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A CHRONIC inflammatory airway disorder, asthma is marked by air- way hyperresponsiveness with re- current episodes of wheezing, coughing, tightness of the chest, and shortness of breath. Typically, these episodes are associated with airflow obstruction that may be re- versed spontaneously or with treatment. Asthma affects approximately 300 million people around the world. In children, males have a higher asthma risk; in adults, fe- males have a higher prevalence. Experts believe asthma results from various host factors, environ- mental factors, or a combination. Host factors include gender, obesi- ty, and genetics. Genetic factors in- clude atopy. Defined as a genetic tendency to develop allergic dis- eases, such as asthma and allergic rhinitis, atopy commonly is linked to an immunoglobulin E (IgE)–me- diated response to allergens. Pathophysiology Understanding asthma pathophysi- ology helps you understand how the condition is diagnosed and treated. Our knowledge of asthma pathogenesis has changed dramati- cally in the last 25 years, as re- searchers have found various asth- ma phenotypes. Asthma involves many patho- physiologic factors, including bronchiolar inflammation with airway constriction and resist- ance that manifests as epi- sodes of coughing, shortness of breath, and wheezing. Asthma can affect the tra- chea, bronchi, and bronchi- oles. Inflammation can exist even though obvious signs and symptoms of asthma may not al- ways occur. Bronchospasms, edema, exces- sive mucus, and epithelial and muscle damage can lead to bron- choconstriction with broncho- spasm. Defined as sharp contrac- tions of bronchial smooth muscle, bronchospasm causes the airways to narrow; edema from microvascu- lar leakage contributes to airway narrowing. Airway capillaries may dilate and leak, increasing secre- tions, which in turn causes edema and impairs mucus clearance. (See How bronchospasm constricts the airway.) Asthma also may lead to an in- crease in mucus-secreting cells with expansion of mucus-secreting glands. Increased mucus secretion can cause thick mucus plugs that block the airway. Injury to the ep- ithelium may cause epithelial peel- ing, which may result in extreme airway impairment. Loss of the Understanding asthma pathophysiology, diagnosis, and management Learn about new research findings and current treatment strategies for this common disorder. By Shari J. Lynn, MSN, RN, and Kathryn Kushto-Reese, MS, RN www.AmericanNurseToday.com July 2015 American Nurse Today 49

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A CHRONIC inflammatory airwaydisorder, asthma is marked by air-way hyperresponsiveness with re-current episodes of wheezing,coughing, tightness of the chest,and shortness of breath. Typically,these episodes are associated withairflow obstruction that may be re-versed spontaneously or withtreatment.

Asthma affects approximately300 million people around theworld. In children, males have ahigher asthma risk; in adults, fe-males have a higher prevalence.

Experts believe asthma results

from various host factors, environ-mental factors, or a combination.Host factors include gender, obesi-ty, and genetics. Genetic factors in-clude atopy. Defined as a genetictendency to develop allergic dis-eases, such as asthma and allergicrhinitis, atopy commonly is linkedto an immunoglobulin E (IgE)–me-diated response to allergens.

PathophysiologyUnderstanding asthma pathophysi-ology helps you understand howthe condition is diagnosed andtreated. Our knowledge of asthmapathogenesis has changed dramati-cally in the last 25 years, as re-searchers have found various asth-ma phenotypes.

Asthma involves many patho-physiologic factors, includingbronchiolar inflammation withairway constriction and resist-ance that manifests as epi -sodes of coughing, shortnessof breath, and wheezing.Asthma can affect the tra-chea, bronchi, and bronchi-oles. Inflammation can exist

even though obvious signs andsymptoms of asthma may not al-ways occur.

Bronchospasms, edema, exces-sive mucus, and epithelial andmuscle damage can lead to bron-choconstriction with broncho -spasm. Defined as sharp contrac-tions of bronchial smooth muscle,bronchospasm causes the airwaysto narrow; edema from microvascu-lar leakage contributes to airwaynarrowing. Airway capillaries maydilate and leak, increasing secre-tions, which in turn causes edemaand impairs mucus clearance. (SeeHow bronchospasm constricts theairway.)

Asthma also may lead to an in-crease in mucus-secreting cellswith expansion of mucus-secretingglands. Increased mucus secretioncan cause thick mucus plugs thatblock the airway. Injury to the ep-ithelium may cause epithelial peel-ing, which may resultin extreme airwayimpairment.Loss ofthe

Understanding asthmapathophysiology, diagnosis,

and managementLearn about new research findings and currenttreatment strategies for this common disorder.

By Shari J. Lynn, MSN, RN, and Kathryn Kushto-Reese, MS, RN

www.AmericanNurseToday.com July 2015 American Nurse Today 49

50 American Nurse Today Volume 10, Number 7 www.AmericanNurseToday.com

epithelium’s barrier function allowsallergens to penetrate, causing theairways to become hyperrespon-sive—a major feature of asthma.The degree of hyperresponsivenessdepends largely on the extent ofinflammation and the individual’simmunologic response.

Asthma also causes loss of en-zymes that normally break downinflammatory mediators, with ensu-ing reflexive neural effects fromsensory nerve exposure. Withoutproper treatment and control, asth-ma may cause airway remodelingleading to changes to cells and tis-sues in the lower respiratory tract;these changes cause permanent fi-brotic damage. Such remodelingmay be irreversible, resulting inprogressive loss of lung functionand decreased response to therapy.

Classifying asthmaAsthma may be atopic, nonatopic,or a combination.• Atopic asthma begins in child-

hood and is linked to triggersthat initiate wheezing. It mayarise after exposure and re-sponse to a specific allergen,such as dust mites, grass or tree

pollen, pet dander, smoke, orcertain drugs or foods. On ex-posure to a trigger, excessive re-lease of IgE occurs, which initi-ates B-lymphocyte activation.IgE binds to cells related to in-flammation. This action causesrelease of inflammatory media-tors (such as chemokines, nitricoxide, prostaglandin D2, cyto -kines, histamine, and leuko -trienes), in turn triggering airway inflammation and bron-choconstriction. Women whosmoke during pregnancy maypredispose their unborn chil-dren to higher IgE levels, caus-ing hyperresponsiveness andasthma development. Exposureto pollution may have the sameeffect.

• Nonatopic asthma doesn’t in-

volve an IgE response. It mayhave fewer obvious triggers andusually occurs in adults, possiblysecondary to a viral infection.

DiagnosisAsthma diagnosis goes beyondsymptoms, such as coughing, chesttightness, wheezing, and dysp-nea—and even beyond signs andsymptoms that worsen at night andimprove after treatment. Diagnosismay require pulmonary functiontests (PFTs) and peak expiratoryflow (PEF) measurements. Withasthma, the ratio of forced expira-tory volume in 1 second (FEV1) toforced vital capacity (FVC, alsocalled FEV1%) typically declines.

Asthma symptoms can be re-versed by a rapid-acting beta2-agonist, such as albuterol, as meas-ured by spirometry. The general-ly acceptable response to beta2-agonists is a 12% or 200-mL increasein FEV1 or FVC. PEF measurementsnot only aid diagnosis but also helpclinicians monitor the disease.

Some patients with asthma signsand symptoms may have normalPFT results. They may need fur-ther diagnostic testing, such as air-way response testing using a bron -chial challenge. (See Bronchialchallenge.)

Clinicians must rule out otherconditions that may decrease FEV1and cause signs and symptoms thatmimic asthma. These conditions in-clude vocal cord dysfunction, gas-troesophageal reflux disease, is-chemic cardiac pain, chronicobstructive pulmonary disease,heart failure, upper-airway obstruc-tion, cystic fibrosis, hyperventila-tion, and foreign-body aspiration.Viral respiratory infections maylead to asthma exacerbations orcontribute to eventual develop-ment of the disorder.

ManagementAsthma management involves bothacute and long-term treatment.Medication selection hinges on the

How bronchospasm constricts the airwayThese illustrations compare a normal airway (left) to an asthmatic one (middle) and anasthmatic airway during an asthma attack (right).

Without proper treatment

and control, asthma may

cause airway remodeling.

www.AmericanNurseToday.com July 2015 American Nurse Today 51

patient’s age, disease severity, andcomorbidities.

Be sure to obtain a completemedication history before the pa-tient starts taking asthma medica-tions. Some drugs, including beta-blockers, angiotensin-convertingenzyme inhibitors, cholinergics,and nonpotassium-sparing diuret-ics, may be contraindicated for patients receiving certain asthmaagents.

Rescue (quick-relief) drugsMeant for short-term symptom re-lief, rescue drugs cause bronchodi-lation and are used mainly to pre-vent or treat an asthma attack.They begin working within min-utes and may remain effective forup to 6 hours. Potential side ef-fects include jitteriness and palpita-tions. Rescue drugs include iprat-ropium bromide inhaler (Atrovent),short-acting beta2-agonists, andoral corticosteroids. • Ipratropium bromide, an anti-

cholinergic, may be given incombination with short-actingbeta2-agonists in some cases.

• Beta2-agonists used for quick re-lief include albuterol, leval-buterol, metaproterenol, andterbutaline.

• Oral corticosteroids, such asprednisone and methylpred-nisolone, sometimes are usedfor brief periods during acuteasthma attacks that don’t re-spond to usual treatments.Long-term use can lead to highblood pressure, muscle weak-ness, cataracts, osteoporosis, decreased ability to resist infec-tion, and reduced growth inchildren.

Long-term control agentsUsed to prevent asthma attacksand control chronic symptoms,these agents include inhaled corti-costeroids, leukotriene modifiers,long-acting beta-agonists (LABAs),theophylline, and combination in-halers that contain both a corticos-

teroid and an LABA. These drugsmay take days or weeks to reachmaximal effect.

Leukotriene modifiers help pre-vent symptoms for up to 24 hours.LABAs, which may last up to 12hours, usually are given in combi-nation with an inhaled corticos-teroid, because when used alonethey may lead to a severe asthmaattack. LABAs also are prescribedto prevent nocturnal asthma symp-toms, such as coughing. Theoph -ylline, given orally, acts as a bron-chodilator and also is used to treatnocturnal symptoms.

Patient educationPatient education is crucial in asth-ma management. Teach patientsand their families how to use apeak flow meter, optimize environ-mental controls, and recognizeasthma signs and symptoms. Stressthe importance of smoking cessa-

tion. Urge patients to receive an-nual vaccinations, as asthma in-creases the risk of complicationsfrom respiratory diseases, such aspneumonia and influenza. �

Selected referencesAsthma overview. American Academy of Aller-gy Asthma and Immunology. www.aaaai.org/conditions-and-treatments/asthma.aspx

Corbridge S, Corbridge TC. Asthma in ado-lescents and adults. Am J Nurs. 2010;110(5):28-38.

Fanta CH. Treatment of acute exacerbationof asthma in adults. Last updated February 5,2015. www.uptodate.com/contents/treatment-of-acute-exacerbations-of-asthma-in-adults

Global Initiative for Asthma. Pocket Guidefor Asthma Management and Prevention (forAdults and Children Older than 5 Years).Updated 2015. www.ginasthma.org/local/uploads/files/GINA_Pocket_2015.pdf

Johnson J. Asthma assessment tips. J NursePract. 2010;6(5):383-4.

Kaufman G. Asthma: pathophysiology, diag-nosis and management. Nurs Stand. 2011;26(5):48-56.

Martinez FD, Vercelli D. Asthma. Lancet Sem.2013;382(9901):1360-72.

National Asthma Education and PreventionProgram. Expert Panel Report 3: Guidelinesfor the Diagnosis and Management of Asth-ma. Section 2: Definition, pathophysiologyand pathogenesis of asthma and natural his-tory of asthma. Bethesda, MD: NationalHeart, Lung, and Blood Institute; 2007; 1-24.

Pruitt B, Lawson R. Assessing and managingasthma: a Global Initiative for Asthma up-date. Nursing. 2011;41(5):46-52.

Shari J. Lynn and Kathryn Kushto-Reese are instruc-tors at the Johns Hopkins University School of Nurs-ing in Baltimore, Maryland.

Bronchial challengeIn the bronchial challenge, a patient with airway hypersensitivity inhales an aggra-vating agent with the potential to cause bronchoconstriction. The inhaled agentmay act directly (such as inhaled histamine or methacholine) or indirectly (such asmannitol).

The agent’s histamine properties increase mucus production and bronchocon-striction. Cholinergic properties of methacholine cause wheezing and shortness ofbreath. The mannitol inhalation challenge (approved in some countries) maycause airway narrowing in asthmatic patients by altering the osmolarity of airwaysurface liquid, in turn resulting in mast cell granulation and release of inflammato-ry mediators.

In these tests, a decrease of 15% to 20% from the patient’s baseline forced ex-piratory volume in 1 second indicates asthma.

Be sure to obtain a

complete medication

history before the patient

starts taking asthma

medications.