Emp Asthma

EMERGENCY MEDICINE PRACTICE
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E

Asthma: An Evidence-Based
Management Update

T

HE young man looks bad. The medics struggle to keep him
upright as they wheel him past, but his skin is slippery from the
torrents of sweat that surge from his cyanotic torso. You yell to him, but he
does not respond. His whole being is focused on getting one more nearly
impossible breath. The boy’s neck muscles strain, his chest heaves, but you
detect no breath sounds as you quickly listen to his lungs. As the team moves
him to the ED stretcher, the terrified light in his eyes begins to dim, and the
gasps start to quiet. This young asthmatic is slipping away.
In the past two decades, our knowledge and understanding of the
pathophysiology and treatment of asthma has steadily increased. We rely
on an ever-growing pharmacological armamentarium and continue to
expand our means of preventative care. Furthermore, as increasing
numbers of patients seek emergency care for the treatment of their
asthma, the role of the emergency physician also grows. Our task now
includes not only acute treatment, but also initiation of preventative and
maintenance care.
This issue of Emergency Medicine Practice addresses acute treatment
decisions involved with patients with an acute asthma exacerbation, as
well as their long-term care requirements.

February 2001
Volume 3, Number 2
Authors
Mary K. Reilly, MD
Chief Resident, Emergency Medicine, Case Western
Reserve University/MetroHealth Medical Center,
Cleveland, OH.
Michael A. Kaufmann, MD
Chief Resident, Emergency Medicine, Case Western
Reserve University/MetroHealth Medical Center,
Cleveland, OH.
Rita K. Cydulka, MD, FACEP
Associate Professor, Case Western Reserve University;
Attending Physician, MetroHealth Medical Center;
Consultant, Cleveland Clinic Foundation; Cleveland, OH.
Peer Reviewers
Alfred Sacchetti, MD, FACEP
Research Director, Our Lady of Lourdes Medical Center,
Camden, NJ; Assistant Clinical Professor of Emergency
Medicine, Thomas Jefferson University, Philadelphia, PA.
Jeffrey Mann, MD
Attending Emergency Physician, Somerset Medical
Center, Somerville, NJ.
CME Objectives

Epidemiology And Pathophysiology
Despite continuing advances in treatment and prevention, asthma is
increasing in prevalence worldwide,1 reaching 4%-5% in the developed
nations2,3 and affecting more than 15 million Americans.4 In the United
States, it is the most prevalent chronic disease among children.4 The death
rate from asthma among those 19 years and younger has increased by
almost 80% since 1980.4 Asthma carries higher morbidity and is even more
lethal in the elderly, among whom 7%-10% are affected.5,6

Editor-in-Chief
Stephen A. Colucciello, MD, FACEP,
Assistant Chair, Director of
Clinical Services, Department of
Emergency Medicine, Carolinas
Medical Center, Charlotte, NC;
Associate Clinical Professor,
Department of Emergency
Medicine, University of North
Carolina at Chapel Hill, Chapel
Hill, NC.

Associate Editor
Andy Jagoda, MD, FACEP, Professor
of Emergency Medicine; Director,
International Studies Program,
Mount Sinai School of Medicine,
New York, NY.

Editorial Board
Judith C. Brillman, MD, Residency
Director, Associate Professor,
Department of Emergency

Medicine, The University of
New Mexico Health Sciences
Center School of Medicine,
Albuquerque, NM.
W. Richard Bukata, MD, Assistant
Clinical Professor, Emergency
Medicine, Los Angeles County/
USC Medical Center, Los Angeles,
CA; Medical Director, Emergency
Department, San Gabriel Valley
Medical Center, San Gabriel, CA.
Francis M. Fesmire, MD, FACEP,
Director, Chest Pain—Stroke
Center, Erlanger Medical Center;
Assistant Professor of Medicine,
UT College of Medicine,
Chattanooga, TN.
Valerio Gai, MD, Professor and Chair,
Department of Emergency
Medicine, University of Turin, Italy.
Michael J. Gerardi, MD, FACEP,
Clinical Assistant Professor,
Medicine, University of Medicine
and Dentistry of New Jersey;
Director, Pediatric Emergency
Medicine, Children’s Medical

Center, Atlantic Health System;
Chair, Pediatric Emergency
Medicine Committee, ACEP.
Michael A. Gibbs, MD, FACEP,
Residency Program Director;
Medical Director, MedCenter Air,
Department of Emergency
Medicine, Carolinas Medical
Center; Associate Professor of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Charlotte, NC.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor,
MI; Clinical Professor, Department
of Emergency Medicine,
University of Michigan Medical
School, Ann Arbor, MI; President,
American Physicians Assurance
Society, Ltd., Bridgetown,
Barbados, West Indies; Past
President, ACEP.
Jerome R. Hoffman, MA, MD, FACEP,
Professor of Medicine/
Emergency Medicine, UCLA

Upon completing this article, you should be able to:
1. assess the severity of an acute asthma exacerbation;
2. treat a range of asthma exacerbations, from mild to
severe; and
3. identify the appropriate disposition for an asthmatic
presenting to the ED.

Date of original release: February 9, 2001.
Date of most recent review: February 7, 2001.
See “Physician CME Information” on back page.

School of Medicine; Attending
Physician, UCLA Emergency
Medicine Center;
Co-Director, The Doctoring
Program, UCLA School of
Medicine, Los Angeles, CA.
John A. Marx, MD, Chair and Chief,
Department of Emergency
Medicine, Carolinas Medical
Center, Charlotte, NC; Clinical
Professor, Department of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Michael S. Radeos, MD, MPH, FACEP,
Attending Physician in
Emergency Medicine, Lincoln
Hospital, Bronx, NY; Research
Fellow in Emergency Medicine,
Massachusetts General Hospital,
Boston, MA; Research Fellow in
Respiratory Epidemiology,
Channing Lab, Boston, MA.
Steven G. Rothrock, MD, FACEP,
FAAP, Associate Professor
of Emergency Medicine,

University of Florida; Orlando
Regional Medical Center; Medical
Director of Orange County
Emergency Medical Service,
Orlando, FL.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Department of Emergency
Medicine, Vanderbilt University
Hospital, Nashville, TN.
Mark Smith, MD, Chairman,
Department of Emergency
Medicine, Washington Hospital
Center, Washington, DC.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
Emergency Medicine, University
of Alabama at Birmingham,
Birmingham, AL.

exposure to various chemicals, dusts, or fumes.
The astute emergency physician should be able to
differentiate these common presentations with a careful
history and physical, combined with the judicious use of
diagnostic studies. Past medical history can be an
important determinant. Has the patient ever had a
history of asthma or wheezing before? Has he or she ever
used an inhaler? A history of CHF or cardiac disease may
increase the likelihood of pulmonary edema masquerading as reactive airway disease.

Asthma is the third-leading cause of preventable
hospitalization in the United States7 and each year
accounts for approximately 2 million visits to the nation’s
EDs.8 The direct costs for the treatment of asthma are
projected to have been higher than $14.5 billion in the
year 2000, more than double the cost one decade ago.4
Although asthma is characterized by reversible airflow
obstruction, it is a chronic disease with long-term implications. It can cause a permanent decline in lung function,
resulting in increased mortality.9,10 Appropriate treatment
and long-term care, therefore, are critical to preserve normal
lung function and minimize long-term mortality.
The pathophysiology of asthma is multifactorial.
Asthma is a chronic inflammatory condition, which is
caused by an array of factors, including genetic, allergenic, infectious, socioeconomic, psychosocial, and
environmental triggers.11-14 Because all of these can
influence the pattern of episodic and variable airflow
obstruction, treatment involves understanding and
addressing the underlying etiologies. (See Table 1.)
Despite this seemingly complex array of inciting
factors, emergency treatment of the asthmatic patient
traditionally has included pharmacological therapy that
works in one of two ways: by relaxing bronchial smooth
muscle (bronchodilation) or reducing airway inflammation (anti-inflammatory action).15 While pharmacologic
therapy is the mainstay of emergency treatment of
asthma, we can improve long-term outcomes by recognizing the genesis of the disease.

“‘Healing,’ Papa would tell me, ‘is not a science,
but the intuitive art of wooing nature.’”
—W.H. Auden

Clinical Practice Guidelines
And Systematic Reviews
The National Heart, Lung, and Blood Institute of the
National Institutes of Health (NIH) first published guidelines for the diagnosis and management of asthma in 1991
and updated these recommendations in 1997. However,
there is no consistent or widespread acceptance of these
guidelines.16 In fact, the management of asthma in many
EDs deviates significantly from published guidelines.17
Furthermore, there is little evidence that these (or other)
guidelines actually improve outcomes.18 As we will show in
the ensuing pages, many of the NIH guidelines are not
evidence-based. A number of recommendations are based
on the opinion of the panel, and unlike most evidence-based
guidelines, they did not use a ranking system to establish a
hierarchy of “best evidence.” (In such a hierarchical system,
a large, prospective, randomized, controlled trial free from
significant bias is specifically designated as more valid than
a case report.)
Nonetheless, as many as 40% of hospitals have
developed some critical pathways for asthma. Hospitals
that use asthma clinical guidelines are more likely to
engage in asthma-specific quality improvement efforts
than hospitals that do not use such guidelines.19 There is
some evidence that an acute asthma quality improvement
initiative can advance patient care. In one urban teaching
hospital, such an initiative decreased delays to β-agonist
and steroid therapy by approximately 16 minutes and 34
minutes, respectively. The program decreased median ED
length of stay by 58 minutes and resulted in fewer
inpatient admissions.20
In some hospitals, the triage or treatment area nurses
will initiate asthma protocols in order to speed interventions and decrease resource utilization. One study
prospectively examined 149 patients with asthma treated
by a pathway protocol and compared them with a
historical cohort of 97 patients with asthma who were
treated by conventional means. Protocol patients had less
oxygen use, fewer handheld nebulizer treatments, fewer
saline locks, and received fewer intravenous steroids.
There was a significant increase in the use of metereddose inhalers with spacer and oral steroids in patients
treated by protocol.21
Even scientific reviews and meta-analysis regarding

Differential Diagnosis
Although wheezing, cough, and dyspnea are the clinical
hallmarks of asthma, all that wheezes is not asthma.
Other common conditions present in a similar fashion.
Differential diagnoses include pneumonia, bronchitis,
croup, bronchiolitis, chronic obstructive lung disease,
congestive heart failure, pulmonary embolism, allergic
reactions, and upper airway obstruction. Less common
entities include cystic fibrosis, hypersensitivity pneumonitis, and carcinoid syndrome. Even those with no
predisposition to asthma may develop wheezing after

Table 1. Pathophysiology Of Asthma.
Etiology
Cellular

Relevance to treatment
Interaction of mast cells with IgE
molecules leading to the flood of
pro-inflammatory molecules in the
pulmonary system10,13

Infectious disease

Connection between viral
respiratory infections and the
development of asthma14

Social

Psychological and emotional factors
that act via modification of vagal
efferent activity

Public health

Influence of other precipitants like
environmental pollutants and
pharmacologic agents

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February 2001

respond as rapidly to therapy. In one study, patients with
sudden-onset asthma were less likely to report an upperrespiratory-tract infection (17% vs 40%) and more likely
to have an unidentifiable trigger (40% vs 19%) than those
with a less subacute attack. Contrary to the ED mythology that sudden-onset asthma presages respiratory
failure, a recent study concluded that sudden onset of
symptoms predicted rapid response to therapy and was
less likely to lead to admission.25
Confirm whether the current attack feels like their
typical exacerbation; if it does not, find out why. Identify
any factors that may lead to concomitant or even contrary
diagnosis, such as fever or a productive cough. Acuteonset chest pain may denote potential pneumothorax,
pneumomediastinum, pneumonia, or pulmonary
embolism (in addition to possible cardiac disease). Newonset wheezing in a person with no prior attacks may not
represent asthma. (Of course, wheezing in a known
asthmatic may also be due to causes other than reactive
airway disease. The prior history just makes asthmarelated bronchospasm more likely.)
There appear to be significant differences in the way
different ethnic groups describe the symptoms of asthma.
In one study, African-Americans used upper-airway
terms such as “tight or itchy throat,” “scared-agitated,”
“voice tight,” and “tough breath.” Whites were more
likely to use lower-airway or chest-wall descriptors such
as “deep breath,” “light-headed,” “out of air,” “aware of
breathing,” and “hurts to breathe.”26
Next, determine the type of medication and amount
used prior to arrival in the ED. This information will help
guide therapy, both in the ED and beyond. Ask when the
patient was last on steroids.
Patients with a chronic disease such as asthma are
often the best judges of their own condition. Ask the
patient how the current attack compares to prior episodes. Some physicians have the asthmatic rate the
present episode on a visual analog scale. These scales
correlate well with pulmonary function tests (PFTs) in
individual patients.27

asthma are plagued with problems (except perhaps this
one). In a systematic review of systematic reviews, the
asthma literature was found wanting. Half of the reviews
and meta-analyses never included a comprehensive
search or reported their methods. Few included measures
to avoid selection bias, evaluated study validity, or used
appropriate criteria for validity assessment.22

Prehospital Care
The prehospital care of the asthmatic closely parallels the
ED management. Medics should either give oxygen to
patients with asthma, measure their oxygen saturation
using pulse oximetry, or both. Patients with minimal
symptoms, however, may require neither.
Clinical trials demonstrate that the prehospital
administration of either aerosolized albuterol or subcutaneous terbutaline significantly reduces respiratory
distress.23 In this study, albuterol provided greater
subjective improvement.
Some limited data suggest that 125 mg of intravenous methylprednisolone given by paramedics may
reduce the need for admission in asthmatics.24 Once
again, patients with mild exacerbations would not
require this intervention.

ED Evaluation
The acute asthmatic can present with an array of signs
and symptoms. Some patients complain of wheezing and
shortness of breath, while others report a relentless
cough. The degree of dyspnea will dictate the ability to
perform a thorough history and physical. Immediate
attention must be directed to the patient’s appearance,
vital signs, and chest examination. If needed, aggressive
therapy directed at relieving airway obstruction must
begin as soon as the diagnosis is suspected.

History
The patient’s history will not only help determine the
course of immediate treatment in the ED, but it will also
place the exacerbation in the context of the disease.

Past Exacerbations
The patient’s history offers the backdrop for his current
exacerbation. Does the patient have a history of asthma?
Many patients will report no history of asthma but admit

History Of Present Illness
Establish any precipitants of the attack and its duration.
Be aware of attacks that are prolonged, as they may not

Key Points In Treating The Asthmatic Patient
this presentation should spur consideration of
alternative or concomitant diagnoses.
3. Every asthmatic requiring more than one β-agonist
treatment should receive corticosteroids in the ED and
should be discharged to home on a pulse regimen.
4. Suggest short-term follow-up (within 3-4 days of the ED
visit) to patients with asthma. Tell them to return to the
ED if they get worse. ▲

1. Most asthmatics can be appropriately assessed
with a history and physical, vital signs, PEFR, or
spirometry and ongoing clinical evaluation. Specific
signs and the severity of the asthmatic’s exacerbation
should guide the addition of extra tests, such as ABG
and chest radiography.
2. Always place the context of the asthmatic’s current
attack into his past history—significant differences in

February 2001

3

Emergency Medicine Practice

a variety of the clinical clues outlined below.

they “wheeze all the time” or have lots of “bronchitis”
attacks. Ask whether he or she has ever been given an
inhaler or breathing treatments in the past. Document the
frequency of ED visits, prior hospitalizations (including
admission to intensive-care settings), a previous need for
steroids, and most recent steroid use. Recent discontinuation of steroids may be a factor in the current attack.
Determine any history of intubation or noninvasive
ventilation. Prior history of intubation or chest-tube
placement is an important predictor of severe disease. In
one study of near-fatal asthma, univariate analysis
identified a history of previous mechanical ventilation
(OR: 27.5); admission to the intensive care unit (OR: 9.9);
history of worse asthma during January and February
(OR: 3.5); and use of air-conditioning (OR: 15.0) as
important risk factors for respiratory failure.28 A nearfatal episode of asthma is a risk factor for future lifethreatening attacks; approximately 10% of such patients
die in the year after the event.29

“No one fakes diaphoresis.”
—Ancient ED saying

General Appearance
The patient’s general appearance will often determine the
pace of subsequent interventions. Upon entering the room,
assess for the general level of distress. A patient who is
sweating and unable to speak in full sentences is in trouble.
The number of seconds a patient can spend counting
correlates well with pulmonary function.30 In the first
several moments, quickly appraise the patient’s mental
status. Both lethargy and agitation presage respiratory
failure. Cyanosis is a very late finding in asthma. By the
time it appears, it is likely that the patient is moribund.31
While these suggestions are considered “common
knowledge,” studies that focus on clinical examination
show that inter-observer agreement regarding respiratory
signs in adults is low.32 However, one study indicates that
inter-observer agreement may be better in the assessment
of acute asthma in children.33

Past Medical History, Social History, Medications
Obtaining a history of other medical problems, allergies,
current medications, and social history is vital to the
course of medical management. The patient with a
history of asthma may also have a history of cardiovascular disease, pulmonary embolism, or DVT. Ignoring this
history could lead to misfortune if “shortness of breath”
is automatically attributed to asthma. This is especially
important if the patient states that the current problem is
not similar to previous attacks.
Ask patients whether they are using an inhaler, and in
particular whether they are using it with a spacer chamber.
How many puffs a day are they using? Many patients may
list albuterol as one of their medications without informing
the physician that their inhaler is empty. Because proper
technique is critical to the efficacy of an MDI, have them
demonstrate how they use their inhaler. This simple
intervention may have a dramatic impact on their disease if
they are able to learn the proper technique.
Questioning the patient about tobacco use or exposure
may lead to an explanation for the asthmatic who seems to
be on the right pharmacologic regimen but continues to
have frequent exacerbations. Finally, the ubiquitous “list of
meds” can offer insight into both this exacerbation and the
severity of the patient’s asthma. For example, recently
prescribed timolol ophthalmic drops may have worsened
the disease due to their β-blocking effect.

Vital Signs
Tachycardia and tachypnea do not always correlate with
the degree of airway obstruction.34,35 Tachycardia will
often resolve with appropriate β-agonist therapy, not
worsen. A decreasing respiratory rate can simply mean
the patient is tiring, rather than improving.
There is little research that examines the relationship
of blood pressure to respiratory distress. However, if the
blood pressure is extremely high (or extremely low),
consider cardiac etiologies such as CHF or cardiogenic
shock in the differential diagnosis of wheezing.
If the determination of fever is important, consider
obtaining a rectal temperature. Oral temperatures are
notoriously inaccurate in patients with tachypnea.

Pulse Oximetry
Pulse oximetry—the “fifth vital sign”—is often useful in
the assessment of asthma. It will rapidly alert the ED staff
to hypoxia and the need for supplemental oxygen.
Hypoxemia generally reflects the extent of ventilation/
perfusion mismatch.36 Remember, however, that pulse
oximetry does not reflect ventilation status. Patients with
near-normal saturations while on oxygen may be
hypercarbic and in danger of incipient respiratory failure.
Pulse oximetry may also predict the need for
admission in children. Children with initial low oxygen
saturation (below 90% or 91% depending on the study)
often require admission regardless of their response to
therapy.37-39 In one study, children who presented with an
oxygen saturation level of 92% or less had a greater-thansixfold relative risk for requiring prolonged treatment.40
Another study showed that in children, a posttreatment
SpO2 level of 91% or less increased the odds of admission
16-fold.41 As opposed to some previous studies, this
study found pretreatment SpO2 levels to be a relatively
poor predictor of admission.
The initial room air pulse oximetry can accelerate

Physical Examination
Be wary when performing the physical exam. A patient’s
ventilatory status can change rapidly. Remember that
patients with no wheezing may actually be in extremis;
they cannot move enough air to produce the turbulent
whistle of asthma. Such patients, however, will appear
dyspneic and will not be able to speak normally. Others
who are “just holding their own” may tire and rapidly
become acidotic and hypercarbic. Many experienced
physicians use their gestalt to rapidly assess the severity
of distress. They may overtly or subliminally incorporate

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February 2001

patient. The short-term prognosis in the acute asthmatic
is challenging and often not obvious. In addition to the
history and physical exam, diagnostic studies may prove
useful in determining the disposition for some patients.46

treatment intervention in adults (if low) or provide reassurance (if high). However, the initial oxygen saturation has
little prognostic utility in the adult asthmatic.42

Head And Neck
Asthma Index Scores And Pulmonary Function Tests

A careful cardiopulmonary evaluation is central to the ED
evaluation. Findings such as increased jugular venous
pressure, lymphadenopathy, and carotid bruits may
signal alternative diagnoses. Pay special attention to the
patient’s neck veins. If they distend during inspiration
(Kussmaul’s sign), then the patient has a significant
increase in right-sided venous pressure that might
possibly be due to right ventricular infarction, tension
pneumothorax, pulmonary embolism, or pericardial
tamponade.43 In the unlikely event of a deviated trachea,
consider the possibility of a tension pneumothorax on the
side opposite the deviation. The strap muscles of the
anterior neck will bulge when the patient is in significant
distress in an attempt to pull air into the lungs. Those in
respiratory distress may breathe with pursed lips.

The chest exam is, of course, central to the evaluation of
an asthmatic. Look for intercostal retractions and
accessory muscle use. Next, careful auscultation of the
lungs may reveal wheezing, rhonchi, rales, or a silent
chest. The latter can be ominous, as wheezing can be
absent when airflow is minimal.34
The presence of unilateral wheezing or rales should
lead one to consider the possibility of pneumonia or
other causes of obstruction. Unequal breath sounds
suggest a variety of diagnoses. While this finding may be
present in asthma, it also occurs with pneumothorax,
pulmonary embolism, pneumonia, pleural effusion, or
foreign body. Stridor should be distinguished from
wheezing. When listening with a stethoscope, stridor is
most prominent over the glottis, while wheezing is
louder in the chest fields. Stridor is associated with
tracheal or laryngeal obstruction and is usually more
distinct upon inspiration.
A complete cardiac exam includes evaluation of the
heart sounds. A gallop rhythm, in particular an S3, is
evidence of cardiac failure.
Pulsus paradoxus (> 20 mmHg) is associated with
severe obstruction in some individuals, although it is absent
in up to one-third of severe asthmatics.34 It is not clear that
this finding is useful in clinical practice. No study proves
that it adds any further information to that provided by
routine clinical assessment. In one British trial, pulsus
paradoxus did not correlate with either the severity of acute
asthma in individuals or with peak flow. The authors
suggested that it be abandoned as an indicator of asthma
severity.44 Furthermore, physicians differ widely in their
ability to measure pulsus paradoxus.45

Scoring systems are usually employed to help with
management and triage decisions. Asthma index scores,
once commonly used for predicting emergency disposition and treatment, have proven to be no better than
clinical judgment in predicting outcome.47-49
The peak expiratory flow rate (PEFR) measures the
obstruction in larger airways.50 Beware of the patient
making a poor effort with his peak flow; peak flow data
alone should not dictate disposition but should be used
in the context of the patient’s overall clinical picture.
Despite its shortcomings, PEFRs are easy to obtain,
inexpensive, and less time-consuming than FEV1 measurements. In the appropriate setting, with good patient
cooperation, many emergency physicians consider them
useful. In addition, PEFRs may be used to avoid other
invasive tests (see the “Arterial Blood Gas” section later
in this article).
The forced expiratory volume in the first second
(FEV1) tends to be a more sensitive reflection of the
patient’s overall airway obstruction, as well as the
patient’s ability to ventilate.51 In addition, FEV1 is much
less dependent on patient effort, making it more reliable
than PEFR. However, FEV1 requires a more involved
maneuver and significant patient cooperation.52-55 A pretreatment PEFR or FEV1 of less than 50% predicted
indicates severe obstruction.56
The National Guidelines recommend PEFR or FEV1
measurements to assist in ED management decisions.
While pulmonary function tests such as PEFR may be
valuable in the home management of asthma, there is
considerable controversy regarding their utility in the
ED. Only one study shows that the use of PEFR initially
and at 30 minutes (combined with assessment of accessory muscle use) might help predict which patients may
require hospitalization.57
However, a better-designed large prospective trial
demonstrated that peak flow rates could not predict
which patients would return to the ED with a relapse.58
Another study looked at the “personal best” PEFR
scores—a value that the asthma guidelines champion as
an important benchmark for ED management—among
inner-city ED patients with acute asthma. The authors
found that the “personal best” PEFR was inaccurate and
argue that “in contradistinction to NAEPP guidelines,
these values should not be used routinely (or preferentially) as part of the ED discharge decision.”59
Other studies confirm that PEFRs do not correlate well
with need for admission or with return visits to the ED.60,61

Diagnostic Studies

Chest Radiography

The therapeutic quandary with asthma is not usually in
the diagnosis, but in the treatment and disposition of the

Chest radiography should not be routine in the ED
evaluation of acute asthma. Unless the patient’s history
or physical exam suggests the possibility of additional or

Pulmonary And Cardiac Exam

February 2001

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Emergency Medicine Practice

corticosteroid treatment can cause modest leukocytosis,66
which can mislead the physician into diagnosing an
infectious etiology. Finally, a theophylline level should be
obtained in those patients maintained on chronic therapy.

competing diagnoses, such as congestive heart failure,
foreign body, pneumonia, or pneumothorax, chest
radiography is probably not warranted.
White et al carried out a prospective study of asthmatics that identified a “major” abnormality in 34% of chest
radiographs in patients requiring admission for acute
asthma.62 “Major abnormality” included infiltrate, pneumothorax, and cardiomegaly.62 The prevalence of abnormal
chest radiographs in all-comers to the ED (not just those ill
enough to require admission) is significantly lower.63,64
Indications for chest films may include:63,64
• Asthma severe enough to require hospitalization
• Severe respiratory distress
• Clinical suspicion of pneumothorax, CHF, pneumonia, or foreign body
• Failure to improve in the ED
• Compromised host
• Unexplained fever

Treatment
The most urgent goal in the ED is to rapidly reverse
airflow obstruction and ensure adequate oxygenation.
The initial therapeutic interventions in any asthmatic
should include the basic ABCs, with intravenous access,
oxygen, and cardiac monitoring instituted for those
in severe distress. It is useful to quickly identify the
asthmatic as either unstable or stable (recognizing that
the initial designation is subject to rapid change). The
clinical pathway “Management Of Patients With An
Acute Asthma Exacerbation” on page 14 begins with
this classification.
The unstable patient mandates emergency airway
equipment at the bedside (including the availability of
rapid-sequence intubation agents). Systemic β-agonists
(e.g., subcutaneous terbutaline or epinephrine) may
replace or be combined with aerosolized treatments.
Assess the improvement of that patient with several
measures: mental status, air exchange, oxygenation, and
ventilation. Progressive deterioration or failure to
improve with maximal therapy may require intubation.
Thankfully, the majority of asthmatics who present to the
ED will not require such extreme measures.
The most standard therapies can be grouped
into three primary categories: β-adrenergic agonists,
glucocorticoids, and anticholinergics. A fourth category
of drugs, the methylxanthines, has no significant role in
emergency management, while a fifth and sixth category
of drugs, the cromones and leukotriene modifiers, are
generally reserved for maintenance therapy. Magnesium
is emerging as a treatment for very severe asthma
exacerbations. The role of other agents, including βagonist isomers (e.g., levalbuterol), heliox, anesthetics,
and anti-hypertensive agents are currently the topics of
intensive clinical research in the management of acute
asthma exacerbations.

Patients with COPD are more likely to have abnormalities on chest film, and their need for chest radiography depends on a variety of factors.65

Arterial Blood Gas
Measurement of arterial blood gases is expensive,
painful, and is occasionally associated with significant
morbidity (arterial thrombosis). It is also unnecessary in
the vast majority of patients who are suffering an acute
exacerbation. ABG may be useful in patients experiencing
severe or prolonged attacks, those with a PEFR or FEV1
less than 25% of predicted who appear in significant
distress,56 or in those with altered mental status.
Pulmonary function tests can usually exclude the
possibility of respiratory failure. Martin et al demonstrated
that PEFR accurately predicted hypercarbia or acidosis. In
his study, no patient with a PEFR greater than 25% predicted had a PaCO2 greater than 45 or a pH less than 7.35.36
When an ABG is obtained, some pitfalls await the
unwary physician. In the patient with significant tachypnea, a “normal” PaCO2 is actually a worrisome finding,
since the tachypneic patient is expected to be hypocarbic.
A near-normal value reflects the fact that the patient is
tiring and should warn of impending ventilatory failure.

β-agonists

Cardiac monitoring and ECG testing are not indicated in
the evaluation of the acute asthmatic unless co-existing
cardiac conditions are suspected. When present, typical
ECG patterns include findings consistent with pulmonary disease, including right ventricular strain, right
atrial enlargement or nonspecific ST-T wave abnormalities that resolve with treatment.

β-adrenergic agonists are the mainstays in the treatment
of acute bronchospastic disease. They exert their effects
by increasing cyclic adenosine monophosphate (cAMP).
A series of interactions cause intracellular calcium to bind
to cell membranes with greater affinity, thus dropping the
myoplasmic calcium concentration. This results in
bronchial smooth-muscle relaxation, inhibition of
mediator release, and increased mucociliary clearance.

Routine Laboratory Evaluation

Types Of Agents

Electrocardiography And Cardiac Monitoring

The older catecholamine bronchodilators include
isoproterenol, isoetharine, and epinephrine. Isoproterenol
is a more selective β-adrenergic agent than epinephrine,
but a number of deaths were associated with isoproterenol inhalation in England in the 1960s. Use of this agent

Blood tests, including a complete blood count, are rarely
indicated in the evaluation of acute asthma exacerbations. Again, the exceptions may include those patients in
whom other diagnoses are being considered.
If a CBC is obtained, note that β-agonist therapy and

Emergency Medicine Practice

6

February 2001

exist for the latter devices: dry powder inhalers (DPIs) or
an MDI utilizing a novel hydrofluorocarbon (HFC).
When making this transition, physicians should be aware
of potential efficacy differences between the two methods
of drug delivery.78
Nebulizer therapy is still widely used in EDs, despite
the fact that numerous studies show that the MDI
combined with a spacer chamber is therapeutically
equivalent.79-83 The combination of an MDI with spacer is
less expensive, easier to administer, and provides an
opportunity for the physician to evaluate whether the
patient is using the device correctly (an essential component of home management). For these reasons, many
hospitals have switched from the nebulizer to the MDI
with spacer in the emergency treatment of asthma. Other
EDs may give the first treatment via nebulizer and switch
to an MDI plus spacer if the patient meets certain clinical
criteria (respiratory rate, pulmonary function tests,
oxygen saturation, etc.). Children randomized to an MDI
plus holding chamber as compared to a nebulizer
improve faster, have fewer side effects, fewer admissions,
and shorter lengths of stay in the ED.79,80,84

is not generally warranted.
Isoetharine is also a more β2-selective agent than
epinephrine and is as effective a bronchodilator as
albuterol.67 It is available as a metered-dose inhaler or as
an aerosol solution. Doses may be repeated every 20-30
minutes during an acute attack.
Epinephrine is a nonselective β- and α-adrenergic
agonist. While it can be nebulized, it is usually administered subcutaneously, and occasionally intravenously for
the patient in extremis. It is found in over-the-counter
inhalers and the nebulized form increasingly used in the
treatment of bronchiolitis. Complications of its use
include myocardial irritability, dysrhythmias, and
nervousness. However, in one interesting study, when
patients with a history of recent myocardial infarction or
of angina were excluded, the administration of subcutaneous epinephrine did not cause an increase in
dysrhythmias, despite the fact that it was given to
asthmatics as old as 96.68 The subcutaneous dose in adults
is 0.3-0.5 cc of a 1:1000 solution, which may be repeated
every 20 minutes to a total of three doses.
The agents listed above have nearly been replaced by
newer, longer-acting derivatives and, with the exception
of epinephrine, do not have a place in the routine care of
asthmatics. Albuterol is currently one of the most widely
used of the β-agonists. Despite its popularity, researchers
have not consistently validated its clinical superiority.69
Other β-agonists include metaproterenol, terbutaline,
fenoterol, and carbuterol. They are similar to albuterol in
that they all share greater β2-specificity and longer
duration of action than the catecholamines.

Dosage
The most effective dose of inhaled β-agonist remains
unknown. Standard doses of albuterol for adults range from
2.5-5.0 mg per treatment; however, continuous nebulization
may involve administering 20 mg or more per hour. In one
study, two 5.0 mg treatments of aerosolized albuterol at a
40-minute interval were more effective than three treatments of 2.5 mg given every 20 minutes. The high-dose
regimen improved pulmonary function more rapidly and to
a greater extent than standard-dose therapy and resulted in
shorter ED length of stay (in addition to lower charges to
third-party payors).85
β-agonist doses may be administered nebulized
every 15-20 minutes or as a continuous aerosol.86 Recent
literature has failed to demonstrate the superiority of
either method.87 Continuous nebulization has a theoretical advantage in departments with limited personnel; if
the respiratory therapist or nurse is unable to return
every 20 minutes to initiate additional treatments,
continuous nebulization can potentially bridge these
gaps in the patient who is in moderate distress.
One study showed that 2.5 mg of nebulized albuterol
is therapeutically equivalent to 1 mg of salbutamol by
MDI/spacer (11 puffs). In this randomized trial of acute
severe asthma, the MDI-spacer group received four puffs
of albuterol at 10-minute intervals (24 puffs per hour).
Although patients in the MDI and nebulizer group
showed similar improvement, nebulizer therapy produced greater adverse side effects.88 Other studies have
employed 6-12 puffs per treatment using an albuterol
MDI, even in children.89

Levalbuterol And Its Isomer Counterparts
Levalbuterol is the R-isomer of racemic albuterol (a
mixture of 50:50 R- and S-albuterol). The bronchodilator
effects of racemic albuterol depend on the R-isomer; for
many years, the S-isomer was felt to be biologically
inert.70 However, a more in-depth evaluation of the
S-isomer indicates that it may have pharmacological
properties separate from its R counterpart.71 Theoretically,
levalbuterol could provide equivalent bronchodilatation
to albuterol with fewer side effects. It costs significantly
more than albuterol, and its therapeutic effects have not
been directly compared to albuterol in patients with acute
exacerbations.72 Even when used on a non-emergent
basis, the current literature does not uniformly support
the use of levalbuterol over its racemic counterpart.73-75

Routes Of Administration
Aerosol therapy (either nebulization or via metered-dose
inhaler [MDI]) is the preferred route for ED use. This is
because aerosols achieve topical administration of drug
in small doses and produce local bronchodilation with
minimal systemic absorption and side effects. The addition
of a spacer chamber is an important adjunct when using the
MDI, dramatically increasing effective drug delivery.76,77
Worldwide, healthcare providers are transitioning
from chlorofluorocarbons (CFCs) as propellants for
metered-dose inhalers to non-CFC devices. Two choices

February 2001

Parenteral Therapy
Parenteral β-agonist therapy usually involves subcutaneous
injections of epinephrine or terbutaline. These are sometimes given in the distressed patient when aerosol therapy is

7

Emergency Medicine Practice

either unavailable or will be delayed. Some physicians,
believing that bronchoconstriction may be so profound as to
impair aerosol delivery to the lungs, use parenteral therapy
in the patient in extremis. However, the presumed advantages of this approach remains unproven.
The evidence regarding the utility of intravenous
β-agonists is limited. Although a few studies have
examined intravenous terbutaline in adults resistant to
maximal therapy,90,91 it is best studied in children who are
in status asthmaticus.
Intravenous terbutaline is well tolerated in asthmatic
children at varying doses up to a maximum of 10 mcg/
kg/min.92 In another study, children with acute severe
asthma given 15 mcg/kg of intravenous albuterol over 10
minutes showed significant improvement compared to
those who received nebulized albuterol.93

over another, oral administration is the preferred route,
particularly in children and even in moderately ill
asthmatics if they are able to tolerate the drug (i.e., they
do not regurgitate it within the hour).
Intramuscular steroids have also been well studied in
the treatment of asthma. Studies on the use of intramuscular
“depo” steroids show they are as effective as a seven- to 10day course of oral prednisone.103 Side effects are rare.
In one randomized study, a single intramuscular
injection (approximately 1.7 mg/kg) of dexamethasone
acetate (Decadron, Dexasone, Dexone, Hexadrol) was as
effective as a five-day course of oral prednisone (approximately 2 mg/kg/day) in children with mild-to-moderate
asthma exacerbations. In a similar study involving adults,
a single 40 mg dose of intramuscular triamcinolone
diacetate (Aristocort, Kenalog, Aristospan) proved
equivalent to prednisone (40 mg/d PO for 5 days) after
ED treatment of mild-to-moderate exacerbations of
asthma.104 Intramuscular methylprednisolone sodium
acetate (Depo-Medrol) is therapeutically equivalent to an
eight-day course of oral prednisone.105
Inhaled corticosteroids are currently under investigation for the treatment of the acute exacerbation and may
be beneficial for asthmatics who have a more severe
exacerbation.101,106,107 Home use of inhaled budesonide
and oral prednisone is equally effective in patients
discharged from the ED after treatment with systemic
corticosteroids for a severe acute exacerbation of asthma.
In one study, patients randomized to receive either
inhaled budesonide (Turbuhaler) 600 mcg QID (3 puffs
QID) or prednisone 40 mg each morning for 7-10 days
showed no difference in relapse rates.108
However, combining inhaled with oral steroids does not
consistently provide an additive effect.109 In one study, the
addition of high-dose inhaled flunisolide to standard
therapy (including oral steroids) did not benefit inner-city
patients with acute asthma in the first 24 days after ED
discharge.110 Other studies have confirmed this finding.111
On the flip side, however, Rowe et al did show
improved outcomes in patients who were prescribed
inhaled corticosteroids at the time of discharge.112 In this
study, patients with acute asthma who were discharged
from the ED were prescribed inhaled budesonide (1600
mcg/d) or placebo added to a fixed course of oral
prednisone. Those who received the inhaled budesonide
had fewer relapses, fewer asthma symptoms, a decreased
need for inhaled β-agonists, and reported an improved
quality of life over the next 21 days.

Oral Therapy
Oral administration of β-agonists is generally discouraged.94 Short-acting oral agents such as oral albuterol do
not improve quality of life when added to inhaled
therapy and significantly increase side effects such as
tremor and palpitations.95 Children with wheezing
should receive home therapy using an MDI with spacer
(and mask in the case of the younger child), not oral
agents. In certain situations, long-acting oral agents such
as bambuterol (not yet available in the United States) can
be helpful in nocturnal asthma.96

Glucocorticoids
Early administration (within one hour) of glucocorticoids in the
treatment of acute reactive airway disease results in fewer hospital
admissions and a lower rate of relapse after ED discharge.97-99
Therefore, steroids should be administered to all asthmatics
whose acute exacerbation is not relieved by one nebulized
bronchodilator aerosol and given urgently to those who
appear in moderate to severe distress.
While the exact mechanism of action is unclear, one
theory proposes a reduction of airway inflammation, as
well as restoration of β-adrenergic responsiveness in the
constricted airways. Accepted dosage regimens in adults
include prednisone (40-60 mg PO), a 60-125 mg intravenous bolus of methylprednisolone, or a 60-125 mg
intramuscular dose of methylprednisolone. No clear
benefit has been demonstrated by using “high-dose”
steroids (> 80 mg/d of methylprednisolone) for those
patients requiring hospitalization for their exacerbation,100 though it is commonplace for adult patients to
receive 120 mg of methylprednisolone in the ED.
Oral, intravenous, and intramuscular routes of
administration of steroids share equal efficacy and have
an onset of action of approximately four hours.98,101 In
prolonged ED stays or ED observation units, steroids
should be re-administered every 6-8 hours, whether they
are given orally or intravenously. In one study, 125 mg of
intravenous methylprednisolone increased PEFR and
percent-predicted PEFR over time compared to placebo.102 However, because no well-designed trial has
demonstrated a “head to head” superiority of one route

Emergency Medicine Practice

Anticholinergics
Anticholinergic therapy, including ipratropium bromide
and glycopyrrolate, antagonizes the neuromuscular
transmitter acetylcholine at the postganglionic parasympathetic receptor, which reduces vagally mediated
bronchoconstriction in the larger central airways. Anticholinergic bronchodilation peaks within 1-2 hours. Simultaneous treatment with β-adrenergic agents and anticholinergics may produce an additive effect.113,114 The pooled
results of five randomized, controlled trials (RCTs) showed

8

February 2001

that the addition of ipratropium to standard therapy with
steroids and β-agonists results in fewer hospitalizations
when compared to placebo (P = 0.007). The addition of
ipratropium bromide also improves pulmonary function in
the first 90 minutes of treatment.115 Rodrigo et al demonstrated the most benefit with those who present with severe
asthma (FEV1 < 35% predicted ).115 The NIH guidelines
recommend that ipratropium bromide (0.5 mg via either
nebulizer or MDI) be administered to all patients with a
PEFR or FEV1 less than 80% predicted.
Ipratropium is useful in pediatric asthma as well. One
study showed significant improvement in pulmonary
function studies over 120 minutes in children with severe
asthma who were given nebulized ipratropium (combined
with albuterol and oral steroids) compared with children
who received the albuterol and steroids alone.116 In a
systematic review of 10 studies regarding the use of
anticholinergic inhalations added to the β-agonist regimen,
children who received multiple-dose ipratropium had
improved pulmonary function and a trend to reduced
hospitalization. Single-dose ipratropium improved FEV1 but
did not decrease hospitalizations. However, the single-dose
studies tended to focus on children with less severe
exacerbations, while the multiple-dose studies involved
children with more severe attacks.117
When nebulized, ipratropium may be combined in
the same holding chamber with the β-agonist. It also is
marketed as a single agent in an MDI (Atrovent) and as a
combination inhaler with albuterol (Combivent). At
present, ipratropium bromide is the only anticholinergic
agent recommended for use during an acute asthma
exacerbation.115 Other anticholinergics, such as aerosolized atropine sulfate and glycopyrrolate, have fallen
out of favor.118 These medications have a high incidence
of side effects, including tachycardia, restlessness,
irritability, dry mouth, thirst, and difficulty swallowing.

magnesium over 10-15 minutes.
Magnesium is now being used as a vehicle for
nebulized albuterol. In acute asthma, nebulized magnesium-albuterol increases the peak flow when compared to
albuterol plus normal saline.123

Controversies/Cutting Edge
Heliox
Heliox, an 80:20 mixture of helium and oxygen, can be
considered in patients with respiratory acidosis who fail
conventional therapy. Helium is a low-density, inert gas
that lowers airway resistance and decreases respiratory
work.124 Significant improvement may be noted within
10-20 minutes of initiating therapy in the asthmatic with
severe bronchospasm.125
Kass and Terregino compared the effect of heliox to
30% oxygen in asthmatics with severe symptoms. Patients
who received heliox had significant improvement in PEFRs
compared to controls.126 In contrast, Henderson et al did not
demonstrate a difference in spirometry or admission rates
for mild-to-moderate asthmatics treated with heliox.127 This
disparity may relate to differences in disease severity
between the study populations. Ultimately, further studies
are necessary to determine the role of heliox in current
asthma management.

Nitric Oxide
Inhaled nitric oxide (NO) may be valuable in status
asthmaticus refractory to other therapies. In one series,
it was administered to five consecutive children with
life-threatening status asthmaticus who required mechanical ventilation. Four showed a greater than 20%
decrease in baseline PaCO2 soon after the administration
of inhaled NO.128

Anesthetics
Certain anesthetic agents such as halothane and
isoflurane are potent bronchodilators.129,130 These agents
produce rapid bronchodilatation but are also myocardial
depressants. Halothane can produce arrhythmias and
intrapulmonary shunting of blood. Close monitoring of
heart rate and blood pressure is essential when using
anesthetics to treat status asthmaticus.129
Though general anesthetics have theoretical benefits
in the acute treatment of an intubated asthmatic, it is
unlikely that such agents will be available in the ED.
They are most appropriate for an intensive-care setting in
consultation with the anesthesiologist.

Magnesium
Magnesium sulfate is efficacious for the relief of severe
bronchoconstriction but adds little to the treatment of mildto-moderate bronchospasm.119-121 This medication regulates
intracellular calcium flux, inhibits the release of histamine
from mast cells, inhibits the action of acetylcholine, and
directly inhibits bronchial smooth-muscle contraction.
Bronchodilation is observed within 2-5 minutes after
the initiation of therapy but disappears rapidly after
termination of treatment. Side effects of magnesium therapy
potentially include hypotension, malaise, and a warm,
flushing sensation. Monitoring of cardiac rhythm, blood
pressure, pulse, neurologic status, and renal function is
prudent, but a recent systematic review demonstrated no
clinically significant changes in vital signs or presence of
side effects with the administration of magnesium.122
In a systematic review of 27 studies and seven trials,
the authors found that magnesium reduced hospital
admission rates and improved pulmonary function for
patients with severe asthma. However, no difference was
shown for patients with mild-to-moderate asthma.120 For
patients with severe asthma, consider giving 2 g of

February 2001

Leukotriene-Receptor Antagonists
Leukotriene modifiers result in improved lung function,
diminished symptoms, and less need for short-acting
β-agonists over a wide spectrum of asthma severity.
However, they are not currently indicated for acute
exacerbations.131 In one ED study, patients were given
either 10 mg chewable montelukast or placebo within 20
minutes of presentation (in addition to standard therapy).
There were no significant differences in the final PEFR

9

Emergency Medicine Practice

scores or the need for hospitalization.132

Airway Management

Lidocaine And Anti-Hypertensives

Intubation
If the patient deteriorates or fails to improve despite
intensive therapy, intubation and mechanical ventilation
must be considered. Fortunately, fewer than 1% of asthmatics require mechanical ventilation. Although there are no
absolute criteria other than respiratory arrest and coma, the
following are indications for acute airway intervention:
• Worsening pulmonary function tests despite vigorous bronchodilator therapy
• Decreasing PaO2
• Increasing PaCO2
• Progressive respiratory acidosis
• Declining mental status
• Increasing agitation

Lidocaine surfaces in anecdotal reports as an agent that
may succeed when conventional therapies fail.133 Despite
these reports, prospective study into this choice of
pharmacologic therapy is needed. Likewise, reports of
improvement with calcium-channel blockers and
clonidine should spur further investigation into their
possible role in the acute treatment of asthma.134

Theophylline—The Drug That Won’t Die
Theophylline/aminophylline is not generally recommended therapy in the ED. The vast majority of studies
show that it provides no additional benefit to short-acting
inhaled β-agonists and frequently causes adverse
effects.135-140 In hospitalized patients, most data indicate
that intravenous methylxanthines are not beneficial in
children with severe asthma,141-143 and they remain
controversial for adults.144,145 While the occasional study
suggests some positive effect in severely ill children
unresponsive to standard treatment,146 its marginal
benefit and poor safety profile argue against routine use.

Many experienced emergency physicians believe that
the decision to intubate is best made on clinical grounds
(“looks bad and not getting better”) as opposed to using
objective parameters such as PEFR or ABG. This contention is difficult to prove one way or another.
Intubation of the asthmatic patient is a daunting task
fraught with potential for serious complications. Rapidsequence intubation is the method of choice. (For a full
discussion of airway management, please see the May 2000
issue of Emergency Medicine Practice, “Emergency Endotracheal Intubations: An Update On The Latest Techniques.”)
Despite some advantages of the nasal route of intubation
(minimal use of sedation), the oral route is the preferred
route in asthmatics. Most asthmatics who are in enough
distress to require intubation will not be able to readily
cooperate with a nasal intubation; in addition, there is
increased risk of trauma and bleeding with the nasal route,
and it necessitates the use of a smaller endotracheal tube,
thereby increasing airflow resistance.153
Some authors suggest pre-treating the asthmatic with
lidocaine in the presumption that this will decrease the
reflex bronchospasm associated with cord manipulation.
While no study has directly evaluated pre-treating the
moribund asthmatic with lidocaine, one interesting study
suggests that this is unnecessary. In a group of asthmatics
undergoing elective surgery, inhaled albuterol blunted
airway response to tracheal intubation in asthmatic patients,
whereas intravenous lidocaine did not.154 The use of
inhalational lidocaine has been shown to worsen
bronchoconstriction and does not have a role at this time in
the rapid-sequence intubation of asthmatics.155,156
Consider the use of the dissociative agent ketamine for
the induction agent. Ketamine indirectly stimulates
catecholamine release and, in a dose of up to 2 mg/kg, will
produce bronchodilation in the critically ill asthmatic.157,158
Ketamine is contraindicated in patients with ischemic heart disease, severe hypertension, preeclampsia,
or increased intracranial pressure. Side effects of
ketamine include hallucinations, increased secretions,
and, on rare occasions, laryngospasm.
Once intubation has been successfully performed,
mechanical ventilation should be initiated. However,

Therapies Not Recommended
For Treating Exacerbations
Narcotics, sedatives, and tranquilizers should be avoided in
an acute asthmatic because respiratory arrest may occur
after their use. The combative asthmatic is more likely to
need aggressive therapy or even intubation than sedation.
Mucolytics, expectorants, and aggressive hydration do not
aid in the treatment of asthma. A meta-analysis regarding
the use of antihistamines in adult asthmatics showed that
these agents increase side effects without improving
pulmonary function. The literature does not generally
support their use.147 While some physicians prescribe
antihistamines for allergen- and exercise-induced asthma,
the scientific basis for this remains thin.
Nedocromil and cromolyn inhibit mast cell mediator
release through the blockage of chlorine channels.
Although efficacious in preventing the acute release of
these pro-inflammatory cytokines, mast cell mediators
play no role in the actively wheezing patient.
Continuous infusions of ketamine have been
occasionally used as an adjunct to treat status
asthmaticus in the non-intubated patient.148 However, a
randomized trial suggests ketamine infusion is not useful
in this situation.149
Many alternative or complementary medicine
therapies are used to treat asthma. Of note, manual
therapy (performed by chiropractors, respiratory therapists, or osteopaths) is sometimes touted to improve lung
function. There are no data or very poor data to suggest
that any manual therapy is appropriate to treat patients
with asthma.150 Likewise, no well-controlled trials
support the use of other alternative therapies (acupuncture, homeopathy). Currently, these have no place in the
acute or long-term treatment of asthma.151,152

Emergency Medicine Practice

10

February 2001

with a square waveform.153 (See the clinical pathway
“Ventilatory Management Of The Asthmatic” on page
16.) Once the initial ventilatory settings have been
chosen, continued close monitoring of the patient is
essential. According to Williams et al, the most sensitive
indication of the patient’s ongoing risk for barotrauma or
volutrauma is his end inspiratory volume, which is a
measure of dynamic hyperinflation.163 Because this is
difficult to measure, a practical substitute is the plateau
pressure (Pplat), which reflects the pressure in the alveoli.
The goal should be to keep Pplat less than 30 cmH2O; if the
plateau pressure is consistently higher than this, lower
the patient’s minute ventilation.
As mentioned, this lowered minute ventilation to
decrease hyperinflation often results in hypercapnia and

mechanical ventilation carries its own peculiar risks in
the asthmatic. In the early phases of treatment, airflow
obstruction results in larger tidal volumes secondary to
air trapping. This produces “auto-PEEP” or increased
residual volumes and may lead to barotrauma and
possibly tension pneumothorax.
Mechanical ventilation with rapid-flow rates,
reduced respiratory frequency, combined with a prolonged expiratory phase, helps prevent this distressing
condition. This pattern of mechanical ventilation is
commonly referred to as controlled mechanical
hypoventilation or permissive hypercapnia.159-162
Jain et al recommend initial ventilatory settings of a
VT of 6-8 cc/kg, no extrinsic PEEP, a respiratory rate of
8-10 per minute, and an inspiratory flow of 80-100 L/min

Ten Excuses That Don’t Work In Court
1. “Really, he wasn’t wheezing when I discharged him. It’s
right there on the chart.”
Other things are on the chart as well. The nurse
documented that the respiratory rate was 35 and the room
air pulse oximetry was 90%. The patient wasn’t wheezing
because he still wasn’t moving any air.
No wheezing can be a very ominous sign in the
asthmatic. Interpret a silent chest on initial evaluation or
after pharmacologic interventions in the clinical context of
the patient—somnolence with this physical exam finding
necessitates immediate intervention, including the
possibility of invasive ventilation.

he’s obviously in need of additional treatment or he
wouldn’t have come to the ED.
6. “I didn’t instruct him how to use the MDI because they
are so simple to use.”
Every patient should be instructed on the proper use
of the MDI and discharged with a spacer (or a prescription
for a spacer) to accompany it. If the patient has the
medication but can’t use the delivery device properly,
he is in a canoe without a paddle—and possibly up some
sort of creek.
7. “After intubating him, I just figured a large tidal volume
would open his airway. How was I supposed to know we
were out of chest tubes?”
Intubating asthmatics is fraught with difficulty, and the
emergency physician must be acutely aware of the possible
complications, including high airway pressures leading to
barotrauma. Consider lower tidal volumes (5-7 cc/kg) and
monitor the plateau pressures. If they arrest on the
ventilator, decompress the chest!

2. “Really, he wasn’t wheezing when I first evaluated him.”
Ditto.
3. “I thought I would let his primary doctor start him
on steroids.”
Steroids play an integral role in the treatment of an acute
asthma exacerbation, and nearly all asthmatics should be
discharged with a pulse-course of oral steroids (except
those with minimal symptoms who responded to a single
inhalation treatment). Inhaled or intramuscular steroids
remain other options.

8. “I reserve ipratropium for elderly COPD patients.”
Anticholinergics are indicated for moderate-to-severe
asthma exacerbations. They are safe, effective, and offer at
least some benefit to many asthmatics.

4. “He couldn’t move the peak-flow meter, but I just
assumed he wasn’t cooperating.”
If the PEFR is documented, then be prepared to use the
data. If a patient has a difficult time using this device,
document other indicators of the patient’s improvement
(such as an ability to count to five or speak in full
sentences). Documenting a smiling patient who states, “I
feel great, doc!” may be as useful as a “good” peak flow.

9. “Of course I’m sorry he died, but no one can predict who
will have a fatal attack.”
Not quite true. The past may guide the future. Patients with
a history of prior intubations or intensive care admissions
are more likely to suffer fatal asthma in the future. Ask.
10. “I thought a small dose of midazolam would help
relax him.”
Make sure you aren’t making a patient permanently
relaxed. Most asthmatics who are in distress are not
breathing well. Their distress will resolve with treatment of
their primary respiratory disease, not their anxiety. ▲

5. “He had just used his β-agonists at home, so I thought I
would wait to treat him.”
Let the patient’s presentation dictate the treatment—if he
is in distress and wheezing, start therapy. No matter how
much pharmacologic intervention he received at home,

February 2001

11

Emergency Medicine Practice

respiratory acidosis. A PaCO2 as high as 80 mmHg, resulting
in a pH of 7.15, is well within the acceptable limits for this
type of ventilatory management. Indeed, multiple studies
have shown minimal adverse effects from this
hypoventilation and clearly improved outcomes resulting
from a lower incidence of barotrauma.164-167 Few relative
contraindications exist for permissive hypercapnia, but they
include severe hypertension, severe metabolic acidosis, and
severe hypoxemia.153
Any patient undergoing hypoventilation will require
heavy sedation and at times the use of neuromuscular-

blocking agents, as this type of ventilatory management
is usually poorly tolerated. Although corticosteroidtreated patients with severe asthma who undergo
prolonged neuromuscular paralysis may develop
protracted muscle weakness,233 this is not a concern in
emergency management. Rarely, the use of buffer therapy
to maintain pH is indicated; this decision should be
undertaken in consultation with an intensivist and in the
context of the patient’s comorbid medical conditions.
Once a patient has been intubated and initial ventilatory management determined, β-agonist therapy must be

Cost-Effective Strategies For Patients With Asthma
Strategies That Focus On ED Care

2. Give the patient a spacer.
Only 40% of ED asthma patients own a spacer.208 Increase this
number to 100% by dispensing them in the ED. Patients can
even make their own spacer using a 500 mL plastic bottle. A
sealed 500 mL soda bottle produces similar bronchodilation
when compared to a conventional spacer in children with
asthma.227 (Whether Coke or Pepsi bottles yield better PEFRs
remains to be studied.)
Even giving the patient a nebulizer can be cost-effective.
In one study, providing home nebulizers for selected
outpatients resulted in significant savings due to reduced ED
and office visits.228

1. Increase the ED use of MDIs and spacers, as opposed to
nebulizers.
MDIs plus spacers are at least as effective and less expensive
than nebulizer therapy.
Risk-Management Caveat: These devices are less well
studied in the moribund asthmatic.
2. Use oral instead of parenteral steroids.
There is no convincing evidence that intravenous steroids
are more effective than the less expensive oral route. In
one pediatric study of severe asthma, there was no
difference in length of hospital stay between asthmatic
patients receiving oral prednisone and those receiving
intravenous methylprednisolone.225
Risk-Management Caveat: Moribund patients as well as
those who are vomiting may require intravenous steroids.
Consider intramuscular steroids for non-compliant or
indigent patients (see below).

4. Avoid unnecessary antibiotics.
Many healthy young adults with wheezing are given
antibiotics for “bronchitis.” Most of these patients have
a virus that results in reactive bronchospasm. Randomized,
placebo-controlled trials do not support routine antibiotic
treatment of uncomplicated acute bronchitis. However,
RCTs do show that inhaled albuterol decreases the
duration of cough in adults with uncomplicated acute
bronchitis.229 Despite this fact, as many as 74% of patients
with acute uncomplicated bronchitis are given antibiotics,
while only about 17% receive bronchodilators.230 These
numbers should be reversed. (Better yet, no antibiotics and
100% bronchodilators.)
Risk-Management Caveat: Antibiotics are certainly indicated
in asthmatics who suffer concurrent pneumonia. They also
decrease the relapse rate for patients with an acute
exacerbation of COPD.231

3. Avoid unnecessary laboratory tests.
Most asthmatics will not require bloodwork. The CBC is rarely
helpful. If you suspect pneumonia, order a chest x-ray, not a
CBC. Blood gases are seldom necessary. A pulse ox will detect
hypoxia, and a patient with a PEFR above 25% of predicted
will rarely (if ever) be hypercarbic.
Risk-Management Caveat: Patients taking theophylline
(especially those who are tremulous and vomiting) may be
theophylline toxic and will require a blood level.
4. Avoid unnecessary x-rays.
Most patients with a history of asthma who present with
wheezing will not require chest film.
Risk-Management Caveat: If you suspect pneumonia,
foreign body, congestive heart failure, or other asthma
mimics, get the film.

Strategies For Indigent Patients

Strategies That Focus On Preventing Relapse

1. Give the patient discharge medications such as an MDI
and steroids.
One study showed that providing medications and
increasing the use of steroids decreased “bounce-backs” in
patients with asthma.232

1. Educate the patient.
Patient education programs can decrease ED visits.226 This
education ranges from the proper use of the MDI to
developing an action plan for exacerbations.

2. Consider the use of intramuscular steroids for noncompliant patients.
Intramuscular steroids are therapeutically equivalent to a
week’s therapy with oral steroids. ▲

Emergency Medicine Practice

12

February 2001

will present to the ED one or more times for an acute
exacerbation.179 Multiple factors may contribute to the
change in a pregnant asthmatic’s disease, but the important lesson is that these patients require close monitoring
and may present with worsening of their disease.177,180
Early therapy is vital to the prevention of fetal
hypoxemia, and under-treatment can lead to increased
perinatal mortality and prematurity, as well as low birth
weight.181-184 Demissie et al also found an increased risk of
preeclampsia in pregnant asthmatics as well as congenital
malformations in their babies.185
The management of pregnant asthmatics is essentially the same as for non-pregnant asthmatics, but there
are a few exceptions. Subcutaneous epinephrine should
be avoided since it causes uterine artery constriction,
whereas subcutaneous terbutaline probably does not.
Inhaled β-agonists and corticosteroids are considered safe
in pregnancy.181-184,186,187 Ipratropium is also acceptable and
is listed as category “B” (presumed safe) in pregnancy.
Despite the data demonstrating the importance and
safety of steroids in the pregnant asthmatic, Cydulka et al
demonstrated that pregnant women were 30% less likely
to receive this therapy when compared to their nonpregnant cohorts, despite similar symptomatology and
PEFRs.178 Current guidelines can be found in the
National Asthma Education and Prevention Program
(NAEPP) expert panel guidelines for the treatment of
acute asthma exacerbations.188

continued. Bronchodilators may be administered via an
MDI or by nebulization. Both methods have been shown to
be efficacious in the literature.168 The use of an MDI offers
the advantages of ease of administration, lower cost, and
ability to maintain ventilatory settings. Dhand et al documented good efficacy and safety with the use of four puffs
of an albuterol MDI administered at the beginning of
inspiration through an in-line spacer device.169
If a patient with severe asthma suddenly arrests
while on the ventilator, quickly place bilateral chest
tubes. (Okay, first auscultate the lungs, look for tracheal
deviation, and evaluate the peak pressures on the
ventilator—then place bilateral chest tubes.) Tension
pneumothorax is an important cause of sudden death in
the intubated asthmatic.
In patients with persistent and markedly elevated
peak pressures, high-frequency jet ventilation may
improve gas exchange.170 This, however, is rarely employed in the ED setting.

Non-Invasive Ventilation
Non-invasive ventilation (NIV) offers an attractive
alternative to intubation in the patient with a severe
asthma exacerbation. The trials evaluating this method of
ventilatory support are small but promising; most
involve bi-level positive airway pressure (BiPAP).171-173
Initial settings can begin at 8 or 10 cmH2O inspiratory
positive airway pressure (IPAP), while the expiratory
positive airway pressure (EPAP) can be set at 3 or 5
cmH2O. The settings are then adjusted according to
clinical response. In one study, the authors suggested that
for hypoxemic patients, EPAP should be raised in
increments of 2 cmH2O while maintaining the IPAP at a
fixed interval above EPAP (i.e., the difference between
IPAP and EPAP is kept at 5 cmH2O). For hypercapnic
patients, IPAP was raised in increments of 2 cmH2O with
EPAP increased at a slower rate (1 cm increase in EPAP
for every 2.5 cm increase in IPAP).172 β-agonists given
via BiPAP appear to be more effective than those administered by small-volume nebulizers.174 At this time, NIV
represents a reasonable alternative to invasive ventilation
for selected asthmatics.175 However, such patients must
be monitored very closely, as some will ultimately
require intubation.

Elderly Patients

Special Circumstances: Pregnant Patients,
The Elderly, And The Young

Elderly patients represent the fastest-growing segment of
our population and therefore consume a relatively larger
amount of the healthcare dollar. Skobeloff et al cited an
asthma prevalence of 7%-10% in the elderly population.189
When hospitalized, the elderly have longer hospital stays
and more are discharged to skilled facilities, rather than
to home.189
Elderly patients also present a diagnostic dilemma—
how often do we hear, “I have asthma,” when the patient
really means, “I have emphysema”? Fortunately, the
acute treatment of these two disease entities is similar.
Remember that elderly patients with new-onset wheezing may be in CHF.
Be particularly aware of medication side effects in
the elderly—for example, steroids in the diabetic or
theophylline in the patient with underlying coronary
artery disease. Though the emergency physician didn’t
start the theophylline, consider that he or she might be
treating a patient in multifocal atrial tachycardia with a
theophylline level of 25 mg/dL! Likewise, consider the
example of an asthmatic patient just placed on timolol for
his glaucoma. Caution is the advisory in the elderly.

Pregnant Patients

Pediatric Patients

“The cheeks are ruddy; eyes protuberant, as if from
strangulation…they breathe standing, as if desiring to draw in
all the air which they possibly can inhale.”
—Aretaeus the Cappadocian (81-138?) on asthma176

Asthma affects approximately 4% of pregnant women. Of
these, approximately one-third improve during pregnancy, one-third remain unchanged, and one-third
become worse.177,178 Forty-two percent of pregnant
asthmatics will require hospitalization, and up to 18%

February 2001

Children with asthma are treated in a similar manner to
the adult: β-agonists, anticholinergics, and systemic
steroids. Assess fluid status and make appropriate
corrections for infants and children, particularly in the
Continued on page 17

13

Emergency Medicine Practice

Clinical Pathway: Management Of Patients
With An Acute Asthma Exacerbation
•
•
•
•

ABCs
IV/O2/Monitor*
Physical exam
Vital signs

→
Is the pa tient stable?

→

→

No

Yes

• Inhaled β2-agonists by MDI or nebulizer (Class IIa)
• O2 as needed to keep saturation > 90%
• Multiple-dose ipratropium for moderate-to-severe
attacks (Class IIb)
• Systemic corticosteroids* (Class IIa)

Prepare for intubation
• Continuous β2-agonists 0.1 mg/kg/h (Class IIb) OR
• Subcutaneous terbutaline 10 mcg/kg (Class IIb) OR
• Consider subcutaneous epinephrine 0.01 mg/kg (Class
IIb) PLUS
• Ipratropium bromide 0.5 mg >10 kg < 0.25 mg (Class IIa)
• Systemic corticosteroids 1-2 mg/kg (Class IIa)
• Magnesium 2 g IV over 5-10 minutes (Class IIb)

→

→

Repeat evaluation
• Clinical examination
• May include evaluation of PEFR or FEV1 (Class IIb)

Proceed with airway management
• Rapid-sequence intubation (Class IIb)
• BiPAP (Class indeterminate)

→

Yes

Go to top of next page

→

No

Is the pa tient impr oving?

→

→

* Patients with very mild attacks may not require
IV/O2 monitoring or systemic corticosteroids.
The evidenc e for recommenda tions is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II a: Acceptable and useful. Very good evidence provides support. Class II b: Acceptable and useful.
Fair-to-good evidence provides support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright  2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited
copying privileges for educational distribution within your facility or program. Commercial distribution to
promote any product or service is strictly prohibited.
Emergency Medicine Practice

14

February 2001

Clinical Pathway: Management Of Patients
With An Acute Asthma Exacerbation
(continued)

Mild to minimal exacerbation?
• Asymptomatic
• Normal physical examination
• PFTs > 70%

Moderate exacerbation?
• Moderate symptoms present
• PFTs 50%-80% predicted/
personal best

• Continue treatment for 1-3 hours
(Class indeterminate)
• β2-agonists (Class IIa)
• Anticholinergics (Class IIa)
• Corticosteroids (Class IIa)

→

→

→
The evidenc e for recommenda tions
is graded using the following scale. For
complete definitions, see back page.
Class I: Definitely recommended.
Definitive, excellent evidence provides
support. Class II a: Acceptable and
useful. Very good evidence provides
support. Class II b: Acceptable and
useful. Fair-to-good evidence provides
support. Class III: Not acceptable, not
useful, may be harmful. Indeterminate: Continuing area of research.

• β2-agonists
(Class IIa)
• Anticholinergics
(Class IIa)
• Systemic
corticosteroids
(Class IIa)
• Monitor FEV1 and
O2 saturations
(Class IIb)

Reassess need
for in tubation

→

• Continued ED
therapy (Class
indeterminate)
OR
• Admit to clinical
observation unit
(Class indeterminate) OR
• Admit to hospital
floor (Class
indeterminate)

Poor response
• PCO2 > 42mmHg
• Drowsiness or confusion
• FEV1 or PEFR < 50%

→

Incomplete response
• Mild to moderate symptoms
• Persistent wheezing
• FEV1 or PEFR > 50% and < 70%

Discharge to home
• β2-agonist MDIs (Class IIa)
• Systemic corticosteroids
(Class IIa)
• Patient education (Class
indeterminate)
• Early outpatient follow-up
• Consider inhaled steroids
(Class indeterminate)

Continue treatments OR
• Continuous aerosols with β2-agonists
(Class IIb)
• Multiple-dose anticholinergics
(Class IIb)
• Intravenous corticosteroids (Class IIa)
• Consider magnesium 2 g IV (Class IIb)

→

→

→
Good response
• Response sustained longer
than 60 minutes
• Physical exam normal
• FEV1 or PEFR > 70%

How is
the pa tient
responding?

→

Discharge to home
• β2-agonist MDIs (Class IIa)
• Systemic corticosteroids (Class IIa)
• Patient education (Class indeterminate)
• Early outpatient follow-up
• Consider inhaled steroids (Class
indeterminate)

→

→

→

Severe exacerbation?
• Symptoms at rest, retractions,
accessory muscle use
• No improvement
• FEV1 or PEFR < 50% predicted/
personal best

No

•
•
•
•
•
•
•

Yes

→

• Proceed
with RSI
• Low tidal
volumes
• ABG

Admit to hospital ICU or stepdown unit (Class indeterminate)
β2-agonists hourly or continuously (Class IIb)
Anticholinergic agents (Class IIa)
Systemic corticosteroids (Class IIa)
Oxygen
Chest x-ray (Class IIb)
Consider ABG (Class IIb)

• Consider need for alternative therapies if continued deterioration or failure to improve (Class indeterminate)
• Magnesium 2 g IV (Class IIb)
• Intravenous β-agonists (continuous drip) (Class indeterminate)
• Heliox (Class indeterminate)
• Inhalation anesthesia (Class indeterminate)
• BiPAP if not intubated (Class indeterminate)

This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright  2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited
copying privileges for educational distribution within your facility or program. Commercial distribution to
promote any product or service is strictly prohibited.
February 2001

15

Emergency Medicine Practice

Clinical Pathway: Ventilatory Management Of The Asthmatic
Initial ventilator settings:
Mode = Assist control, FiO2 = 1.0
RR = 8-10/min, VT = 80-100 L/min
PEEP = 0, sensitivity = 1.0 cmH2O (Class indeterminate)

Physiological objectives:
Pplat < 30 cmH2O (Class indeterminate)

Physiological
objectives achieved?

→

→

Change ventilator mode to SIMV or pressure support
(Class indeterminate)

Reduce minute ventilation
(may require heavy sedation/NMB) (Class indeterminate)

Yes

No

→

Yes

Measure pH (Class indeterminate)
pH ≥ 7.15?

No

Unconventional therapies—
Heliox, anesthetic agents
(Class indeterminate)

→

→

→

Yes

No

→

Continue aggressive
medical therapy
(Class IIa)

→

→

→

Physiological objective achieved?

Consider buffer
therapy
(Class indeterminate)

LEGEND
FiO2 = fraction of inspired oxygen
VT = tidal volume
RR = respiratory rate
PEEP = positive end-expiratory pressure
Pplat = plateau airway pressure
SIMV = synchronized intermittent mandatory ventilation
NMB = neuromuscular blockade
Adapted from Figure 4 in: Jain S, Hanania NA, Guntupalli KK. Ventilation of patients with asthma and obstructive lung disease.
Crit Care Clin 1998;14:685-705.
The evidenc e for recommenda tions is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II a: Acceptable and useful. Very good evidence provides support. Class II b: Acceptable and useful.
Fair-to-good evidence provides support. Class III: Not acceptable, not useful, may be harmful. Indeterminate: Continuing area of research.

This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.

Copyright  2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited
copying privileges for educational distribution within your facility or program. Commercial distribution to
promote any product or service is strictly prohibited.
Emergency Medicine Practice

16

February 2001

Continued from page 13

controlled asthma may result in poor growth.192,193
The majority of studies evaluating the use of inhaled
beclomethasone (at dosages of 400-800 mcg/d) revealed
no negative effect on growth,194-196 although several shortterm studies did demonstrate a dose-related phenomenon.197,198 At this time, the use of inhaled steroids is not
only safe, but considered usual care.

face of notable tachypnea. Since they may be less dexterous than adults, be sure to prescribe a “spacer” or
“valved holding chamber” for use with MDIs. Smaller
children and infants will need a spacer with a mask.
These devices are a necessity for children, as well as
most adults. There are versions with holding chambers
(with or without face masks) for both infants and older
children alike. Even in very young children with acute
wheezing, RCTs show that the MDI plus spacer is at least
as effective as a nebulizer.80,190
In the child with asthma, consider inhaled steroids.
In one RCT, children who received 1.5 mg/kg of nebulized dexamethasone in the ED had fewer short-term
relapses than children treated with 2 mg/kg of oral
prednisone.191 Though a concern about the long-term
growth effects of inhaled steroids exists, their efficacy
usually outweighs the potential risk. In fact, poorly

Radiography
As in adults, chest radiographs rarely influence the
management of children with a history of asthma and
should not be routine.199 Overall, fewer than 14% of films
show significant findings (such as infiltrates, atelectasis,
pneumothorax, or pneumomediastinum).200 When a
wheezing child presents to the ED, a trial of inhaled βagonists is appropriate before any imaging studies.
Children who improve during ED observation rarely
need a chest film.

Tool 1. Sample Discharge Instructions For The Patient With Asthma.
Copyright  2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited
copying privileges for educational distribution within your facility or program. Commercial distribution to
promote any product or service is strictly prohibited.
Asthma is a chronic disease of the breathing passages that affects about one in 10 people—it is not an infection,
and it cannot be cured. People of all ages and backgrounds can have asthma. There are more than 15 million
Americans with asthma—including almost 5 million children—and their numbers are increasing.
Asthma can be well controlled with appropriate therapy. When you have an asthma attack, your airways
become small in response to some form of irritation, or “trigger,” making breathing difficult.
Asthma “attacks” can be mild or life-threatening. Common asthma triggers include pollen, molds, animal
dander, dust mites, smoke, strong odors or fumes, respiratory infections, cold air, and sometimes exercise. By
knowing what your triggers are, you may be able to reduce your daily risk of having an asthma attack.

What Are The Symptoms Of Asthma?
The main symptoms of asthma are shortness of breath, wheezing, tightness in the chest, and prolonged cough
(greater than one week). Although wheezing is a hallmark of asthma, not all people with asthma wheeze. For
some, coughing may be the only symptom of asthma. Coughing often occurs during the night or after exercise.

Treatment
There are two basic categories of asthma medications. Long-term control medications are taken regularly (often
every day) to prevent or reduce inflammation in the airways. Using these medications makes the asthma sufferer
less likely to have an asthma attack. Quick-relief or “rescue” medications are designed to open the airways
rapidly and are taken when symptoms of an asthma attack are first noticed.
You can help prevent asthma attacks by taking the following steps: Take your asthma medication(s) exactly
as directed by your doctor. Use a peak-flow meter—to monitor your breathing—as often as instructed by your
doctor. Keep track of your condition and learn to recognize when your asthma symptoms are worsening. Know
how to respond when an asthma attack is beginning. A severe asthma attack is a medical emergency. Untreated,
it can be fatal.
Asthma episodes rarely occur without warning. Most people with asthma have warming signs (physical
changes) that occur hours before symptoms appear. Warning signs are not the same for everyone. You may have
different signs at different times. By knowing your warning signs and acting on them, you may be able to avoid
a serious episode of asthma.
February 2001

17

Emergency Medicine Practice

body, or heart failure

However, there is considerable controversy regarding the need for routine chest radiography in children
who present with a first-time episode of wheezing. Some
authors suggest chest films for all children who have no
prior history of bronchospasm in order to identify
important mimics such as foreign body, pneumonia, CHF,
or other cardiopulmonary disease. In one study of firsttime wheezing in children, the authors stated that they
were unable to identify any individual or combination of
clinical factors that could accurately predict a positive
chest film. They suggested routine use of chest radiography for the initial episode of childhood bronchospasm.201
In contrast, another group found several clinical
characteristics among children with first-time wheezing that
were associated with a positive chest x-ray. These included
elevated temperature (37.9˚C vs 37.5˚C; P = 0.04), absence of
family history of asthma (72.6% vs 27.4%; P < 0.01), and the
presence of localized wheezes (76.0% vs 24.0%; P = 0.02) or
localized rales (76.0% vs 24.0%; P < 0.01).202
Chest x-rays may be worthwhile in asthmatic children
with fever or those with persistent rales and rhonchi. The
following are indications for chest x-rays in children with
wheezing and a history of reactive airway disease:203
• Toxicity
• Significant respiratory distress
• Persistent rales and rhonchi
• Fever with no obvious viral source
• Poor response to ED treatment
• Suspicion of pneumothorax, pneumonia, foreign

Disposition
Numerous guidelines exist to help the emergency
physician form an educated decision with regards to
patient disposition. (See also the bottom part of the
clinical pathway “Management Of Patients With An
Acute Asthma Exacerbation,” which starts on page 14.)
Response assessment should be based on subjective
improvement of wheezing, air exchange, and dyspnea;
objective criteria such as improvement in FEV1 or PEFR;
and the patient’s risk for relapse and poor outcomes, in
part predicted by his or her past history.
Complete resolution of symptoms and a PEFR or FEV1
greater than 70% predicted signifies a good response to
treatment.204 When determining improvement, one group
suggests that a 12% (of predicted) improvement in PEFR
and a 2 cm improvement on a 10 cm dyspnea visual analog
scale may represent the minimum clinically significant
response.205 Individuals who demonstrate significant
improvement, as well as those with minimal symptoms,
may be safely discharged home. An five- to 10-day course
of oral corticosteroids and a 10-day regimen of intense
β-agonist therapy remain the mainstay of outpatient
therapy. This seems to be true despite conflicting data on
relapse rates of discharged patients.60
Even with the most aggressive of therapies, some
asthmatics may fail to respond. Poor response to treat-

Tool 2. Your MDI: Guidelines To Proper Use.
Copyright  2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited
copying privileges for educational distribution within your facility or program. Commercial distribution to
promote any product or service is strictly prohibited.
The guidelines that follow will help you use the inhaler the right way. Ask your doctor or nurse to show you
how to use the inhaler.

Using The Inhaler
1. Remove the cap and hold the inhaler upright.
2. Shake the inhaler; attach the inhaler to your spacer.
3. Tilt your head back slightly and breathe out.
4. Place your lips around the spacer.
5. Press down on the inhaler to release the medicine as you start to breathe in slowly.
6. Breathe in slowly for 3-5 seconds.
7. Hold your breath for 10 seconds to allow the medicine to reach deeply into your lungs.
8. Repeat puffs as prescribed. Waiting one minute between puffs may permit the second puff to go deeper into
the lungs.
Note: Dry powder capsules are used differently. To use a dry powder inhaler, close your mouth tightly around
the mouthpiece and inhale very quickly.
Adapted with permission from: National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 2:
Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97-4051. Bethesda, MD, 1997: Figure 4-3.

Emergency Medicine Practice

18

February 2001

gency physician. Consideration of concomitant risk
factors (see Table 2 on page 20), as well as patient input,
should help guide disposition.206
For all patients with an acute asthma exacerbation
who are discharged from the ED, close follow-up is key.
Encourage them to see or call their physician within
several days of their ED visit.

ment is defined as an FEV1 or PEFR of less than 50%
predicted and persistent wheezing. Hospital admission
or continued observation and ongoing aggressive therapy
are warranted for these patients.
An incomplete response or an FEV1 or PEFR that
lingers between 50% and 70% predicted presents a
clinical problem for even the most experienced emer-

Tool 3. Asthma Action Plan.
Copyright  2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber limited
copying privileges for educational distribution within your facility or program. Commercial distribution to
promote any product or service is strictly prohibited.
It is important to keep track of your symptoms, medications, and peak expiratory flow rates (PEFRs) in order to
best treat your asthma. The relative severity of your asthma can be divided into three zones—green, yellow, and
red. At any time, call your doctor if your symptoms worsen while on oral steroids, your inhaled bronchodilator
medication is not lasting four hours, or your peak flow number remains or falls below ______ in spite of following the plan!

Green Zone: GO!
1. PEFR is _____________ (80%-100% of your personal best).
2. Breathing is good with no cough, wheeze, or chest tightness during work, school, exercise, or play.
ACTION:
• Continue the medications prescribed in your daily plan.

Yellow Zone: CAUTION!
1. PEFR is _____________ (50%-79% of your personal best).
2. Asthma symptoms are present, including cough, wheeze, or chest tightness.
3. You have increased need for your “quick-relief” medications, you have increased asthma symptoms when
you wake, or you are waking at night with symptoms.
ACTIONS:
• Take ______ puffs of your quick-relief (bronchodilator) medication _____________
Repeat ______ times.
• Take ______ puffs of _____________ (anti-inflammatory) _____________ times per day.
• Begin or increase treatment with oral steroids.
Take ______ mg of _____________ every a.m. ______ p.m. ______
• Call your doctor (phone) _____________

Red Zone: DANGER!
1. PEFR is _____________ (< 50% of your personal best).
2. You continue to get worse despite treatments started in the yellow zone.
ACTIONS:
• Take ______ puffs of your quick-relief (bronchodilator) medicine _____________
Repeat ______ times.
• Begin/increase treatment with oral steroids: Take ______ mg now.
• Call your doctor (phone) _____________ now.
• If you cannot contact your doctor, go directly to the emergency department.
Adapted with permission from: National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 2:
Guidelines for the Diagnosis and Management of Asthma. National Institutes of Health pub no 97-4051. Bethesda, MD, 1997: Figure 4-3.

February 2001

19

Emergency Medicine Practice

Discharge Medications

followed are successfully treated and discharged.213,214
Choosing which patients to place in an observation unit
is an inexact science. Fortunately, the literature supplies
some guidance. In one study, the change in peak flow in
response to treatment provided clues to the need for
admission or further observation. In this trial, patients with
40% or higher PEFR after the third treatment had an 89%
probability of reaching 50% predicted in 12 hours and were
thus good candidates for an observation unit. Those with a
third-treatment PEFR lower than 32% predicted had only a
22% probability of reaching 50% predicted in 12 hours and
were more likely to ultimately require admission.215

Patients will need to obtain medications that will prevent
a relapse. Providing indigent patients with medications
may avoid an ED “bounce-back.”
The best outpatient strategy for administering
β-agonists is unclear. Many physicians prescribe
β-agonists every 4-6 hours. However, some studies
show that PRN use (“on-demand inhalation”) of shortacting β2-agonists in moderate-to-severe asthma is safe and
effective. In severe asthma, a reduction from regular to ondemand β2-agonist inhalation can even improve asthma
control.207 Make sure that the patient either has or can get a
spacer. Only 40% of ED asthma patients own a spacer.208
Increase this number to 100% by dispensing them in the ED.
Give corticosteroids. Corticosteroids have multiple
positive effects in the patient treated in the ED for acute
asthma. They decrease the need for β-agonists and reduce
both the relapse rate and need for subsequent hospitalization in the ensuing 7-10 days.103 When giving oral
steroids, there is no evidence that a taper is necessary.209
Prescribe prednisone (30-50 mg/d) for anywhere from
five to 10 days and stop them without a taper.

Education
Asthma education in the ED may decrease future
emergency visits. One successful education program
included topics such as prevention of asthma, decreasing
inflammation as a means of improving asthma control
(stressing inhaled corticosteroids), self-monitoring with a
peak flow meter, and demonstrating the correct inhalation technique with metered-dose inhalers and a spacer
device.216 In another study, ED asthma education using a
nurse educator led to reduced symptoms, improved lung
function, less time off work, and fewer consultations with
health professionals.217
Despite some evidence that self-management
programs with a written action plan reduce hospitalizations,218 only 28% of the adult patients hospitalized for
asthma had written action plans that defined how to
manage their asthma and control an exacerbation.219
Furthermore, Emond et al recently surveyed 77 emergency departments to assess the presence of formal
asthma education programs. Only 16% of the sites had
asthma education programs, and the majority of those
were at pediatric facilities.220 This is an arena in which
emergency physicians could play a greater role.
Simple handouts including an “Asthma Action Plan”
(see the sample on page 19) should be dispensed at discharge or at admission. Patients should be taught to monitor
their peak flows: A drop in peak flow below 80% of personal
best indicates need for added medications, while a drop
below 50% indicates a severe exacerbation. In addition,
provide handouts with written information about the
symptoms and treatment of asthma, as well as instructions
on the use of an MDI. (See “Tool 1: Sample Discharge
Instructions For The Patient With Asthma” on page 17 and
“Tool 2: Your MDI: Guidelines To Proper Use” on page 18.)
This last strategy of proper MDI use is deceptively
simple yet profoundly important. Only about 20% of
asthmatics use their MDI correctly.221 The physician or
respiratory therapist should critically observe the
patient’s technique before discharge. Many asthmatics
casually use their inhaler as if it were a breath freshener.

Peak-Flow Meters And Pulmonologists
In one large study, prescribing peak-flow meters and giving
self-management guidelines to all asthma patients did not
improve mortality or morbidity.210 This study, however, did
not focus on ED patients with asthma. Patients whose
asthma is severe may benefit from these interventions.
Emergency physicians often act as the gatekeepers
for referral to specialized care—patients may come to us
just to “get a referral.” Studies show that physicians
differ widely in their opinions as to which patients need
specialty consultation.211,212 Some physicians consider
suggesting a pulmonologist for patients with more than
two bursts of oral steroids in one year, patients younger
than 3 years of age, or patients with multiple ED visits for
acute exacerbations. Again, while this recommendation
seems reasonable, there is little to no evidence to show
that it improves outcomes.

Observation Units
Observation units are an option for incomplete responders.
Recent studies indicate that as many as 59% of asthmatics
admitted to observation units where strict care protocols are

Table 2. Risk Factors For Asthma.
Prior intubation
Prior intensive care unit hospitalization
Chronic glucocorticoid use
Comorbidity
Two or more hospitalizations in the past year
Recent ED care
Psychosocial problems
Poor compliance
Poor follow-up

Smoking
Ask the parents of wheezing children if they or anyone
else smokes inside the house. Cigarette smoke in the
home is an important modifiable risk factor in reactive
airway disease among children.222,223 People who will not

Adapted from Table 4 in: Brenner B, Kohn MS. The acute asthmatic
patient in the ED: To admit or discharge. Am J Emerg Med 1998;16:69-75.

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20

February 2001

stop smoking despite their own respiratory agonies may
at least smoke outside in deference to their children.
5.

Summary
Numerous myths and pitfalls of asthma management are
perpetuated despite “modern” medicine. Withholding βagonist therapy in the ED because of recent use at home
is unwarranted, has no scientific basis, and is extremely
dangerous. Likewise, failing to start corticosteroids, lack
of effort toward patient education, and failure to arrange
prompt outpatient follow-up are also concerning. (For
suggestions on how to avoid these pitfalls, see the “Ten
Excuses That Don’t Work In Court” on page 11.)
No established treatment regimen is completely
efficacious. Numerous drugs and drug combinations can
be used in the acute asthmatic to achieve optimal and
maximum bronchodilatory effect. Treatment should begin
with inhaled β-agonists and, if the patient is hypoxic,
oxygen as well. Additional therapy may include anticholinergic agents and corticosteroids. Objective measures of
treatment responsiveness, such as pulmonary function
tests, vital signs, chest and heart exams, as well as the
patient’s subjective assessment of dyspnea, may guide
ED intervention.
On discharge, all patients requiring systemic steroids
in the ED should be prescribed steroid therapy equivalent to oral prednisone 40-60 mg in a non-tapering
burst.224 The steroids may be given by mouth, by inhalation, or by injection. The best duration of therapy remains
unclear; recommendations range from five to 10 days.
Long-acting intramuscular steroids offer the advantage of
foregoing outpatient oral steroids, thereby ensuring full
patient compliance. ▲

6.
7.

8.

9.

10.

11.

12.

13.
14.
15.

16.
17.

18.

References
19.

Evidence-based medicine requires a critical appraisal of
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The findings of a large, prospective, randomized, and
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To help the reader judge the strength of each
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will be included in bold type following the reference,
where available. In addition, the most informative
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Emergency Medicine Practice

Physician CME Questions
17. Despite your best efforts, a patient suffering an
acute asthma attack becomes more anxious and
progresses to respiratory failure. Your next step in
management includes:
a. morphine to ease patient anxiety.
b. a benzodiazepine to calm and relax this patient.
c
ketamine followed by rapid-sequence
intubation.
d. blind nasotracheal intubation.
e. inserting a nasogastric tube to prevent
gastric distension.

26

February 2001

25. All of the following concerning the physical
examination are true except:
a. No wheezing is always a good sign—it means
that bronchoconstriction cannot be occurring.
b. The number of seconds a patient can
spend counting correlates well with
pulmonary function.
c. A patient’s ventilatory status can change
rapidly, so caution is advised.
d. Both lethargy and agitation presage
respiratory failure.

18. Increased airway resistance in an acute asthma
attack is produced by:
a. constriction of airway smooth muscle.
b. mucus secretion.
c. inflammatory changes in the bronchioles.
d. all of the above.
19. A patient has a rapid onset of wheezing and
difficulty breathing after she enters a dust-filled
room and presents to the ED in moderate distress.
Which medication has no role in her management
at this time?
a. Terbutaline
b. Epinephrine
c. Methylprednisolone
d. Cromolyn sodium
e. Albuterol

26. Which of the following findings may suggest a
diagnosis other than (or in addition to) asthma?
a. Increased jugular venous pressure,
lymphadenopathy, or carotid bruits
b. Unilateral wheezing or rales
c. Extremely high or extremely low
blood pressure
d. All of the above

20. All of the following are appropriate first-line
agents in the treatment of a moderate asthma
exacerbation except:
a. inhaled β2-agonists.
b. inhaled anticholinergics.
c. systemic corticosteroids.
d. inhaled lidocaine.
e. supplemental oxygen.

27. Indications for chest radiography include:
a. asthma severe enough to require
hospitalization.
b. clinical suspicion of pneumothorax,
CHF, pneumonia, or foreign body.
c. an immunocompromised host.
d. unexplained fever.
e. all of the above.

21. When evaluating a patient’s pulmonary function,
it’s important to keep in mind that:
a. PEFR is a more sensitive measure of patient’s
overall airway obstruction than FEV1.
b. FEV1 measures the obstruction in larger airways.
c. FEV1 is more dependent on patient effort.
d. PEFR requires less patient cooperation.

28. Early administration (within one hour) of
glucocorticoids in the treatment of acute
reactive airway disease:
a. results in fewer hospital admissions and
a lower rate of relapse after ED discharge.
b. is rarely helpful.
c. has not been proven to be effective.
d. is only useful in asthmatic children.

22. Which of the following ancillary diagnostic tests
should be ordered for the asthmatic presenting to
the ED?
a. Chest radiography in asthmatics being discharged from the ED
b. ABG in asthmatics with a PEFR less than 25%
c. CBC in asthmatics being admitted to
the hospital
d. Glucose test

29. Which of the following is an indication for
discharge in acute asthma?
a. Two ED visits in the past three days for an
acute exacerbation
b. The patient has improved subjectively but is
still wheezing
c. The peak expiratory flow rate after treatment
is 40% predicted
d. A PEFR greater than 70% predicted with
a clear lung exam and subjective patient
improvement
e. Lack of wheezing

23. Which of the following has shown some promise in
the treatment of severe asthma exacerbations?
a. Isoetharine
b. Inhaled lidocaine
c. Magnesium
d. Calcium-channel blockers
24. Asthmatics presenting to the ED should receive
which of the following therapies?
a. Systemic steroids, except in pregnant asthmatics
b. Epinephrine as first-line therapy on presentation
for mild-to-moderate asthma attacks
c. No additional β-agonist therapy if the
patient has received three nebulized
treatments at home
d. Anticholinergic therapy for moderate-tosevere exacerbations

February 2001

30. The addition of ipratropium to standard therapy
with steroids and β-agonists:
a. decreases pulmonary function in the first 90
minutes of treatment.
b. is least beneficial in those with severe asthma.
c. results in fewer hospitalizations when compared
to placebo.
d. is contraindicated in patients with a PEFR or
FEV1 less than 80% predicted.

27

Emergency Medicine Practice

Physician CME Information

31. What proportion of asthmatics use their
inhalers correctly?
a. About one in five
b. About half
c. About four in five
d. Virtually all adults and about 70% of children

This CME enduring material is sponsored by Mount Sinai School of
Medicine and has been planned and implemented in accordance with
the Essentials and Standards of the Accreditation Council for Continuing
Medical Education. Credit may be obtained by reading each issue and
completing the post-tests administered in December and June.
Target Audienc e: This enduring material is designed for emergency
medicine physicians.
Needs A ssessmen t: The need for this educational activity was
determined by a survey of medical staff, including the editorial board
of this publication; review of morbidity and mortality data from the
CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for
emergency physicians.
Date of O riginal R elease: This issue of Emergency Medicine Practice
was published February 9, 2001. This activity is eligible for CME credit
through February 9, 2004. The latest review of this material was
February 7, 2001.
Discussion of I nvestiga tional I nformation: As part of the
newsletter, faculty may be presenting investigational information
about pharmaceutical products that is outside Food and Drug
Administration approved labeling. Information presented as part of
this activity is intended solely as continuing medical education and is
not intended to promote off-label use of any pharmaceutical product.
Disclosure of Off-Label Usage: Clinical trials of β-agonists and
anticholinergics use far higher doses that those approved by the FDA.
Conversely, dosages approved by the FDA are not well-studied in
moderate-to-severe asthma.
Facult y Disclosur e: In compliance with all ACCME Essentials, Standards,
and Guidelines, all faculty for this CME activity were asked to complete
a full disclosure statement. The information received is as follows: Dr.
Cydulka reports research funding for Phase III trials from Sepracor and
Merck. Dr. Reilly, Dr. Kaufmann, Dr. Sacchetti, and Dr. Mann report no
significant financial interest or other relationship with the
manufacturer(s) of any commercial product(s) discussed in this
educational presentation.
Accreditation: Mount Sinai School of Medicine is accredited by the
Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credit D esigna tion: Mount Sinai School of Medicine designates this
educational activity for up to 4 hours of Category 1 credit toward the
AMA Physician’s Recognition Award. Each physician should claim only
those hours of credit actually spent in the educational activity.
Emergency Medicine Practice is approved by the American College of
Emergency Physicians for 48 hours of ACEP Category 1 credit (per
annual subscription).
Earning C redit: Physicians with current and valid licenses in the United
States, who read all CME articles during each Emergency Medicine
Practice six-month testing period, complete the CME Evaluation Form
distributed with the December and June issues, and return it
according to the published instructions are eligible for up to 4 hours
of Category 1 credit toward the AMA Physician’s Recognition Award
(PRA) for each issue. You must complete both the post-test and CME
Evaluation Form to receive credit. Results will be kept confidential.
CME certificates will be mailed to each participant scoring higher than
70% at the end of the calendar year.

32. An asthma attack that differs from a patient’s
prior attacks:
a. is no cause for concern.
b. may indicate a concomitant or even
alternative diagnosis.
c. is only relevant if the patient has a history
of other illnesses.
d. presages respiratory failure.

Class Of Evidence Definitions
Each action in the clinical pathways section of Emergency
Medicine Practice receives an alpha-numerical score based on
the following definitions.
Class I
• Always acceptable, safe
• Definitely useful
• Proven in both efficacy
and effectiveness
• Must be used in the
intended manner for
proper clinical indications
Level of Evidence:
• One or more large
prospective studies
are present (with
rare exceptions)
• Study results consistently
positive and compelling
Class IIa
• Safe, acceptable
• Clinically useful
• Considered treatments
of choice
Level of Evidence:
• Generally higher levels
of evidence
• Results are consistently
positive
Class IIb
• Safe, acceptable
• Clinically useful
• Considered optional or
alternative treatments
Level of Evidence:
• Generally lower or
intermediate levels
of evidence
• Generally, but not
consistently, positive results

Class III:
• Unacceptable
• Not useful clinically
• May be harmful
Level of Evidence:
• No positive high-level data
• Some studies suggest or
confirm harm
Indeterminate
• Continuing area of research
• No recommendations until
further research
Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent,
contradictory
• Results not compelling
Adapted from: The Emergency
Cardiovascular Care Committees
of the American Heart Association
and representatives from the
resuscitation councils of ILCOR:
How to Develop Evidence-Based
Guidelines for Emergency Cardiac
Care: Quality of Evidence and
Classes of Recommendations; also:
Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring
effectiveness of community-wide
emergency cardiac care. JAMA
1992;268(16):2289-2295.

Publisher : Robert Williford. Vice Presiden t/General Manager : Connie Austin.
Executiv e Editor: Heidi Frost.

Direct all editorial or subscription-related questions to Pinnacle
Publishing, Inc.: 1-800-788-1900 or 770-992-9401
Fax: 770-993-4323
Pinnacle Publishing, Inc.
P.O. Box 769389
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E-mail: emer gmed@pinpub .com
Web Site: http://www .pinpub .com/emp
Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year)
by Pinnacle Publishing, Inc., 1000 Holcomb Woods Parkway, Building 200, Suite 280,
Roswell, GA 30076-2587. Opinions expressed are not necessarily those of this
publication. Mention of products or services does not constitute endorsement. This
publication is intended as a general guide and is intended to supplement, rather than
substitute, professional judgment. It covers a highly technical and complex subject and
should not be used for making specific medical decisions. The materials contained
herein are not intended to establish policy, procedure, or standard of care. Emergency
Medicine Practice is a trademark of Pinnacle Publishing, Inc. Copyright 2001 Pinnacle
Publishing, Inc. All rights reserved. No part of this publication may be reproduced in
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Emergency Medicine Practice is not affiliated
with any pharmaceutical firm
or medical device manufacturer.

Emergency Medicine Practice

28

February 2001