fluti-casone (Flovent), and triamcinolone (Azmacort).

Medication regimens used to manage COPD are based ondisease severity. For stage I or mild COPD, a short-acting bron-


FIGURE 24-5 (A) Examples of metered dose inhalers and spacers. (B) A metered dose inhaler and spacer in use.

A B

chodilator may be prescribed. For stage II or moderate COPD,one or more bronchodilators may be prescribed along with in-haled corticosteroids, if symptoms are significant. For stage III orsevere COPD, medication therapy includes regular treatmentwith one or more bronchodilators and inhaled corticosteroids(NIH, 2001).

Other Medications. Patients should receive a yearly influenzavaccine and the pneumococcal vaccine every 5 to 7 years as pre-ventive measures. In most healthy adults, pneumococcal vaccinetiters persist for 5 or more years (George, San Pedro & Stoller,2000). Other pharmacologic treatments that may be used inCOPD include alpha1 antitrypsin augmentation therapy, anti-biotic agents, mucolytic agents, and antitussive agents.

MANAGEMENT OF EXACERBATIONAn exacerbation of COPD is difficult to diagnose, but signs andsymptoms may include increased dyspnea, increased sputum pro-duction and purulence, respiratory failure, changes in mental sta-tus, or worsening blood gas abnormalities. Primary causes for anacute exacerbation include tracheobronchial infection and airpollution (NIH, 2001). Secondary causes are pneumonia; pul-monary embolism; pneumothorax; rib fractures or chest trauma;inappropriate use of sedative, opioid, or beta-blocking agents;and right- or left-sided heart failure. First, the primary cause ofthe exacerbation is identified, and then specific treatment is ad-ministered. Optimization of bronchodilator medications is thefirst-line therapy and involves identifying the best medication orcombinations of medications taken on a regular schedule for thatpatient. Depending on the signs and symptoms, corticosteroids,antibiotic agents, oxygen therapy, and intensive respiratory in-terventions may also be used. Indications for hospitalization of apatient with an acute exacerbation of COPD include severe dys-pnea that does not respond adequately to initial therapy, confu-

sion or lethargy, respiratory muscle fatigue, paradoxical chest wallmovement, peripheral edema, worsening or new onset of centralcyanosis, persistent or worsening hypoxemia, and/or need fornoninvasive or invasive assisted mechanical ventilation (Celli,Snider, Heffner et al., 1995; NIH, 2001).

OXYGEN THERAPYOxygen therapy can be administered as long-term continuoustherapy, during exercise, or to prevent acute dyspnea. Long-term oxygen therapy has been shown to improve the patient’squality of life and survival (NIH, 2001). For patients with anarterial oxygen pressure (PaO2) of 55 mm Hg or less on roomair, maintaining a constant and adequate oxygen saturation(>90%) is associated with significantly reduced mortality andimproved quality of life. Indications for oxygen supplementa-tion include a PaO2 of 55 mm Hg or less or evidence of tissuehypoxia and organ damage such as cor pulmonale, secondarypolycythemia, edema from right heart failure, or impaired men-tal status. In patients with exercise-induced hypoxemia, oxygensupplementation during exercise can improve performance. Pa-tients who are hypoxemic while awake are likely to be so duringsleep. Therefore, nighttime oxygen therapy is recommended aswell, and the prescription for oxygen therapy is for continuous,24-hour use. Intermittent oxygen therapy is indicated for thosewho desaturate only during exercise or sleep.


Table 24-2 • Types of Bronchodilator Medications

METHOD OF ADMINISTRATION

Metered-Dose DURATIONCLASS/DRUG Inhaler Nebulizer Oral OF ACTION

Beta-Adrenergic Agonist AgentsAlbuterol (Proventil, Ventolin, Volmax) X X X ShortBitolerol (Tornate) X X MediumLevalbuterol (Xopenax) X MediumMetaproterenol (Alupent) X X X ShortPirbuterol (Maxair) X ShortSalbutamol (Asmavent) X X X ShortSalmeterol (Serevent) X LongTerbutaline (Brethaire) X Short

Anticholinergic AgentsIpratropium bromide (Atrovent) X X ShortOxitropium bromide (Oxivent) X Medium

MethylxanthinesAminophylline (Phyllocontin) X VariableTheophylline (Slo-bid, Theo-Dur) X Variable

Short-acting: 4–6 hoursMedium-acting: 6–9 hoursLong-acting: 12+ hours

NURSING ALERT Because hypoxemia stimulates respiration inthe patient with severe COPD, increasing the oxygen flow to a highrate may greatly raise the patient’s blood oxygen level. At the sametime, this will suppress the respiratory drive, causing increasedretention of carbon dioxide and CO2 narcosis. The nurse shouldclosely monitor the patient’s respiratory response to oxygen admin-istration via physical assessment, pulse oximetry, and/or arterialblood gases.

!

SURGICAL MANAGEMENT

Bullectomy. A bullectomy is a surgical option for select patientswith bullous emphysema. Bullae are enlarged airspaces that donot contribute to ventilation but occupy space in the thorax;these areas may be surgically excised. Many times these bullaecompress areas of the lung that do have adequate gas exchange.Bullectomy may help reduce dyspnea and improve lung function.It can be done thoracoscopically (with a video-assisted thoraco-scope) or via a limited thoracotomy incision (see Chap. 25).

Lung Volume Reduction Surgery. Treatment options for patientswith end-stage COPD (stage III) with a primary emphysematouscomponent are limited, although lung volume reduction surgeryis an option for a specific subset of patients. This subset includespatients with homogenous disease or disease that is focused in onearea and not widespread throughout the lungs. Lung volume re-duction surgery involves the removal of a portion of the diseasedlung parenchyma. This allows the functional tissue to expand, re-sulting in improved elastic recoil of the lung and improved chestwall and diaphragmatic mechanics. This type of surgery does notcure the disease, but it may decrease dyspnea, improve lung func-tion, and improve the patient’s overall quality of life. Careful se-lection of patients for this procedure is essential to decrease themorbidity and mortality. The long-term outcomes of this surgeryare unknown.

The National Emphysema Treatment Trial (NETT) is a large,multicenter randomized clinical trial that began in 1997 and isongoing. It is attempting to answer many questions regarding therisks and benefits of lung volume reduction surgery in the treat-ment of severe emphysema. All patients in this trial receive a 6-to 10-week pulmonary rehabilitation program and comprehen-sive medical management. Following completion of pulmonaryrehabilitation, patients are randomized to continue medical man-agement or undergo lung volume reduction surgery. The results

of this trial will help to determine the role of lung volume reduc-tion surgery for patients with severe emphysema (NIH, 2001). Itis expected that 2,500 patients will be entered into the study.

Lung Transplantation. Lung transplantation is a viable alterna-tive for definitive surgical treatment of end-stage emphysema. Ithas been shown to improve quality of life and functional capac-ity (NIH, 2001). Specific criteria exist for referral for lung trans-plantation; however, organs are in short supply and manypatients die while waiting for a transplant.

PULMONARY REHABILITATIONPulmonary rehabilitation for patients with COPD is well estab-lished and widely accepted as a means to alleviate symptoms andoptimize functional status. In both randomized and nonrandom-ized clinical trials, pulmonary rehabilitation has been shown toimprove exercise tolerance, reduce dyspnea, and increase health-related quality of life (Rochester, 2000). The primary goal of re-habilitation is to restore patients to the highest level of independentfunction possible and to improve their quality of life. A suc-cessful rehabilitation program is individualized for each patient,is multidisciplinary, and attends to both the physiologic andemotional needs of the patient. Most pulmonary rehabilitationprograms include educational, psychosocial, behavioral, andphysical components. Breathing exercises and retraining and ex-ercise programs are used to improve functional status, and the pa-tient is taught methods to alleviate symptoms.

Pulmonary rehabilitation may be used therapeutically in otherdiseases besides COPD, including asthma, cystic fibrosis, lungcancer, interstitial lung disease, thoracic surgery, and lung trans-plantation. It may be conducted in the inpatient, outpatient, orhome setting; the lengths of programs vary. Selection of a programdepends upon the patient’s physical, functional, and psychosocialstatus; insurance coverage; changing health care trends; availabil-ity of programs; and patient preference (Rochester, 2000).


Oxygen Administration and Dyspnea Management in Patients With AAT Deficiency

PurposeLimitations in activity due to dyspnea are common in persons withemphysema, including patients with alpha1 antitrypsin (AAT) defi-ciency. The purpose of this study was to examine whether short-termoxygen administration decreased dyspnea and improved exercise tol-erance in nonhypoxemic patients with emphysema caused by AATdeficiency.

Study Sample and DesignThirty-one Caucasian subjects participated in a double-blind,crossover study. The subjects’ mean age was 47 ± 7 years; 62% weremale and 38% were female. Twenty-four percent had used oxygensupplementation at some point during their illness. Oxygen satura-tion, 6-minute walk distance, and end-of-walk dyspnea were mea-sured during three practice walks and during walks with nasal cannulaadministration of oxygen (intervention) and compressed air (control).

FindingsResearchers found significant differences in subjects’ oxygen saturationduring walks with oxygen vs. walks with compressed air (p = 0.0001),

NURSING RESEARCH PROFILE 24-2

with oxygen saturation higher with oxygen supplementation than withcompressed air. There was no difference in subjects’ walk distance andseverity of self-reported dyspnea between oxygen and compressed airuse. However, some gender differences were noted. Men showed nobenefit from oxygen supplementation while walking, but women ex-perienced less dyspnea, which corresponded with an increased walkingdistance.

Nursing ImplicationsThe findings demonstrated that oxygen supplementation did not sig-nificantly improve the sensation of dyspnea or the distance walked in6 minutes in the total sample of patients with AAT deficiency. How-ever, there were trends in gender differences in relation to dyspnea lev-els and distance walked while receiving the intervention (oxygensupplementation). Future studies should examine subjects with dif-fering levels of room air hypoxemia and explore potential gender dif-ferences in exercise performance with oxygen supplementation.Nurses should be aware that patients may respond differently to oxy-gen supplementation depending upon the underlying disease process,level of hypoxemia, and gender.

Knebel, A. R., Bentz, E., & Barnes, P. (2000). Dyspnea management in alpha-1 antitrypsin deficiency: Effect of oxygen administration. Nursing Research, 49(6), 333–338.

Nursing ManagementThe nurse plays a key role in identifying potential candidates forpulmonary rehabilitation and in facilitating and reinforcing thematerial learned in the rehabilitation program. Not all patientshave access to a formal rehabilitation program. However, thenurse can be instrumental in teaching the patient and family aswell as facilitating specific services for the patient (eg, respiratorytherapy education, physical therapy for exercise and breathing re-training, occupational therapy for conserving energy during ac-tivities of daily living, and nutritional counseling). In addition,numerous educational materials are available to assist the nurse inteaching patients with COPD. Potential resources include theAmerican Lung Association, the American Association of Cardio-vascular and Pulmonary Rehabilitation, the American ThoracicSociety, the American College of Chest Physicians, and the Amer-ican Association for Respiratory Therapy.

PATIENT EDUCATIONPatient education is a major component of pulmonary rehabili-tation and includes a broad variety of topics. Depending on thelength and setting of the program, topics may include normalanatomy and physiology of the lung, pathophysiology and changeswith COPD, medications and home oxygen therapy, nutrition,respiratory therapy treatments, symptom alleviation, smokingcessation, sexuality and COPD, coping with chronic disease,communicating with the health care team, and planning for thefuture (advance directives, living wills, informed decision makingabout health care alternatives).

Breathing Exercises. The breathing pattern of most people withCOPD is shallow, rapid, and inefficient; the more severe the dis-ease, the more inefficient the breathing pattern. With practice,this type of upper chest breathing can be changed to diaphrag-matic breathing, which reduces the respiratory rate, increasesalveolar ventilation, and sometimes helps expel as much air aspossible during expiration (see Chap. 25 for technique). Pursed-lip breathing helps to slow expiration, prevents collapse of smallairways, and helps the patient to control the rate and depth of res-piration. It also promotes relaxation, enabling the patient to gaincontrol of dyspnea and reduce feelings of panic.

Inspiratory Muscle Training. Once the patient masters dia-phragmatic breathing, a program of inspiratory muscle trainingmay be prescribed to help strengthen the muscles used in breath-ing. This program requires that the patient breathe against resis-tance for 10 to 15 minutes every day. As the resistance is graduallyincreased, the muscles become better conditioned. Conditioningof the respiratory muscles takes time, and the patient is instructedto continue practicing at home (Larson, Covey, Wirtz et al.,1999; NIH, 2001).

Activity Pacing. A patient with COPD has decreased exercisetolerance during specific periods of the day. This is especially trueon arising in the morning, because bronchial secretions collect inthe lungs during the night while the person is lying down. Thepatient may have difficulty bathing or dressing. Activities requir-ing the arms to be supported above the level of the thorax mayproduce fatigue or respiratory distress but may be tolerated bet-ter after the patient has been up and moving around for an houror more. Working with the nurse, the patient can reduce these

limitations by planning self-care activities and determining thebest time for bathing, dressing, and daily activities.

Self-Care Activities. As gas exchange, airway clearance, and thebreathing pattern improve, the patient is encouraged to assumeincreasing participation in self-care activities. The patient istaught to coordinate diaphragmatic breathing with activities suchas walking, bathing, bending, or climbing stairs. The patient shouldbathe, dress, and take short walks, resting as needed to avoid fa-tigue and excessive dyspnea. Fluids should always be readily avail-able, and the patient should begin to drink fluids without havingto be reminded. If postural drainage is to be done at home, thenurse instructs and supervises the patient before discharge or inthe outpatient setting.

Physical Conditioning. Physical conditioning techniques in-clude breathing exercises and general exercises intended to con-serve energy and increase pulmonary ventilation. There is aclose relationship between physical fitness and respiratory fit-ness. Graded exercises and physical conditioning programsusing treadmills, stationary bicycles, and measured level walkscan improve symptoms and increase work capacity and exercisetolerance. Any physical activity that can be done regularly ishelpful. Lightweight portable oxygen systems are available forambulatory patients who require oxygen therapy during physi-cal activity.

Oxygen Therapy. Oxygen supplied to the home comes in com-pressed gas, liquid, or concentrator systems. Portable oxygen sys-tems allow the patient to exercise, work, and travel. To help thepatient adhere to the oxygen prescription, the nurse explains theproper flow rate and required number of hours for oxygen use aswell as the dangers of arbitrary changes in flow rates or durationof therapy. The nurse cautions the patient that smoking with ornear oxygen is extremely dangerous. The nurse also reassures thepatient that oxygen is not “addictive” and explains the need forregular evaluations of blood oxygenation by pulse oximetry orarterial blood gas analysis.

Nutritional Therapy. Nutritional assessment and counseling areimportant aspects in the rehabilitation process for the patientwith COPD. Approximately 25% of patients with COPD areundernourished (NIH, 2001; Ferreira, Brooks, Lacasse & Gold-stein, 2001). A thorough assessment of caloric needs and coun-seling about meal planning and supplementation are part of therehabilitation process.

Coping Measures. Any factor that interferes with normal breath-ing quite naturally induces anxiety, depression, and changes inbehavior. Many patients find the slightest exertion exhausting.Constant shortness of breath and fatigue may make the patientirritable and apprehensive to the point of panic. Restricted activ-ity (and reversal of family roles due to loss of employment), thefrustration of having to work to breathe, and the realization thatthe disease is prolonged and unrelenting may cause the patient toreact with anger, depression, and demanding behavior. Sexualfunction may be compromised, which also diminishes self-esteem.In addition, the nurse needs to provide education and support tothe spouse/significant other and family because the caregiver rolein end-stage COPD can be difficult.


NURSING PROCESS: THE PATIENT WITH COPDAssessmentAssessment involves obtaining information about current symp-toms as well as previous disease manifestations. Chart 24-3 listssample questions that may be used to obtain a clear history of thedisease process. In addition to the history, the nurse also reviewsthe results of available diagnostic tests.

DiagnosisNURSING DIAGNOSESBased on the assessment data, the patient’s major nursing diag-noses may include the following:

• Impaired gas exchange and airway clearance due to chronicinhalation of toxins

• Impaired gas exchange related to ventilation–perfusioninequality

• Ineffective airway clearance related to bronchoconstriction,increased mucus production, ineffective cough, broncho-pulmonary infection, and other complications

• Ineffective breathing pattern related to shortness of breath,mucus, bronchoconstriction, and airway irritants

• Activity intolerance due to fatigue, ineffective breathingpatterns, and hypoxemia

• Deficient knowledge of self-care strategies to be performedat home.

• Ineffective coping related to reduced socialization, anxiety,depression, lower activity level, and the inability to work

COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONSBased on the assessment data, potential complications that maydevelop include:

• Respiratory insufficiency or failure• Atelectasis• Pulmonary infection• Pneumonia• Pneumothorax• Pulmonary hypertension

Planning and GoalsThe major goals for the patient may include smoking cessation,improved gas exchange, airway clearance, improved breathingpattern, improved activity tolerance, maximal self-management,improved coping ability, adherence to the therapeutic programand home care, and absence of complications.

Nursing InterventionsPROMOTING SMOKING CESSATIONBecause smoking has such a detrimental effect on the lungs, thenurse must discuss smoking cessation strategies with patients.Although patients may believe that it is too late to reverse the dam-age from years of smoking and that smoking cessation is futile,they should be informed that continuing to smoke impairs themechanisms that clear the airways and keep them free of irritants.The nurse should educate the patient regarding the hazards ofsmoking and cessation strategies and provide resources regardingsmoking cessation, counseling, and formalized programs availablein the community.

IMPROVING GAS EXCHANGEBronchospasm, which occurs in many pulmonary diseases, re-duces the caliber of the small bronchi and may cause dyspnea,static secretions, and infection. Bronchospasm can sometimes bedetected when wheezing or diminished breath sounds are heardon auscultation with a stethoscope. Increased mucus production,along with decreased mucociliary action, contributes to furtherreduction in the caliber of the bronchi and results in decreasedairflow and decreased gas exchange. This is further aggravated bythe loss of lung elasticity that occurs with COPD (NIH, 2001).

These changes in the airway require that the nurse monitor thepatient for dyspnea and hypoxemia. If bronchodilators or corti-costeroids are prescribed, the nurse must administer the medica-tions properly and be alert for potential side effects. The relief ofbronchospasm is confirmed by measuring improvement in expi-ratory flow rates and volumes (the force of expiration, how longit takes to exhale, and the amount of air exhaled) and assessingwhether the patient has less dyspnea.


Chart 24-3 • ASSESSMENT

Chronic Obstructive Pulmonary Disease

Health History• How long has the patient had respiratory difficulty?• Does exertion increase the dyspnea? What type of exertion?• What are limits of the patient’s tolerance for exercise?• At what times during the day does the patient complain most

of fatigue and shortness of breath?• Which eating and sleeping habits have been affected?• What does the patient know about the disease and his or her

condition?• What is the patient’s smoking history (primary and secondary)?• Is there occupational exposure to smoke or other pollutants?• What are the triggering events (exertion, strong odors, dust,

exposure to animals, etc.)?

Inspection and Examination Findings• What position does the patient assume during the interview?• What are the pulse and the respiratory rates?• What is the character of respirations? Even and without effort?

Other?• Can the patient complete a sentence without having to take a

breath?• Does the patient contract the abdominal muscles during

inspiration?• Does the patient use accessory muscles of the shoulders and

neck when breathing?• Does the patient take a long time to exhale

(prolonged expiration)?• Is central cyanosis evident?• Are the patient’s neck veins engorged?• Does the patient have peripheral edema?• Is the patient coughing?• What is the color, amount, and consistency of the sputum?• Is clubbing of the fingers present?• What types of breath sounds (ie, clear, diminished or distant,

crackles, wheezes) are heard? Describe and document findingsand locations.

• What is the status of the patient’s sensorium?• Is there short-term or long-term memory impairment?• Is there increasing stupor? • Is the patient apprehensive?

ACHIEVING AIRWAY CLEARANCEDiminishing the quantity and viscosity of sputum can clear theairway and improve pulmonary ventilation and gas exchange. Allpulmonary irritants should be eliminated or reduced, particularlycigarette smoking, which is the most persistent source of pul-monary irritation. The nurse instructs the patient in directed orcontrolled coughing, which is more effective and reduces thefatigue associated with undirected forceful coughing. Directedcoughing consists of a slow, maximal inspiration followed bybreath-holding for several seconds and then two or three coughs.“Huff” coughing may also be effective. The technique consists ofone or two forced exhalations (“huffs”) from low to medium lungvolumes with the glottis open.

Chest physiotherapy with postural drainage, intermittentpositive-pressure breathing, increased fluid intake, and blandaerosol mists (with normal saline solution or water) may be use-ful for some patients with COPD. The use of these measuresmust be based on the patient’s response and tolerance.

IMPROVING BREATHING PATTERNSIneffective breathing patterns and shortness of breath are due tothe ineffective respiratory mechanics of the chest wall and lung re-sulting from air trapping, ineffective diaphragmatic movement,airway obstruction, the metabolic cost of breathing, and stress. In-spiratory muscle training and breathing retraining may help to im-prove breathing patterns. Training in diaphragmatic breathingreduces the respiratory rate, increases alveolar ventilation, andsometimes helps expel as much air as possible during expiration.Pursed-lip breathing helps to slow expiration, prevents collapse ofsmall airways, and helps the patient to control the rate and depthof respiration. It also promotes relaxation, which enables the pa-tient to gain control of dyspnea and reduce feelings of panic.

IMPROVING ACTIVITY TOLERANCEPatients with COPD experience progressive activity and exerciseintolerance. Education is focused on rehabilitative therapies topromote independence in executing activities of daily living.These may include pacing activities throughout the day or usingsupportive devices to decrease energy expenditure. The nurseevaluates the patient’s activity tolerance and limitations andteaching strategies to promote independent activities of daily liv-ing. Also, the patient may be a candidate for exercise training tostrengthen the muscles of the upper and lower extremities andimprove exercise tolerance and endurance. Other health care pro-fessionals (rehabilitation therapy, occupational therapy, physicaltherapy) may be consulted as additional resources.

ENHANCING SELF-CARE STRATEGIESIn addition to a pulmonary rehabilitation program, the nursehelps the patient manage self-care by emphasizing the importanceof setting realistic goals, avoiding temperature extremes, andmodifying lifestyle (particularly stopping smoking) as applicable.

Setting Realistic GoalsA major area of teaching is the importance of setting and accept-ing realistic short-term and long-range goals. If the patient is se-verely disabled, the objectives of treatment are to preserve currentpulmonary function and relieve symptoms as much as possible.If the disease is mild, the objectives are to increase exercise toler-ance and prevent further loss of pulmonary function. It is im-portant to plan and share the goals and expectations of treatmentwith the patient. The patient and those providing care need pa-tience to achieve these goals.

Avoiding Temperature ExtremesThe nurse instructs the patient to avoid extremes of heat andcold. Heat increases the body temperature, thereby raising oxy-gen requirements; cold tends to promote bronchospasm. Air pol-lutants such as fumes, smoke, dust, and even talcum, lint, andaerosol sprays may initiate bronchospasm. High altitudes aggra-vate hypoxemia.

Modifying LifestylePatients with COPD should adopt a lifestyle of moderate activ-ity, ideally in a climate with minimal shifts in temperature andhumidity. As much as possible, the patient should avoid emo-tional disturbances and stressful situations that might trigger acoughing episode. The medication regimen for patients withCOPD can be quite complex; patients receiving aerosol medica-tions by an MDI may be particularly challenged. It is crucial toreview this material and to have the patient perform a returndemonstration before discharge, during follow-up visits to thecaregiver’s office or clinic, and during home visits (Chart 24-4).

Smoking cessation goes hand in hand with lifestyle changes,and reinforcement of the patient’s efforts is a key nursing activ-ity. Smoking cessation is the single most important therapeuticintervention for patients with COPD. There are many strategies,including prevention, cessation with or without oral or topicalpatch medications, and behavior modification techniques.

ENHANCING INDIVIDUAL COPING STRATEGIESCOPD and its progression promote a cycle of physical, social,and psychological consequences, all which are interrelated. Pa-tients experience depression, altered mood states, social isolation,and altered functional status. The nurse is key to identifying thiscycle and promoting interventions for improved physical func-tioning, psychological and emotional stability, and social sup-port. Following the initial assessment of the patient, the nursemay provide referrals to health care professionals in these specificareas.

MONITORING AND MANAGING POTENTIAL COMPLICATIONSThe nurse caring for the patient with COPD must assess for var-ious complications, such as life-threatening respiratory insuffi-ciency and failure and respiratory infection and atelectasis, whichmay increase the patient’s risk for respiratory failure. The nursealso monitors for cognitive changes (personality and behavioralchanges, memory impairment), increasing dyspnea, tachypnea,and tachycardia, which may indicate increasing hypoxemia andimpending respiratory failure.

The nurse monitors pulse oximetry values to assess the pa-tient’s need for oxygen and administers supplemental oxygen asprescribed. The nurse also instructs the patient about signs andsymptoms of respiratory infection that may worsen hypoxemiaand reports changes in the patient’s physical and cognitive statusto the physician. Other activities require assisting with the man-agement of developing complications, with possible intubationand mechanical ventilation (see Chap. 25).

Bronchopulmonary infections must be controlled to diminishinflammatory edema and to permit recovery of normal ciliary ac-tion. Minor respiratory infections that are of no consequence tothe person with normal lungs can be life-threatening to the personwith COPD. The cough associated with bronchial infection intro-duces a vicious cycle with further trauma and damage to the lungs,progression of symptoms, increased bronchospasm, and increasedsusceptibility to bronchial infection. Infection compromises lung


function and is a common cause of respiratory failure in patientswith COPD.

In COPD, infection may be accompanied by subtle changes.The nurse instructs the patient to report any signs of infection,such as a fever or change in sputum color, character, consistency,or amount. Any worsening of symptoms (increased tightness of thechest, increased dyspnea and fatigue) also suggests infection andmust be reported. Viral infections are hazardous to these patientsbecause they are often followed by infections caused by bacterialorganisms, such as Streptococcus pneumoniae and Haemophilusinfluenzae.

The nurse should encourage patients with COPD to be im-munized against influenza and S. pneumoniae because these pa-tients are prone to respiratory infection. It is important to cautionpatients to avoid going outdoors if the pollen count is high or ifthere is significant air pollution because of the risk of bron-

chospasm. The patient also should avoid exposure to high out-door temperatures with high humidity.

Pneumothorax is a potential complication of COPD. Patientswith severe emphysematous changes can develop large bullae,which may rupture and cause a pneumothorax. The developmentof a pneumothorax may be spontaneous or related to an activitysuch as severe coughing or large intrathoracic pressure changes. Ifthe patient develops a rapid onset of shortness of breath, the nurseshould quickly evaluate the patient for a potential pneumothoraxby assessing the symmetry of chest movement, differences inbreath sounds, and pulse oximetry. A pneumothorax is a life-threatening event in the patient with COPD who has minimalpulmonary reserve.

Over time, pulmonary hypertension may occur as a result ofchronic hypoxemia. The pulmonary arteries respond to hypox-emia by constriction, thus leading to pulmonary hypertension.


Chart 24-4Home Care Checklist • Use of Metered-Dose Inhaler (MDI)

At the completion of the home care instruction, the patient or caregiver will be able to:

• Describe the rationale for using the MDI to administer inhaled medicine. ✓ ✓

• Describe how the medication enters the lungs. ✓ ✓

• Demonstrate the correct steps in administering medication with an MDI:Remove the cap and hold the inhaler upright. ✓Shake the inhaler. ✓Tilt your head back slightly and breathe out slowly. ✓Position the inhaler approximately 1–2 inches away from the open mouth, or use a spacer/holding chamber. ✓When using a medicine chamber, place the lips around the mouthpiece.Press down on the inhaler to release the medication as you start to breathe in slowly through the mouth. ✓Continue breathing in as the medication is released (press the cartridge down).

Patient Caregiver

Breathe in slowly and deeply for 3–5 seconds. ✓Hold your breath for 8–10 seconds to allow the medication to reach down into your airways. ✓Repeat puffs as directed, allowing 1–2 minutes between puffs. ✓Apply the cap to the MDI for storage. ✓After inhalation, rinse mouth with water when using a corticosteroid-containing MDI. ✓

• Describe how to clean the MDI. ✓ ✓

• Describe how to assess the amount of medication remaining in the MDI. ✓ ✓

• Describe how and when to contact the health care provider for assessment, and how to obtain a refill of the MDI prescription. ✓ ✓

Nurse teaches patient to use a metered dose inhaler. © B. Proud.

Expert Panel Report II. (1997). Guidelines for the diagnosis and management of asthma. National Asthma Education andPrevention Program, National Institutes of Health.

The complication may be prevented by maintaining adequateoxygenation through an adequate hemoglobin level, improvedventilation/perfusion of the lungs, or continuous administrationof supplemental oxygen (if needed).

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-CareTeaching is essential throughout the course of COPD and shouldbe part of the nursing care given to every patient with COPD. Pa-tients’ and family members’ knowledge and comfort level withtheir knowledge should be assessed and considered when provid-ing instructions about self-management strategies. In addition tothe aspects of patient education previously described, patientsand family members must become familiar with the medicationsthat are prescribed and knowledgeable about potential side ef-fects. Patients and family members need to learn the early signsand symptoms of infection and other complications so that theyseek appropriate health care promptly.

Continuing CareReferral for home care is important to enable the nurse to assessthe patient’s home environment and physical and psychologicalstatus, to evaluate the patient’s adherence to the prescribed regi-men, and to assess the patient’s ability to cope with changes inlifestyle and physical status. The nurse assesses the patient’s andfamily’s understanding of the complications and side effects ofmedications. The home care visit provides an opportunity to re-inforce the information and activities learned in the inpatient oroutpatient pulmonary rehabilitation program and to have the pa-tient and family demonstrate correct administration of medicationsand oxygen, if indicated, and performance of exercises. If the pa-tient does not have access to a formal pulmonary rehabilitationprogram, it is important for the nurse to provide the educationand breathing retraining necessary to optimize the patient’s func-tional status.

The nurse may direct patients to community resources suchas pulmonary rehabilitation programs and smoking cessationprograms to help improve their ability to cope with their chroniccondition and the therapeutic regimen and to give them a senseof worth, hope, and well-being. In addition, the nurse remindsthe patient and family about the importance of participating ingeneral health promotion activities and health screening.

EvaluationEXPECTED PATIENT OUTCOMESExpected patient outcomes may include:

1. Demonstrates knowledge of hazards of smokinga. Verbalizes willingness/interest to quit smokingb. Verbalizes information about smoking, risks of contin-

uing, benefits of quitting, and techniques to optimizecessation efforts

2. Demonstrates improved gas exchangea. Shows no signs of restlessness, confusion, or agitationb. Has stable pulse oximetry or arterial blood gas values

(but not necessarily normal values due to chronicchanges in the gas exchange ability of the lungs)

3. Achieves maximal airway clearancea. Stops smokingb. Avoids noxious substances and extremes of temperaturec. Maintains adequate hydrationd. If indicated, performs postural drainage correctly

e. Knows signs of early infection and is aware of how andwhen to report them if they occur

f. Performs controlled coughing without experiencingexcessive fatigue

4. Improves breathing patterna. Practices and uses pursed-lip and diaphragmatic breath-

ingb. Shows signs of decreased respiratory effort (decreased

respiratory rate, less dyspnea)5. Demonstrates knowledge of strategies to improve activity

tolerance and maintain maximum level of self-carea. Performs self-care activities within tolerance rangeb. Paces self to avoid fatigue and dyspneac. Uses controlled breathing while performing activitiesd. Uses devices to assist with activity tolerance and de-

crease energy expenditure6. Demonstrates knowledge of self-care strategies

a. Participates in determining the therapeutic programb. Understands the rationale for activities and medicationsc. Follows the medication pland. Uses bronchodilators and oxygen therapy as prescribede. Stops smokingf. Maintains acceptable activity level

7. Uses effective coping mechanisms for dealing with conse-quences of diseasea. Uses self-care strategies to lessen stress associated with

diseaseb. Verbalizes resources available to deal with psychological

burden of diseasec. Participates in pulmonary rehabilitation, if appropriate

8. Uses community resources and home-based carea. Verbalizes knowledge of community resources (eg,

smoking cessation, hospital/community-based supportgroups)

b. Participates in pulmonary rehabilitation, if appropriate9. Avoids or reduces complications

a. Has no evidence of respiratory failure or insufficiencyb. Maintains adequate pulse oximetry and arterial blood

gas valuesc. Shows no signs or symptoms of infection, pneumotho-

rax, or pulmonary hypertensionFor more information, see Plan of Nursing Care: Care of the

Patient With COPD.

BronchiectasisBronchiectasis is a chronic, irreversible dilation of the bronchiand bronchioles. Under the new definition of COPD, it is considered a separate disease process from COPD (NIH,2001). Bronchiectasis may be caused by a variety of conditions,including:

• Airway obstruction• Diffuse airway injury• Pulmonary infections and obstruction of the bronchus or

complications of long-term pulmonary infections• Genetic disorders such as cystic fibrosis• Abnormal host defense (eg, ciliary dyskinesia or humoral

immunodeficiency)• Idiopathic causes


(text continues on page 586)


Plan of Nursing CareCare of the Patient With COPD

Nursing Interventions Rationale Expected Outcomes

1. Evaluate current smoking status, educateregarding smoking cessation, and facili-tate efforts to quit.a. Evaluate current smoking habits of

patient and family.b. Educate regarding hazards of smoking

and relationship to COPD.c. Evaluate previous smoking cessation

attempts.d. Provide educational materials.e. Refer to a smoking cessation program

or resource.2. Evaluate current exposure to occupa-

tional exposures and indoor/outdoorpollution.a. Evaluate current exposures to occupa-

tional toxins, indoor and outdoor airpollution (eg, smog, toxic fumes,chemicals).

b. Emphasize primary prevention tooccupational exposures. This is bestachieved by elimination or reductionof exposures in the workplace.

c. Educate regarding types of indoor andoutdoor air pollution (eg, biomass fuelburned for cooking and heating inpoorly ventilated buildings, outdoorair pollution).

d. Advise patient to monitor publicannouncements regarding air quality.

1. Smoking causes permanent damage tothe lung and diminishes the lungs’protective mechanisms. Airflow is ob-structed, secretions are increased, andlung capacity is reduced. Continuedsmoking increases morbidity and mortal-ity in COPD and is also a risk factor forlung cancer.

2. Chronic inhalation of both indoor andoutdoor toxins causes damage to theairways and impairs gas exchange.

• Identifies the hazards of cigarette smoking• Enrolls in smoking cessation program• Reports success in stopping smoking• Identifies resources for smoking cessation• Verbalizes types of inhaled toxins• Minimizes or eliminates exposures• Monitors public announcements regarding

air quality and minimizes or eliminatesexposures during episodes of severepollution

Nursing Diagnosis: Impaired gas exchange related to ventilation–perfusion inequalityGoal: Improvement in gas exchange

1. Administer bronchodilators as prescribed:a. Inhalation is the preferred route.b. Observe for side effects: tachycardia,

dysrhythmias, central nervous systemexcitation, nausea, and vomiting.

c. Assess for correct technique ofmetered-dose inhaler (MDI)administration.

2. Evaluate effectiveness of nebulizer orMDI treatments.a. Assess for decreased shortness of

breath, decreased wheezing or crackles,loosened secretions, decreased anxiety.

b. Ensure that treatment is given beforemeals to avoid nausea and to reducefatigue that accompanies eating.

3. Instruct and encourage patient indiaphragmatic breathing and effectivecoughing.

1. Bronchodilators dilate the airways. Themedication dosage is carefully adjustedfor each patient, in accordance withclinical response.

2. Combining medication with aerosolizedbronchodilators is typically used tocontrol bronchoconstriction in an acuteexacerbation. Generally, however, theMDI with spacer is the preferred route(less cost and time to treatment).

3. These techniques improve ventilation byopening airways to facilitate clearing theairways of sputum. Gas exchange isimproved and fatigue is minimized.

• Verbalizes need for bronchodilators andfor taking as prescribed

• Evidences minimal side effects; heart ratenear normal, absence of dysrhythmias,normal mentation

• Reports a decrease in dyspnea• Shows an improved expiratory flow rate• Uses and cleans respiratory therapy equip-

ment as applicable• Demonstrates diaphragmatic breathing

and coughing• Uses oxygen equipment appropriately

when indicated• Evidences improved arterial blood gases or

pulse oximetry• Demonstrates correct technique for use

of MDI

(continued)

Nursing Diagnosis: Impaired gas exchange and airway clearance due to chronic inhalation of toxinsGoal: Improvement in gas exchange


Plan of Nursing CareCare of the Patient With COPD (Continued)


4. Administer oxygen by the method pre-scribed.a. Explain rationale and importance to

patient.b. Evaluate effectiveness; observe for signs

of hypoxemia. Notify physician if rest-lessness, anxiety, somnolence, cyanosis,or tachycardia is present.

c. Analyze arterial blood gases and com-pare with baseline values. When arter-ial puncture is performed and a bloodsample is obtained, hold puncture sitefor 5 minutes to prevent arterial bleed-ing and development of ecchymoses.

d. Initiate pulse oximetry to monitoroxygen saturation.

e. Explain that no smoking is permittedby patient or visitors while oxygen is in use.

4. Oxygen will correct the hypoxemia. Care-ful observation of the liter flow or thepercentage administered and its effect onthe patient is important. If the patient haschronic CO2 retention, excessive oxygencould suppress the hypoxic drive and res-pirations. These patients generally needlow-flow oxygen rates of 1 to 2 L/min.Periodic arterial blood gases and pulseoximetry help to evaluate adequacy ofoxygenation. Smoking may render pulseoximetry inaccurate because the carbonmonoxide from cigarette smoke alsosaturates hemoglobin.

Nursing Diagnosis: Ineffective airway clearance related to bronchoconstriction, increased mucus production,ineffective cough, bronchopulmonary infection, and other complications

Goal: Achievement of airway clearance

1. Adequately hydrate the patient.

2. Teach and encourage the use ofdiaphragmatic breathing and coughingtechniques.

3. Assist in administering nebulizer or MDI.

4. If indicated, perform postural drainagewith percussion and vibration in themorning and at night as prescribed.

5. Instruct patient to avoid bronchial irri-tants such as cigarette smoke, aerosols,extremes of temperature, and fumes.

6. Teach early signs of infection that are tobe reported to the clinician immediately:a. Increased sputum productionb. Change in color of sputumc. Increased thickness of sputumd. Increased shortness of breath, tightness

in chest, or fatiguee. Increased coughingf. Fever or chills

7. Administer antibiotics as prescribed.

8. Encourage patient to be immunizedagainst influenza and Streptococcuspneumoniae.

1. Systemic hydration keeps secretions moistand easier to expectorate. Fluids must begiven with caution if right- or left-sidedheart failure is present.

2. These techniques help to improve venti-lation and mobilize secretions withoutcausing breathlessness and fatigue.

3. This ensures adequate delivery of medica-tion to the airways.

4. Uses gravity to help raise secretions sothey can be more easily expectorated orsuctioned.

5. Bronchial irritants cause broncho-constriction and increased mucusproduction, which then interferes with airway clearance.

6. Minor respiratory infections that are ofno consequence to the person with nor-mal lungs can produce fatal disturbancesin the lungs of the person with emphy-sema. Early recognition is crucial.

7. Antibiotics may be prescribed to preventor treat infection.

8. People with respiratory conditions areprone to respiratory infections and areencouraged to be immunized.

• Verbalizes need to drink fluids• Demonstrates diaphragmatic breathing

and coughing• Performs postural drainage correctly• Coughing is minimized• Does not smoke• Verbalizes that pollens, fumes, gases,

dusts, and extremes of temperature andhumidity are irritants to be avoided

• Identifies signs of early infection• Is free of infection (no fever, no change in

sputum, lessening of dyspnea)• Verbalizes need to notify health care

provider at the earliest sign of infection• Verbalizes need to stay away from crowds

or people with colds in flu season• Discusses flu and pneumonia vaccines

with clinician to help prevent infection

(continued)




1. Teach patient diaphragmatic and pursed-lip breathing.

2. Encourage alternating activity with restperiods. Allow patient to make some de-cisions (bath, shaving) about care basedon tolerance level.

3. Encourage use of an inspiratory muscletrainer if prescribed.

1. Helps patient prolong expiration timeand decreases air trapping. With thesetechniques, patient will breathe moreefficiently and effectively.

2. Pacing activities permits patient to per-form activities without excessive distress.

3. Strengthens and conditions the respira-tory muscles.

• Practices pursed-lip and diaphragmaticbreathing and uses them when short ofbreath and with activity

• Shows signs of decreased respiratory effortand paces activities

• Uses inspiratory muscle trainer as pre-scribed

Nursing Diagnosis: Self-care deficits related to fatigue secondary to increased work of breathing and insufficientventilation and oxygenation

Goal: Independence in self-care activities

1. Teach patient to coordinate diaphragmaticbreathing with activity (eg, walking,bending).

2. Encourage patient to begin to bathe self,dress self, walk, and drink fluids. Discussenergy conservation measures.

3. Teach postural drainage if appropriate.

1. This will allow the patient to be more ac-tive and to avoid excessive fatigue or dys-pnea during activity.

2. As condition resolves, patient will be ableto do more but needs to be encouraged toavoid increasing dependence.

3. Encourages patient to become involvedin own care. Prepares patient to manageat home.

• Uses controlled breathing while bathing,bending, and walking

• Paces activities of daily living to alternatewith rest periods to reduce fatigue anddyspnea

• Describes energy conservation strategies• Performs same self-care activities as before• Performs postural drainage correctly

(continued)

Nursing Diagnosis: Ineffective breathing pattern related to shortness of breath, mucus, bronchoconstriction, and airway irritants

Goal: Improvement in breathing pattern

Nursing Diagnosis: Activity intolerance due to fatigue, hypoxemia, and ineffective breathing patternsGoal: Improvement in activity tolerance

1. Support patient in establishing a regularregimen of exercise using treadmill andexercycle, walking, or other appropriateexercises, such as mall walking.a. Assess the patient’s current level of

functioning and develop exercise planbased on baseline functional status.

b. Suggest consultation with a physicaltherapist or pulmonary rehabilitationprogram to determine an exercise pro-gram specific to the patient’s capability.Have portable oxygen unit available ifoxygen is prescribed for exercise.

1. Muscles that are deconditioned consumemore oxygen and place an additional bur-den on the lungs. Through regular, gradedexercise, these muscle groups becomemore conditioned, and the patient can domore without getting as short of breath.Graded exercise breaks the cycle ofdebilitation.

• Performs activities with less shortness ofbreath

• Verbalizes need to exercise daily anddemonstrates an exercise plan to be carriedout at home

• Walks and gradually increases walkingtime and distance to improve physicalcondition

• Exercises both upper and lower bodymuscle groups

Nursing Diagnosis: Ineffective coping related to reduced socialization, anxiety, depression, lower activity level,and the inability to work

Goal: Attainment of an optimal level of coping

1. Help the patient develop realistic goals.

2. Encourage activity to level of symptomtolerance.

1. Developing realistic goals will promote asense of hope and accomplishment ratherthan defeat and hopelessness.

2. Activity reduces tension and decreasesdegree of dyspnea as patient becomesconditioned.

• Expresses interest in the future• Participates in the discharge plan• Discusses activities or methods that can be

performed to ease shortness of breath• Uses relaxation techniques appropriately• Expresses interest in a pulmonary rehabili-

tation program




3. Teach relaxation technique or provide arelaxation tape for patient.

4. Enroll patient in pulmonary rehabilita-tion program where available.

3. Relaxation reduces stress, anxiety, anddyspnea and helps patient to cope withdisability.

4. Pulmonary rehabilitation programs havebeen shown to promote a subjective im-provement in a patient’s status and self-esteem as well as increased exercisetolerance and decreased hospitalizations.

Nursing Diagnosis: Deficient knowledge about self-management to be performed at home.Goal: Adherence to therapeutic program and home care

1. Help patient understand short- and long-term goals.a. Teach the patient about disease, med-

ications, procedures, and how andwhen to seek help.

b. Refer patient to pulmonaryrehabilitation.

2. Give strong message to stop smoking.Discuss smoking cessation strategies. Pro-vide information about resource groups(eg, SmokEnders, American Cancer Soci-ety, American Lung Association).

1. Patient needs to be a partner in develop-ing the plan of care and needs to knowwhat to expect. Teaching about the con-dition is one of the most important as-pects of care; it will prepare the patient tolive and cope with the condition andimprove quality of life.

2. Smoking causes permanent damage to thelung and diminishes the lungs’ protectivemechanisms. Air flow is obstructed andlung capacity is reduced. Smoking in-creases morbidity and mortality and isalso a risk factor for lung cancer.

• Understands disease and what affects it• Verbalizes the need to preserve existing

lung function by adhering to the pre-scribed program

• Understands purposes and proper admin-istration of medications

• Stops smoking or enrolls in a smokingcessation program

• Identifies when and whom to call for assis-tance

(continued)

Collaborative Problem: AtelectasisGoal: Absence of atelectasis on x-ray and physical examination

1. Monitor respiratory status, including rateand pattern of respirations, breath sounds,signs and symptoms of respiratorydistress, and pulse oximetry.

2. Instruct in and encourage diaphragmaticbreathing and effective coughingtechniques.

3. Promote use of lung expansion techniques(eg, deep-breathing exercises, incentivespirometry) as prescribed.

1. A change in respiratory status, includingtachypnea, dyspnea, and diminished orabsent breath sounds, may indicateatelectasis.

2. These techniques improve ventilationand lung expansion and ideally improvegas exchange.

3. Deep-breathing exercises and incentivespirometry promote maximal lungexpansion.

• Normal (baseline for patient) respiratoryrate and pattern

• Normal breath sounds for patient• Demonstrates diaphragmatic breathing

and effective coughing• Performs deep-breathing exercises, incen-

tive spirometry as prescribed• Pulse oximetry is ≥ 90%

Collaborative Problem: PneumothoraxGoal: Absence of signs and symptoms of pneumothorax

1. Monitor respiratory status, including rateand pattern of respirations, symmetry ofchest wall movement, breath sounds,signs and symptoms of respiratorydistress, and pulse oximetry.

2. Assess pulse.

3. Assess for chest pain and precipitatingfactors.

4. Palpate for tracheal deviation/shift awayfrom the affected side.

1. Dyspnea, tachypnea, tachycardia, acutepleuritic chest pain, tracheal deviationaway from the affected side, absence ofbreath sounds on the affected side, anddecreased tactile fremitus may indicatepneumothorax.

2. Tachycardia is associated with pneumo-thorax and anxiety.

3. Pain may accompany pneumothorax.

4. Early detection of pneumothorax andprompt intervention will prevent otherserious complications.

• Normal respiratory rate and pattern forpatient

• Normal breath sounds bilaterally• Normal pulse for patient• Normal tactile fremitus• Absence of pain• Tracheal position is midline• Pulse oximetry ≥ 90%• Maintains normal oxygen saturation and

arterial blood gas measurements forpatient

• Exhibits no hypoxemia and hypercapnia(or returns to baseline values)


A person may be predisposed to bronchiectasis as a result ofrecurrent respiratory infections in early childhood, measles, in-fluenza, tuberculosis, and immunodeficiency disorders.

PathophysiologyThe inflammatory process associated with pulmonary infectionsdamages the bronchial wall, causing a loss of its supporting struc-ture and resulting in thick sputum that ultimately obstructs thebronchi. The walls become permanently distended and distorted,impairing mucociliary clearance. The inflammation and infection

extend to the peribronchial tissues; in the case of saccularbronchiectasis, each dilated tube virtually amounts to a lung ab-scess, the exudate of which drains freely through the bronchus.Bronchiectasis is usually localized, affecting a segment or lobe ofa lung, most frequently the lower lobes.

The retention of secretions and subsequent obstruction ulti-mately cause the alveoli distal to the obstruction to collapse (at-electasis). Inflammatory scarring or fibrosis replaces functioninglung tissue. In time the patient develops respiratory insufficiencywith reduced vital capacity, decreased ventilation, and an increasedratio of residual volume to total lung capacity. There is impair-



5. Monitor pulse oximetry and if indicatedarterial blood gases.

6. Administer supplemental oxygen therapy,as indicated.

7. Administer analgesics, as indicated, forchest pain.

8. Assist with chest tube insertion and usepleural drainage system, as prescribed.

5. Recognition of a deterioration in respira-tory function will prevent seriouscomplications.

6. Oxygen will correct hypoxemia; adminis-ter it with caution.

7. Pain interferes with deep breathing, re-sulting in a decrease in lung expansion.

8. Removal of air from the pleural space willreexpand the lung.

• Absence of pain• Symmetric chest wall movement• Lung is reexpanded on chest x-ray• Breath sounds are heard on the affected

side

Collaborative Problem: Respiratory failureGoal: Absence of signs and symptoms of respiratory failure; no evidence of respiratory failure on laboratory tests

1. Monitor respiratory status, including rateand pattern of respirations, breath sounds,and signs and symptoms of acute respira-tory distress.

2. Monitor pulse oximetry and arterialblood gases.

3. Administer supplemental oxygen and ini-tiate mechanisms for mechanical ventila-tion, as prescribed.

1. Early recognition of a deterioration inrespiratory function will avert furthercomplications, such as respiratory failure,severe hypoxemia, and hypercapnia.

2. Recognition of changes in oxygenationand acid–base balance will guide in cor-recting and preventing complications.

3. Acute respiratory failure is a medicalemergency. Hypoxemia is a hallmarksign. Administration of oxygen therapyand mechanical ventilation (if indicated)are critical to survival.

• Normal respiratory rate and pattern forpatient with no acute distress

• Recognizes symptoms of hypoxemia andhypercapnia

• Maintains normal arterial blood gases/pulse oximetry or returns to baselinevalues

Collaborative Problem: Pulmonary hypertensionGoal: Absence of evidence of pulmonary hypertension on physical examination or laboratory tests

1. Monitor respiratory status, including rateand pattern of respirations, breath sounds,pulse oximetry, and signs and symptomsof acute respiratory distress.

2. Assess for signs and symptoms of right-sided heart failure, including peripheraledema, ascites, distended neck veins,crackles, and heart murmur.

3. Administer oxygen therapy, as prescribed.

1. Dyspnea is the primary symptom of pul-monary hypertension. Other symptomsinclude fatigue, angina, near syncope,edema, and palpitations.

2. Right-sided heart failure is a commonclinical manifestation of pulmonaryhypertension due to increased rightventricular workload.

3. Continuous oxygen therapy is a majorcomponent of management of pulmonaryhypertension by preventing hypoxemiaand thereby reducing pulmonary vascularconstriction (resistance) secondary tohypoxemia.

• Normal respiratory rate and pattern forpatient

• Exhibits no signs and symptoms of right-sided failure

• Maintains baseline pulse oximetry valuesand arterial blood gases

ment in the matching of ventilation to perfusion (ventilation–perfusion imbalance) and hypoxemia.

Clinical ManifestationsCharacteristic symptoms of bronchiectasis include chronic coughand the production of purulent sputum in copious amounts.Many patients with this disease have hemoptysis. Clubbing of thefingers also is common because of respiratory insufficiency. Thepatient usually has repeated episodes of pulmonary infection.Even with modern treatment approaches, the average age at deathis approximately 55 years.

Assessment and Diagnostic FindingsBronchiectasis is not readily diagnosed because the symptoms canbe mistaken for those of simple chronic bronchitis. A definite signis offered by the prolonged history of productive cough, withsputum consistently negative for tubercle bacilli. The diagnosis isestablished by a computed tomography (CT) scan, which demon-strates either the presence or absence of bronchial dilation.

Medical ManagementTreatment objectives are to promote bronchial drainage to clearexcessive secretions from the affected portion of the lungs and toprevent or control infection. Postural drainage is part of all treat-ment plans because draining the bronchiectatic areas by gravityreduces the amount of secretions and the degree of infection.Sometimes mucopurulent sputum must be removed by bron-choscopy. Chest physiotherapy, including percussion and pos-tural drainage, is important in secretion management.

Smoking cessation is important because smoking impairsbronchial drainage by paralyzing ciliary action, increasing bron-chial secretions, and causing inflammation of the mucous mem-branes, resulting in hyperplasia of the mucous glands. Infection iscontrolled with antimicrobial therapy based on the results of sen-sitivity studies on organisms cultured from sputum. A year-roundregimen of antibiotic agents may be prescribed, with differenttypes of antibiotics at intervals. Some clinicians prescribe anti-biotic agents throughout the winter or when acute upper respira-tory tract infections occur. Patients should be vaccinated againstinfluenza and pneumococcal pneumonia. Bronchodilators, whichmay be prescribed for patients who also have reactive airway dis-ease, may also assist with secretion management.

Surgical intervention, although used infrequently, may be in-dicated for the patient who continues to expectorate largeamounts of sputum and has repeated bouts of pneumonia and he-moptysis despite adhering to the treatment regimen. However,the disease must involve only one or two areas of the lung thatcan be removed without producing respiratory insufficiency. Thegoals of surgical treatment are to conserve normal pulmonary tis-sue and to avoid infectious complications. Diseased tissue is re-moved, provided that the postoperative lung function will beadequate. It may be necessary to remove a segment of a lobe(segmental resection), a lobe (lobectomy), or rarely an entire lung(pneumonectomy). (See Chart 25-16 for further information.)Segmental resection is the removal of an anatomic subdivision ofa pulmonary lobe. The chief advantage is that only diseased tis-sue is removed and healthy lung tissue is conserved.

The surgery is preceded by a period of careful preparation.The objective is to obtain a dry (free of infection) tracheo-bronchial tree to prevent complications (atelectasis, pneumonia,

bronchopleural fistula, and empyema). This is accomplished bypostural drainage or, depending on the location, by direct suctionthrough a bronchoscope. A course of antibacterial therapy maybe prescribed. After surgery, the care is the same as for any patientundergoing chest surgery (see Chap. 25).

Nursing ManagementNursing management of the patient with bronchiectasis focuseson alleviating symptoms and assisting the patient to clear pul-monary secretions. Smoking and other factors that increase theproduction of mucus and hamper its removal are targeted in pa-tient teaching. The patient and family are taught to perform pos-tural drainage and to avoid exposure to others with upperrespiratory and other infections. If the patient experiences fa-tigue and dyspnea, strategies to conserve energy while maintain-ing as active a lifestyle as possible are discussed. The patientneeds to become knowledgeable about early signs of respiratoryinfection and the progression of the disorder so that appropriatetreatment can be implemented promptly. Because the presenceof a large amount of mucus may decrease the patient’s appetite andresult in an inadequate dietary intake, the patient’s nutritionalstatus is assessed and strategies are implemented to ensure an ad-equate diet.

AsthmaAsthma is a chronic inflammatory disease of the airways thatcauses airway hyperresponsiveness, mucosal edema, and mucusproduction. This inflammation ultimately leads to recurrentepisodes of asthma symptoms: cough, chest tightness, wheezing,and dyspnea (Fig. 24-6). Estimates show that nearly 17 millionAmericans have asthma, and more than 5,000 die from this dis-ease annually (Centers for Disease Control and Prevention[CDC], 1998; CDC, 1999; NCHS, 2001). In 1998, asthma ac-counted for over 13.9 million outpatient visits to physician of-fices or hospital clinics and over 2.0 million emergency roomvisits (NCHS, 2001).

Asthma differs from the other obstructive lung diseases in thatit is largely reversible, either spontaneously or with treatment. Pa-tients with asthma may experience symptom-free periods alter-nating with acute exacerbations, which last from minutes tohours or days. Asthma can occur at any age and is the most com-mon chronic disease of childhood. Despite increased knowledgeregarding the pathology of asthma and the development of bet-ter medications and management plans, the death rate fromasthma continues to increase. For most patients it is a disruptivedisease, affecting school and work attendance, occupational choices,physical activity, and general quality of life.

Allergy is the strongest predisposing factor for asthma. Chronicexposure to airway irritants or allergens also increases the risk fordeveloping asthma. Common allergens can be seasonal (eg, grass,tree, and weed pollens) or perennial (eg, mold, dust, roaches, oranimal dander). Common triggers for asthma symptoms andexacerbations in patients with asthma include airway irritants(eg, air pollutants, cold, heat, weather changes, strong odors orperfumes, smoke), exercise, stress or emotional upsets, sinusitiswith postnasal drip, medications, viral respiratory tract infections,and gastroesophageal reflux. Most people who have asthma aresensitive to a variety of triggers. A patient’s asthma condition willchange depending upon the environment, activities, manage-ment practices, and other factors (NHLBI, 1998).


PathophysiologyThe underlying pathology in asthma is reversible and diffuse air-way inflammation. The inflammation leads to obstruction fromthe following: swelling of the membranes that line the airways(mucosal edema), reducing the airway diameter; contraction ofthe bronchial smooth muscle that encircles the airways (bron-chospasm), causing further narrowing; and increased mucus pro-duction, which diminishes airway size and may entirely plug thebronchi.

The bronchial muscles and mucus glands enlarge; thick, tena-cious sputum is produced; and the alveoli hyperinflate. Some pa-tients may have airway subbasement membrane fibrosis. This iscalled airway “remodeling” and occurs in response to chronic in-flammation. The fibrotic changes in the airway lead to airway nar-rowing and potentially irreversible airflow limitation (NIH, 2001;NHLBI, 1998).

Cells that play a key role in the inflammation of asthma aremast cells, neutrophils, eosinophils, and lymphocytes. Mast cells,when activated, release several chemicals called mediators. Thesechemicals, which include histamine, bradykinin, prostaglandins,and leukotrienes, perpetuate the inflammatory response, causingincreased blood flow, vasoconstriction, fluid leak from the vascu-lature, attraction of white blood cells to the area, and broncho-constriction (NHLBI, 1998). Regulation of these chemicals is theaim of much of the current research regarding pharmacologictherapy for asthma.

Further, alpha- and beta2-adrenergic receptors of the sympa-thetic nervous system are located in the bronchi. When the alpha-adrenergic receptors are stimulated, bronchoconstriction occurs;when the beta2-adrenergic receptors are stimulated, bronchodila-

tion results. The balance between alpha and beta2 receptors is con-trolled primarily by cyclic adenosine monophosphate (cAMP).Alpha-adrenergic receptor stimulation results in a decrease incAMP, which leads to an increase of chemical mediators released bythe mast cells and bronchoconstriction. Beta2-receptor stimulationresults in increased levels of cAMP, which inhibits the release ofchemical mediators and causes bronchodilation (NHLBI, 1998).

Clinical ManifestationsThe three most common symptoms of asthma are cough, dysp-nea, and wheezing. In some instances, cough may be the onlysymptom. Asthma attacks often occur at night or early in themorning, possibly due to circadian variations that influence air-way receptor thresholds.

An asthma exacerbation may begin abruptly but most fre-quently is preceded by increasing symptoms over the previous fewdays. There is cough, with or without mucus production. Attimes the mucus is so tightly wedged in the narrowed airway thatthe patient cannot cough it up. There may be generalized wheez-ing (the sound of airflow through narrowed airways), first on ex-piration and then possibly during inspiration as well. Generalizedchest tightness and dyspnea occur. Expiration requires effort andbecomes prolonged. As the exacerbation progresses, diaphoresis,tachycardia, and a widened pulse pressure may occur along withhypoxemia and central cyanosis (a late sign of poor oxygenation).Although life-threatening and severe hypoxemia can occur inasthma, it is relatively uncommon. The hypoxemia is secondaryto a ventilation–perfusion mismatch and readily responds to sup-plemental oxygenation.


Predisposing Factors• Atopy• Female gender

Causal Factors• Exposure to indoorand outdoor allergens• Occupationalsensitizers

Contributing Factors• Respiratory infections• Air pollution• Active/passive smoking• Other (diet, small size at birth)

Inflammation

Hyperresponsivenessof airways Airflow limitation

Risk factors for exacerbations• Allergens• Respiratory infections• Exercise and hyperventilation• Weather changes• Exposure to sulfur dioxide• Exposure to food, additives,medications

Symptoms• Wheezing• Cough• Dyspnea• Chest tightness

FIGURE 24-6 Pathophysiology of asthma.Adapted from materials developed for the GlobalInitiative for Asthma (GINA): Global Strategy forAsthma Management and Prevention, NationalInstitutes of Health–National Heart, Lung, andBlood Institute, revised 2002.

Physiology/Pathophysiology

Symptoms of exercise-induced asthma include maximal symp-toms during exercise, absence of nocturnal symptoms, and some-times only a description of a “choking” sensation during exercise.

Asthma is categorized according to symptoms and objectivemeasures of airflow obstruction (Table 24-3) (Expert Panel Re-port II, 1997).

Assessment and Diagnostic FindingsA complete family, environmental, and occupational history is es-sential. To establish the diagnosis, the clinician must determinethat periodic symptoms of airflow obstruction are present, air-flow is at least partially reversible, and other etiologies have beenexcluded. A positive family history and environmental factors,including seasonal changes, high pollen counts, mold, climatechanges (particularly cold air), and air pollution, are primarily as-sociated with asthma. In addition, asthma is associated with a va-riety of occupation-related chemicals and compounds, includingmetal salts, wood and vegetable dust, medications (eg, aspirin,antibiotics, piperazine, cimetidine), industrial chemicals and plas-tics, biologic enzymes (eg, laundry detergents), animal and insectdusts, sera, and secretions. Comorbid conditions that may ac-company asthma include gastroesophageal reflux, drug-inducedasthma, and allergic bronchopulmonary aspergillosis. Other pos-sible allergic reactions that may accompany asthma include eczema,rashes, and temporary edema.

During acute episodes, sputum and blood tests may discloseeosinophilia (elevated levels of eosinophils). Serum levels of im-munoglobulin E may be elevated if allergy is present. Arterial bloodgas analysis and pulse oximetry reveal hypoxemia during acute at-tacks. Initially, hypocapnia and respiratory alkalosis are present. Asthe condition worsens and the patient becomes more fatigued, thePaCO2 may rise. A normal PaCO2 value may be a signal of im-pending respiratory failure. Because CO2 is 20 times more dif-fusible than oxygen, it is rare for PaCO2 to be normal or elevatedin a person who is breathing very rapidly. During an exacerbation,the FEV1 and FVC are markedly decreased but improve with bron-chodilator administration (demonstrating reversibility). Pul-monary function is usually normal between exacerbations.

The occurrence of a severe, continuous reaction is referred to asstatus asthmaticus and is considered life-threatening (see below).

PreventionPatients with recurrent asthma should undergo tests to identifythe substances that precipitate the symptoms. Possible causes aredust, dust mites, roaches, certain types of cloth, pets, horses, de-tergents, soaps, certain foods, molds, and pollens. If the attacksare seasonal, pollens can be strongly suspected. The patient is in-structed to avoid the causative agents whenever possible.

Knowledge is the key to quality asthma care. Although na-tional guidelines are available for the care of the asthma patient,unfortunately health care providers may not follow them. Failureto follow the guidelines in the following areas has been noted:lack of treatment of patients who have symptoms more than 2 daysper week with a regular medication schedule, lack of patient-specific advice on improving the environment and an explanationabout the importance of doing so, lack of encouragement for pa-tients to monitor their peak flow measurements with a diary, andlack of written, up-to-date educational materials (Plaut, 2001).

A 1998 survey by a group called “Asthma in America” foundthat 11% of physicians were unaware of the national asthmaguidelines. Only 35% of patients with asthma who were surveyedreported having pulmonary function testing in the past year.

While 83% of physicians reported prescribing peak flow metermonitoring, only 62% of patients had ever heard of a peak flowmeter (Rickard & Stempel, 1999). All health care providers caringfor asthma patients need to be aware of the national guidelinesand use them (Expert Panel Report II, 1997).

ComplicationsComplications of asthma may include status asthmaticus, respira-tory failure, pneumonia, and atelectasis. Airway obstruction,particularly during acute asthmatic episodes, often results in hy-poxemia, requiring the administration of oxygen and the moni-toring of pulse oximetry and arterial blood gases. Fluids areadministered because people with asthma are frequently dehydratedfrom diaphoresis and insensible fluid loss with hyperventilation.

Medical ManagementImmediate intervention is necessary because the continuing andprogressive dyspnea leads to increased anxiety, aggravating thesituation.

PHARMACOLOGIC THERAPYTwo general classes of asthma medications are long-acting med-ications to achieve and maintain control of persistent asthma andquick-relief medications for immediate treatment of asthmasymptoms and exacerbations (Table 24-4). Because the under-lying pathology of asthma is inflammation, control of persistentasthma is accomplished primarily with regular use of anti-inflammatory medications. These medications have systemic sideeffects when used long term. The route of choice for administra-tion of these medications is the MDI because it allows for topicaladministration. Critical to the success of inhaled therapy is theproper use of the MDI (see Chart 24-4). If the patient has diffi-culty with this procedure, the use of a spacer device is indicated.Table 24-3 presents a stepwise approach for managing asthma(Expert Panel Report II, 1997). Information on use of the MDIand spacer device is given in the previous section on COPD.

Long-Acting Control Medications. Corticosteroids are the mostpotent and effective anti-inflammatory medications currentlyavailable. They are broadly effective in alleviating symptoms, im-proving airway function, and decreasing peak flow variability.Initially, the inhaled form is used. A spacer should be used withinhaled corticosteroids and the patient should rinse the mouthafter administration to prevent thrush, a common complicationof inhaled corticosteroid use. A systemic preparation may be usedto gain rapid control of the disease; to manage severe, persistentasthma; to treat moderate to severe exacerbations; to acceleraterecovery; and to prevent recurrence (Dhand, 2000).

Cromolyn sodium (Intal) and nedocromil (Tilade) are mild tomoderate anti-inflammatory agents that are used more com-monly in children. They also are effective on a prophylactic basisto prevent exercise-induced asthma or in unavoidable exposure toknown triggers. These medications are contraindicated in acuteasthma exacerbations.

Long-acting beta2-adrenergic agonists are used with anti-inflammatory medications to control asthma symptoms, partic-ularly those that occur during the night. These agents are alsoeffective for preventing exercise-induced asthma. Long-actingbeta2-adrenergic agonists are not indicated for immediate relief ofsymptoms.


(text continues on page 592)


Table 24-3 • Stepwise Approach for Managing Asthma in Adults and Children Over 5 Years Old

Goals of Asthma Treatment• Prevent chronic and troublesome symptoms (eg, coughing or

breathlessness in the night, in the early morning, or after exertion)• Maintain near-normal pulmonary function• Maintain normal activity levels (including exercise and other physical

activity)

• Prevent recurrent exacerbations of asthma and minimize the needfor emergency department visits or hospitalizations

• Provide optimal pharmacotherapy with minimal or no adverse effects• Meet patients’ and families’ expectation of and satisfaction with

asthma care

STEP 4Severe

Persistent*

STEP 3Moderate

Persistent

STEP 2Mild

Persistent

• Continualsymptoms

• Limited physi-cal activity

• Frequent ex-acerbations

• Dailysymptoms

• Daily use ofinhaled short-actingbeta2-agonist

• Exacerbationsaffect activity

• Exacerbations≥2 times aweek; may last days

• Symptoms>2 times aweek but <1time a day

• Exacerbationsmay affectactivity

Frequent

>1 time aweek

>2 timesa month

• FEV1 orPEF ≤60%predicted

• PEFvariability>30%

• FEV1 orPEF 60%to 80%predicted

• PEFvariability>30%

• FEV1 orPEF ≥80%predicted

• PEFvariability20%–30%

Daily medications:• Anti-inflammatory:

inhaled corticosteroid(high dose) AND

• Long-acting bronchodila-tor: either long-actinginhaled beta2-agonist,sustained-release theo-phylline, or long-actingbeta2-agonist tabletsAND

• Corticosteroid tablets orsyrup long term (2 mg/kg/day, generally do notexceed 60 mg per day).

Daily medication:• Either

– Anti-inflammatory:inhaled corticosteroid(medium dose) OR

– Inhaled corticosteroid(low–medium dose) andadd a long-acting bron-chodilator, especially fornighttime symptoms;either long-actinginhaled beta2-agonist,sustained-release theo-phylline, or long-actingbeta2-agonist tablets.

• If needed– Anti-inflammatory:

inhaled corticosteroids(medium–high dose)AND

– Long-acting broncho-dilator, especially fornighttime symptoms;either long-acting in-haled beta2-agonist,sustained-release theo-phylline, or long-actingbeta2-agonist tablets.

Daily medication:• Anti-inflammatory: either

inhaled corticosteroid(low doses) or cromolynor nedocromil (childrenusually begin with a trial of cromolyn ornedocromil).

• Short-acting bron-chodilator: inhaledbeta2-agonists asneeded forsymptoms.

• Intensity of treat-ment will dependon severity ofexacerbation.

• Use of short-actinginhaled beta2-agonists on a dailybasis, or increasinguse, indicates theneed for additionallong-term controltherapy.



• Use of short-actinginhaled beta2-agonists on a dailybasis, or increasinguse, indicates theneed for additionallong-term controltherapy.



(continued)

NIGHTTIME LUNG SYMPTOMS** SYMPTOMS FUNCTION LONG-TERM CONTROL QUICK RELIEF EDUCATION

Steps 2 and 3actions plus:

• Refer toindividualeducation/counseling

Step 1 actionsplus:

• Teach self-monitoring

• Refer to groupeducation ifavailable

• Review andupdate self-managementplan

Step 1 actionsplus:

• Teach self-monitoring

• Refer to groupeducation ifavailable


Table 24-3 • Stepwise Approach for Managing Asthma in Adults and Children Over 5 Years Old (Continued)

NIGHTTIME LUNG SYMPTOMS** SYMPTOMS FUNCTION LONG-TERM CONTROL QUICK RELIEF EDUCATION

STEP 1Mild

Intermittent

• Symptoms ≤2times a week

• Asymptomaticand normalPEF betweenexacerbations

• Exacerbationsbrief (from afew hours to afew days); in-tensity mayvary

≤2 times amonth

• FEV1 orPEF ≥80%predicted

• PEF vari-ability<20%

• Sustained-release theo-phylline to serum concen-tration of 5–15 µg/mL isan alternative. Zafirlukastor zileuton may also beconsidered for patients ≥12 years of age, althoughtheir position in therapy isnot fully established.

• No daily medicationneeded.

• Use of short-actinginhaled beta2-agonists on a dailybasis, or increasinguse, indicates theneed for additionallong-term-controltherapy.



• Use of short-actinginhaled beta2-agonists more than 2 times a week mayindicate the needto initiate long-term controltherapy.

• Review andupdate self-managementplan

• Teach basicfacts aboutasthma

• Teach inhaler/spacer/holdingchamber tech-nique

• Discuss rolesof medications

• Develop self-managementplan

• Develop actionplan for whenand how totake rescueactions

• Discuss appro-priate environ-mental controlmeasures toavoid exposureto knownallergens andirritants

↓Step DownReview treatment every 1 to 6 months; a gradual stepwise reduction

in treatment may be possible.

Notes:• The stepwise approach presents general guidelines to assist clinical

decision making; it is not intended to be a specific prescription.Asthma is highly variable; clinicians should tailor specific medica-tion plans to the needs and circumstances of individual patients.

• Gain control as quickly as possible; then decrease treatment to theleast medication necessary to maintain control. Gaining controlmay be accomplished either by starting treatment at the step mostappropriate to the initial severity of the condition or by starting at ahigher level of therapy (eg, a course of systemic corticosteroids orhigher dose of inhaled corticosteroids).

↑ Step UpIf control is not maintained, consider step up. First, review patient

medication technique, adherence, and environmental control (avoid-ance of allergens or other factors that contribute to asthma severity).

• A rescue course of systemic corticosteroid may be needed at anytime and at any step.

• Some patients with intermittent asthma experience severe and life-threatening exacerbations separated by long periods of normal lungfunction and no symptoms. This may be especially common withexacerbations provoked by respiratory infections. A short course ofsystemic corticosteroids is recommended.

• At each step, patients should control their environment to avoid orcontrol factors that make their asthma worse (eg, allergens, irri-tants); this requires specific diagnosis and education.

PEF, peak expiratory flow*The presence of one of the features of severity is sufficient to place a patient in that category. An individual should be assigned to the mostsevere grade in which any feature occurs. The characteristics noted in this table are general and may overlap because asthma is highly variable.Furthermore, an individual’s classification may change over time.**Patients at any level of severity can have mild, moderate, or severe exacerbations. Some patients with intermittent asthma experience severeand life-threatening exacerbations separated by long periods of normal lung function and no symptoms.Highlights of the Expert Panel Report 2. (1997). Guidelines for the diagnosis and management of asthma. National Institutes of Health, NationalHeart, Lung and Blood Institute, NIH Publication No 97-4051A, p. 29.

Methylxanthines (theophylline [Slo-bid, Theo-24, Theo-Dur])are mild to moderate bronchodilators usually used in addition toinhaled corticosteroids, mainly for relief of nighttime asthmasymptoms. There is some evidence that theophylline may have amild anti-inflammatory effect (NHLBI, 1998).

Leukotriene modifiers (inhibitors) or antileukotrienes are anew class of medications. Leukotrienes are potent bronchocon-strictors that also dilate blood vessels and alter permeability.Leukotriene inhibitors act by either interfering with leukotrienesynthesis or blocking the receptors where leukotrienes exert theiraction (Boushey, Fick, Lazarus & Martin, 2000). At this time,they may provide an alternative to inhaled corticosteroids formild persistent asthma or may be added to a regimen of inhaledcorticosteroids in more severe asthma to attain further control.

In addition, combination products are also available (eg,albuterol/ipratropium [Combivent]) and offer ease of use for thepatient.

Quick-Relief Medications. Short-acting beta-adrenergic agonistsare the medications of choice for relieving acute symptoms andpreventing exercise-induced asthma. They have a rapid onset ofaction. Anticholinergics (eg, ipratropium bromide [Atrovent])may bring added benefit in severe exacerbations, but they are usedmore frequently in COPD patients.

MANAGEMENT OF ASTHMA EXACERBATIONAsthma exacerbations are best managed by early treatment andeducation of the patient (Expert Panel Report II, 1997). Quick-acting beta-adrenergic medications are first used for prompt re-

lief of airflow obstruction. Systemic corticosteroids may be nec-essary to decrease airway inflammation in patients who fail to re-spond to inhaled beta-adrenergic medications. In some patients,oxygen supplementation may be required to relieve hypoxemiaassociated with a moderate to severe exacerbation (Expert PanelReport II, 1997). Also, response to treatment may be monitoredby serial measurements of lung function.

A written action plan is the most useful tool for the patient(Fig. 24-7). This helps to guide the patient in self-managementstrategies regarding an exacerbation and also provides instruc-tions regarding recognition of early warning signs of worseningasthma. Patient self-management and early recognition of prob-lems lead to more efficient communication with health careproviders regarding an asthma exacerbation (Expert Panel ReportII, 1997).

PEAK FLOW MONITORINGPeak flow meters measure the highest airflow during a forced ex-piration (Fig. 24-8). Daily peak flow monitoring is recommendedfor all patients with moderate or severe asthma because it helpsmeasure asthma severity and, when added to symptom monitor-ing, indicates the current degree of asthma control. The patientis instructed in the proper technique, particularly to give maxi-mal effort. The “personal best” is determined after monitoringpeak flows for 2 or 3 weeks after receiving optimal asthma ther-apy. The green (80% to 100% of personal best), yellow (60% to80%), and red (less than 60%) zones are determined, and specificactions are delineated for each zone, enabling the patient to mon-itor and manipulate his or her own therapy after careful instruc-tion (Expert Panel Report II, 1997). This reinforces compliance,independence, and self-efficacy (Reinke, 2000).

Nursing ManagementThe immediate nursing care of the patient with asthma dependson the severity of the symptoms. The patient may be treated suc-cessfully as an outpatient if asthma symptoms are relatively mild,or he or she may require hospitalization and intensive care foracute and severe asthma.

The patient and family are often frightened and anxious be-cause of the patient’s dyspnea. Thus, an important aspect of careis a calm approach. The nurse assesses the patient’s respiratorystatus by monitoring the severity of symptoms, breath sounds,peak flow, pulse oximetry, and vital signs. The nurse obtains ahistory of allergic reactions to medications before administeringmedications and identifies the patient’s current use of medica-tions. The nurse administers medications as prescribed and mon-itors the patient’s responses to those medications. Fluids may beadministered if the patient is dehydrated, and antibiotic agentsmay be prescribed if the patient has an underlying respiratory in-fection. If the patient requires intubation because of acute respi-ratory failure, the nurse assists with the intubation procedure,continues close monitoring of the patient, and keeps the patientand family informed about procedures.

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-Care. A major challenge is to implementbasic asthma management principles at the community level(Reinke, 2000). Key issues include education of health careproviders, establishment of programs for asthma education (forpatients and providers), use of outpatient follow-up care for pa-tients, and a focus on chronic management versus acute episodiccare. The nurse is pivotal to achieving all of these objectives.


Table 24-4 • Classifications of Medications Used in Asthma

MEDICATION CLASS DRUG (BRAND NAME)

Long-Acting Control Medications

Corticosteroids

Mast cell stabilizers

Long-acting beta2-adrenergicagents

Xanthine derivatives

Leukotriene modifiers (inhibitors)

Combination products

Quick-Relief MedicationsShort-acting beta2-adrenergic

agents

Anticholingerics

beclomethasone (Beclovent,Vanceril), budesonide (Pulmi-cort), flunisolide (AeroBid),fluticasone propionate (Flovent),triamcinolone acetonide(Azmacort), prednisone

cromolyn sodium (Intal),nedocromil sodium (Tilade)

salmeterol (Serevent), albuterol(sustained release) (Volmax ER),formoterol fumarate (Foradil)

aminophylline, theophylline (Slo-bid, Theo-24, Theo-Dur)

zafirlukast (Accolate), zileuton(Zyflo), montelukast (Singulair)

albuterol sulfate + ipratropiumbromide (Combivent); flutica-sone propionate + salmeterol in-halation powder (Advair Diskus)

Albuterol (Proventil), levalbuterol(Xopenex), pirbuterol (Maxair),bitolterol (Tornalate)

ipratropium bromide (Atrovent)

Expert Panel Report II. (1997). Guidelines for the diagnosis and management of asthma.National Asthma Education and Prevention Program, National Institutes of Health.

593

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• The nature of asthma as a chronic inflammatory disease• The definition of inflammation and bronchoconstriction• The purpose and action of each medication• Triggers to avoid, and how to do so• Proper inhalation technique• How to perform peak flow monitoring (Chart 24-5)• How to implement an action plan• When to seek assistance, and how to do soAn assortment of excellent educational materials is available

from the Expert Panel Report II (1997) and the National Heart,


FIGURE 24-8 Peak flow meters measure the highest volume of air flow during a forced expiration (left). Volume ismeasured in color-coded zones (right): the green zone signifies 80% to 100% of personal best; yellow, 60% to 80%;and red, less than 60%. If peak flow falls below the red zone, the patient should take the appropriate actions prescribedby his or her health care provider.

Patient teaching is a critical component of care for the patientwith asthma (Plaut, 2001). Multiple inhalers, different types ofinhalers, antiallergy therapy, antireflux medications, and avoid-ance measures are all integral for long-term control. This com-plex therapy requires a patient–provider partnership to determinethe desired outcomes and to formulate a plan to achieve thoseoutcomes. The patient then carries out daily therapy as part ofself-care management, with input and guidance by the health careprovider. Before a partnership can be established, the patientneeds to understand the following:

Chart 24-5Home Care Checklist • Use of Peak Flow Meter

At the completion of the home care instruction, the patient or caregiver will be able to:

• Describe the rationale for using a peak flow meter in asthma management. ✓ ✓

• Explain how peak flow monitoring is used along with symptoms to determine severity of asthma. ✓ ✓

• Demonstrate steps for using the peak flow meter correctly:

• Move the indicator to the bottom of the numbered scale. ✓• Stand up. ✓• Take a deep breath and fill the lungs completely. ✓• Place mouthpiece in mouth and close lips around mouthpiece (do not put tongue inside opening). ✓• Blow out hard and fast with a single blow. ✓• Record the number achieved on the indicator. ✓

• Repeat steps 1–5 two more times and write the highest number in the asthma diary. ✓

• Explain how to determine the “personal best” peak flow reading. ✓ ✓

• Describe the significance of the color zones for peak flow monitoring. ✓ ✓

• Demonstrate how to clean the peak flow meter. ✓ ✓

• Discuss how and when to contact the health care provider about changes or decreases in peak flow values. ✓ ✓

Patient Caregiver

Lung and Blood Institute. The nurse should obtain current edu-cational materials for the patient based on the patient’s diagno-sis, causative factors, educational level, and cultural factors.

Continuing Care. The nurse who has contact with the patient inthe hospital, clinic, school, or office uses the opportunity to as-sess the patient’s respiratory status and ability to manage self-careto prevent serious exacerbations. The nurse emphasizes adherenceto the prescribed therapy, preventive measures, and the need tokeep follow-up appointments with the primary health careprovider. A home visit to assess the home environment for aller-gens may be indicated for the patient with recurrent exacerba-tions. The nurse refers the patient to community support groups.In addition, the nurse reminds the patient and family about theimportance of health promotion strategies and recommendedhealth screening.

STATUS ASTHMATICUSStatus asthmaticus is severe and persistent asthma that does notrespond to conventional therapy. The attacks can last longer than24 hours. Infection, anxiety, nebulizer abuse, dehydration, in-creased adrenergic blockage, and nonspecific irritants may con-tribute to these episodes. An acute episode may be precipitatedby hypersensitivity to aspirin.

PathophysiologyThe basic characteristics of asthma (constriction of the bronchi-olar smooth muscle, swelling of the bronchial mucosa, and thick-ened secretions) decrease the diameter of the bronchi and areapparent in status asthmaticus. A ventilation–perfusion abnor-mality results in hypoxemia and respiratory alkalosis initially, fol-lowed by respiratory acidosis. There is a reduced PaO2 and aninitial respiratory alkalosis, with a decreased PaCO2 and an in-creased pH. As status asthmaticus worsens, the PaCO2 increasesand the pH falls, reflecting respiratory acidosis.

Clinical ManifestationsThe clinical manifestations are the same as those seen in severeasthma: labored breathing, prolonged exhalation, engorged neckveins, and wheezing. However, the extent of wheezing does notindicate the severity of the attack. As the obstruction worsens, thewheezing may disappear, and this is frequently a sign of impend-ing respiratory failure.

Assessment and Diagnostic FindingsPulmonary function studies are the most accurate means of as-sessing acute airway obstruction. Arterial blood gas measure-ments are obtained if the patient cannot perform pulmonaryfunction maneuvers because of severe obstruction or fatigue, or ifthe patient does not respond to treatment. Respiratory alkalosis(low PaCO2) is the most common finding in patients with asthma.A rising PaCO2 (to normal levels or levels indicating respiratoryacidosis) frequently is a danger sign of impending respiratoryfailure.

Medical ManagementIn the emergency setting, the patient is treated initially with ashort-acting beta-adrenergic agonist and corticosteroids. The pa-

tient usually requires supplemental oxygen and intravenous flu-ids for hydration. Oxygen therapy is initiated to treat dyspnea,central cyanosis, and hypoxemia. Humidified oxygen by eitherVenturi mask or nasal catheter is administered. The flow isbased on pulse oximetry or arterial blood gas values. The PaO2

is maintained at 65 to 85 mm Hg. Sedative medications are con-traindicated. If there is no response to repeated treatments, hos-pitalization is required. Other criteria indicating the need forhospitalization include poor pulmonary function test results anddeteriorating blood gas levels (respiratory acidosis), which mayindicate that the patient is tiring and will require mechanical ven-tilation. Although most patients do not need mechanical ventila-tion, it is used for patients in respiratory failure, for those who tireand are too fatigued by the attempt to breathe, or for those whoseconditions do not respond to initial treatment.

Death from asthma is associated with several risk factors,including the following:

• Past history of sudden and severe exacerbations• Prior endotracheal intubation for asthma• Prior admission to the intensive care unit for an asthma

exacerbation• Two or more hospitalizations for asthma within the past

year• Three or more emergency care visits for asthma in the past

year• Excessive use of short-acting beta-adrenergic inhalers (more

than two canisters per month)• Recent withdrawal from systemic corticosteroids• Comorbidity of cardiovascular disease or COPD• Psychiatric disease• Low socioeconomic status• Urban residence (Expert Panel Report II, 1997)

Nursing ManagementThe nurse constantly monitors the patient for the first 12 to 24 hours, or until status asthmaticus is under control. The nursealso assesses the patient’s skin turgor to identify signs of dehy-dration. Fluid intake is essential to combat dehydration, to loosensecretions, and to facilitate expectoration. The nurse administersintravenous fluids as prescribed, up to 3 to 4 L/day, unless con-traindicated. The patient’s energy needs to be conserved, and theroom should be quiet and free of respiratory irritants, includingflowers, tobacco smoke, perfumes, or odors of cleaning agents.A nonallergenic pillow should be used.

Cystic FibrosisCystic fibrosis (CF) is the most common fatal autosomal reces-sive disease among the Caucasian population. An individual mustinherit a defective copy of the CF gene (one from each parent) tohave CF. One in 31 Americans are unknowing symptom carriersof this gene (Katkin, 2002). The frequency of CF is 1 in 2,000 to3,000 live births, and there are approximately 30,000 childrenand adults with this disease in the United States (Cystic FibrosisFoundation, 2002). Although CF was once considered a fatalchildhood disease, approximately 38% of people living with thedisease are 18 years of age or older (Cystic Fibrosis Foundation,2002). Cystic fibrosis is usually diagnosed in infancy or early child-hood, but patients may be diagnosed later in life. For individualsdiagnosed later in life, respiratory symptoms are frequently themajor manifestation of the disease.


PathophysiologyThis disease is caused by mutations in the CF transmembraneconductance regulator protein, which is a chloride channel foundin all exocrine tissues (Katkin, 2002). Chloride transport prob-lems lead to thick, viscous secretions in the lungs, pancreas, liver,intestine, and reproductive tract as well as increased salt contentin sweat gland secretions. In 1989, major breakthroughs weremade in this disease with the identification of the CF gene. Theability to detect the common mutations of this gene allows forroutine screening for this disease as well as the detection of carri-ers. Genetic counseling is an important part of health care forcouples at risk.

Airflow obstruction is a key feature in the presentation of CF.This obstruction is due to bronchial plugging by purulent secre-tions, bronchial wall thickening due to inflammation, and, overtime, airway destruction (Katkin, 2002). These chronic retainedsecretions in the airways set up an excellent reservoir for contin-ued bronchial infections.

Clinical ManifestationsThe pulmonary manifestations of this disease include a productivecough, wheezing, hyperinflation of the lung fields on chest x-ray,and pulmonary function test results consistent with obstructiveairways disease (Katkin, 2002). Colonization of the airways withpathogenic bacteria usually occurs early in life. Staphylococcus au-reus and Haemophilus influenzae are common organisms duringearly childhood. As the disease progresses, Pseudomonas aeruginosais ultimately isolated from the sputum of most patients. Upper res-piratory manifestations of the disease include sinusitis and nasalpolyps.

Nonpulmonary clinical manifestations include gastrointesti-nal problems (eg, pancreatic insufficiency, recurrent abdominalpain, biliary cirrhosis, vitamin deficiencies, recurrent pancreati-tis, weight loss), genitourinary problems (male and female infer-tility), and clubbing of the extremities. (See Chap. 40 for adiscussion of pancreatitis.)

Assessment and Diagnostic FindingsMost of the time, the diagnosis of CF is made based on an ele-vated result of a sweat chloride concentration test, along withclinical signs and symptoms consistent with the disease. Repeatedsweat chloride values of greater than 60 mEq/L distinguish mostindividuals with CF from those with other obstructive diseases.A molecular diagnosis may also be used in evaluating commongenetic mutations of the CF gene.

Medical ManagementPulmonary problems remain the leading cause of morbidity andmortality in CF. Because chronic bacterial infection of the air-ways occurs in individuals with CF, control of infections is key inthe treatment. Antibiotic medications are routinely prescribed foracute pulmonary exacerbations of the disease. Depending uponthe severity of the exacerbation, aerosolized, oral, or intravenousantibiotic therapy may be used. Antibiotic agents are selectedbased upon the results of a sputum culture and sensitivity. Pa-tients with CF have problems with bacteria that are resistant tomultiple drugs and require multiple courses of antibiotic agentsover long periods of time.

Bronchodilators are frequently administered to decrease air-way obstruction. Differing pulmonary techniques are used to en-hance secretion clearance. Examples include manual posturaldrainage and chest physical therapy, high-frequency chest wall os-cillation, and other devices that assist in airway clearance (PEPmasks [masks that generate positive expiratory pressure], “flutterdevices” [devices that provide an oscillatory expiratory pressurepattern with positive expiratory pressure and assist with expecto-ration of secretions]).

Inhaled mucolytic agents such as dornase alfa (Pulmozyme) orN-acetylcysteine (Mucomyst) may also be used. These agentshelp to decrease the viscosity of the sputum and promote expec-toration of secretions.

To decrease the inflammation and ongoing destruction of theairways, anti-inflammatory agents may also be used. These mayinclude inhaled corticosteroids or systemic therapy. Other anti-inflammatory medications have also been studied in CF. Ibupro-fen was studied in children with CF and some benefit wasdemonstrated, but there is little information on its use in youngor older adults with CF (Katkin, 2002).

Supplemental oxygen is used to treat the progressive hypox-emia that occurs with CF. It helps to correct the hypoxemia andmay minimize the complications seen with chronic hypoxemia(pulmonary hypertension).

Lung transplantation is an option for a small, select popula-tion of CF patients. A double lung transplant technique is useddue to the chronically infected state of the lungs seen in end-stageCF. Because there is a long waiting list for lung transplant recip-ients, many patients die while awaiting a transplant.

Gene therapy is a promising approach to management, withmany clinical trials underway. It is hoped that various methodsof administering gene therapy will carry healthy genes to thedamaged cells and correct defective CF cells. Efforts are under-way to develop innovative methods of delivering therapy to theCF cells of the airways.

Nursing ManagementNursing care of the adult with CF includes assisting the patientto manage pulmonary symptoms and to prevent complications ofCF. Specific nursing measures include strategies that promoteremoval of pulmonary secretions; chest physiotherapy, includingpostural drainage, chest percussion, and vibration, and breathingexercises are implemented and are taught to the patient and to thefamily when the patient is very young. The patient is remindedof the need to reduce risk factors associated with respiratory in-fections (eg, exposure to crowds and to persons with known in-fections). The patient is taught the early signs and symptoms ofrespiratory infection and disease progression that indicate theneed to notify the primary health care provider.

The nurse emphasizes the importance of an adequate fluid anddietary intake to promote removal of secretions and to ensure anadequate nutritional status. Because CF is a life-long disorder, pa-tients often have learned to modify their daily activities to ac-commodate their symptoms and treatment modalities. As thedisease progresses, however, assessment of the home environmentmay be warranted to identify modifications required to addresschanges in the patient’s needs, increasing dyspnea and fatigue,and nonpulmonary symptoms.

Although gene therapy and double lung transplantation arepromising therapies for CF, they are limited in availability andlargely experimental. As a result, the life expectancy of adults withCF is shortened. Therefore, end-of-life issues and concerns need


to be addressed in patients when warranted. For the patientwhose disease is progressing and who is developing increasinghypoxemia, preferences for end-of-life care should be discussed,documented, and honored (see Chap. 17). Patients and familymembers need support as they face a shortened life span and anuncertain future.

FitzGerald, J. M. (2001). Evidence-based asthma management. Hamilton,Ontario: B. C. Decker.

George, R. B., San Pedro, G. S., & Stoller, J. K. (2000). Chronic ob-structive pulmonary disease, bronchiectasis, and cystic fibrosis. InR. B. George, R. W. Light, M. A. Matthay & R. A. Matthay (Eds.),Chest medicine: Essentials of pulmonary and critical care medicine(4th ed.). Philadelphia: Lippincott Williams & Wilkins.

Hall, J. B. (2000). Acute asthma: Assessment and management. New York:McGraw-Hill, Health Professions Division.

Katkin, J. P. (2002). Clinical manifestations and diagnosis of cystic fibro-sis. UpToDate, Vol. 10(1), Wellesley, MA.

Kavuru, M. S., & Wiedemann, H. P. (2000). Asthma. In R. B. George,R. W. Light, M. A. Matthay & R. A. Matthay (Eds.), Chest medi-cine: Essentials of pulmonary and critical care medicine (4th ed., pp. 133–173). Philadelphia: Lippincott Williams & Wilkins.

Lieberman, P., & Anderson, J. A. (Eds.). (2000). Allergic diseases: Diag-nosis and treatment. Totowa, NJ: Humana.

National Center for Health Statistics. (2000). US mortality public usedata tape 1998. Centers for Disease Control and Prevention, Hyattsville, MD.

National Center for Health Statistics. (2001). New asthma estimates:Tracking prevalence, health care, and mortality. Fact sheet releasedOct. 5, 2001, Hyattsville, MD.

National Heart, Lung and Blood Institute (1998). Morbidity and mor-tality: 1998 chart book on cardiovascular, lung and blood diseases.

National Heart, Lung and Blood Institute (2000). Morbidity and mor-tality: 2000 chart book on cardiovascular, lung and blood diseases.

National Institutes of Health. (2001) Global initiative for chronic ob-structive lung disease: Global strategy for the diagnosis, management,and prevention of chronic obstructive pulmonary disease. U.S. Depart-ment of Health and Human Services, NIH Publication Number2701B.

O’Byrne, P. M. (2001). Manual of asthma management (2d ed.). Lon-don: W. B. Saunders.

JournalsAsterisks indicate nursing research articles.GeneralACCP/AACVPR Pulmonary Rehabilitation Guidelines Panel. (1997).

Pulmonary rehabilitation: Joint ACCP/AACVPR evidence-basedguidelines. Chest, 112(5), 1363–1396.

Adatsi, G. (1999). Health going up in smoke: How can you prevent it?American Journal of Nursing, 99(3), 63–69.

American Thoracic Society. (1999). Statement on pulmonary rehabili-tation. American Journal of Respiratory and Critical Care Medicine,159(5), 1666–1682.

Lacasse, Y., Guyatt, G., & Goldstein, R. (1997). The components of arespiratory rehabilitation program: A systematic overview. Chest,111(4), 1977–2088.

*McEntee, D. J., & Badenhop, D. T. (2000). Quality of life compar-isons: Gender and population differences in cardiopulmonary reha-bilitation. Heart Lung, 29(5), 340–347.

Rochester, C. L. (2000). Which pulmonary rehabilitation program isbest for your patient? Journal of Respiratory Diseases, 21(9), 539–546.

AsthmaBoushey, H. A., Fick, R. B., Lazarus, S., & Martin, A. (2000). Anti-IgE:

A unique approach to asthma management. Gardiner-CaldwellSynerMed, Califon, NJ, 2–24.

Busse, W. W., & Lemanske, R. F. Jr. (2001). Advances in immunology:Asthma. New England Journal of Medicine, 344(5), 350–362.

Caprioti, T. (1999). Leukotriene antagonists offer a new mechanism forasthma control. MedSurg Nursing, 8(5), 318–322.

Centers for Disease Control and Prevention. (1998). Forecasted state-specific estimates of self-reported asthma prevalence: United States,1998. MMWR Morbidity and Mortality Weekly Report, 47(47),1022–1025.

Centers for Disease Control and Prevention. (1999). Asthma PreventionProgram of the National Center for Environmental Health, At-A-Glance, 1999, 1–6.


1. A 75-year-old woman with end-stage COPD was re-cently admitted to your unit from the emergency room. Shecannot lie flat in bed, she is extremely short of breath, andshe has decreased breath sounds throughout the chest andcrackles in the posterior basilar areas. What is the patho-physiology associated with these findings? What medical andnursing interventions might be used to decrease or alleviatethese signs/symptoms?

2. Your patient at an outpatient asthma clinic is a 35-year-old inner-city Mexican-American mother with asthma. Useof an MDI on a regular daily schedule has been repeatedlyprescribed for her, but she reports that she does not use theMDI except as needed when extremely short of breath. De-scribe teaching techniques you might use to assess the pa-tient’s knowledge of the medication and provide educationabout the action of the MDI, frequency of use, and correctadministration of the medication. What methods would youuse to monitor use of the MDI and reinforce education?

3. As a nurse in your hospital’s community outreach clinic,you are responsible for providing group education and coun-seling to patients with asthma. What areas would you ad-dress regarding triggers for asthma? How might you havepatients assess their home environments?

4. Your 64-year-old patient has a history of bronchiectasisand heart failure following two myocardial infarctions. Topromote removal of pulmonary secretions, his physician hasprescribed chest physiotherapy and postural drainage. Thepatient reports that he is able to breathe easily only in a sit-ting position. Describe how you would modify chest physio-therapy and postural drainage given his statement that hecannot breathe in a supine or prone position.

5. Your 22-year-old patient is a college student with a his-tory of cystic fibrosis; he has been admitted to your unit forintravenous antibiotic therapy. Describe what pulmonary re-habilitation techniques would be appropriate for his diseaseprocess, which are age-specific and consistent with his activ-ity level.

REFERENCES AND SELECTED READINGS

BooksAmerican Association of Cardiovascular & Pulmonary Rehabilitation.

(1998). Guidelines for pulmonary rehabilitation programs (2nd ed.).Champaign, IL: Human Kinetics.

Cystic Fibrosis Foundation (2002). What is CF? http://www.cff.org(accessed June 13, 2002).

Cherniack, N. S., Homma, I., & Altose, M. (Eds.). (1999). Rehabilita-tion of the patient with respiratory disease. New York: McGraw-Hill.

Expert Panel Report II. (1997). Guidelines for the diagnosis and manage-ment of asthma. National Asthma Education and Prevention Pro-gram, National Institutes of Health.

Critical Thinking Exercises??

Dhand, R. (2000). Aerosol therapy in asthma. Current Opinion in Pul-monary Medicine, 6(1), 59–70.

Drazen, J. M., Israel, E., & O’Byrne, P. M. (1999). Treatment ofasthma with drugs modifying the leukotriene pathway. New EnglandJournal of Medicine, 340(3), 197–206.

Janson, S. (1998). National Asthma Education and Prevention Program,Expert Panel Report II: Overview and application for primary care.Lippincott’s Primary Care Practice, 2(6), 578–588.

McGann, E. (1999). Medication compliance in adults with asthma.American Journal of Nursing, 99(3), 45–46.

National Heart, Lung and Blood Institute. (1998). Asthma diagnosisand management. A continuing education module. http://www.nhlbi.nih.gov.

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RESOURCES AND WEBSITES

Agency for Healthcare Research and Quality, 2101 E. Jefferson St., Suite501, Rockville, MD 20852; (301) 594-1364; http://www.ahrq.org.

American Academy of Allergy, Asthma, and Immunology, 611 E. WellsSt., Milwaukee, WI 53202; (414) 272-6071; http://www.aaaai.org.

American Association of Cardiovascular and Pulmonary Rehabilitation,7611 Elmwood Ave., Suite 201, Middleton, WI 53562, (608) 831-5122; http://www.aacvpr.org.

American Association for Respiratory Care, 1720 Regal Row, Dallas, TX75235; (214) 630-3540; http://www.aarc.org.

American Cancer Society, 1599 Clifton Road NE, Atlanta, GA 30329-4251; (800) ACS-2345; http://www.cancer.org.

American College of Chest Physicians, 3300 Dundee Road, North-brook, IL 60062; (847) 498-1400; http://www.chest.org.

American Lung Association, 1740 Broadway, New York, NY 10019-4374; (212) 315-8700; http://www.lungusa.org.

American Thoracic Society, 1740 Broadway, New York, NY 10019;(212) 315-8700; http://www.thoracic.org.

Centers for Disease Control and Prevention, 1600 Clifton Road, NE,Atlanta, GA 30333; http://www.cdc.gov.

Cystic Fibrosis Foundation, 6931 Arlington Road, Bethesda, MD 20814;(310) 951-4422 or (800) FIGHT CF; http://www.cff.org.

National Cancer Institute; (800) 4-Cancer or (301) 496-5585; http://www.cancer.gov or http://www.nci.nih.gov.

National Heart, Lung and Blood Institute, National Institutes of Health,900 Rockville Pike, Bldg. 31, Bethesda, MD 20892; (301) 496-5166; http://www.nhlbi.nih.gov.

Respiratory Nursing Society, 11 Cornell Road, Latham, NY 12110;(518) 782-9400 x286l; e-mail: [email protected].

U.S. Department of Health and Human Services, Department of Healthand Human Services, 200 Independence Avenue, S.W., WashingtonDC 20201; (202) 619-0257; http://www.hhs.gov or http://www.healthfinder.gov.


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