JANUARY 2021 | VOLUME 23 | ISSUE 1

Emergency Medicine Practice Evidence-Based Education • Practical Application

LEARNING OBJECTIVES:

• What are the key aspects of

ECG and patient history that
will help identify STEMI in the
prehospital and ED settings?
• What are common STEMI
mimics and how can you
differentiate them?
• What is the latest evidence on
the therapies for management
of STEMI in the ED?

Authors
Marshall Frank, DO, MPH, FACEP
Assistant Professor of Emergency Medicine,
Florida State University College of Medicine;
Medical Director, Sarasota County Fire
Department, Sarasota, FL

Carson Sanders, BS, NRP, CCEMT-P

Assistant Chief-EMS, Sarasota County Fire
Department, Sarasota, FL

Bryan P. Berry, MD, BCEM, FACEP Evaluation and Management

Associate Clinical Faculty of Emergency
Medicine, Florida State University College
of Medicine; Emergency Medicine Physician,
Sarasota Memorial Hospital, Sarasota, FL
Peer Reviewers
James Morris, MD, MPH
Program Director, Emergency Medicine
Residency, Texas Tech University Health Sciences
Center, Lubbock, TX
Douglas L. Robinson, DO, MS
Medical and Aeromedical Director, Military
Intelligence Battalion, 75th Ranger Regiment,
FBGA; Emergency Medicine Physician, Piedmont
Regional Medical Center, Columbus, GA
Andrew Schmidt, DO, MPH
Assistant Professor, Department of Emergency
Medicine, University of Florida-Jacksonville,
Jacksonville, FL
of ST-Segment Elevation
Myocardial Infarction in the
Emergency Department
n Abstract
ST-segment myocardial infarction (STEMI) is a time-sensitive
emergency that requires swift and seamless integration of
prehospital and emergency department resources in order to
achieve early diagnosis and reperfusion therapy. This issue reviews
the current literature on emergency department management
of STEMI, including recognition of more subtle diagnoses on
electrocardiogram, identification of STEMI mimics, an update
on treatment therapies, and strategies to achieve more effective
management of STEMI across gender and age groups.

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 Case Presentations
A 74-year-old woman with chest pain is delivered to your ED by EMS…
• You greet the paramedics, and they inform you that the patient called 911 from home because she was
having chest pain. They have given her 324 mg of aspirin orally and 3 doses of 0.4 mg of nitroglycerin
CASE 1

sublingually. The patient’s pain improved, but is still present.

• Her vital signs are normal. The paramedic hands you an ECG that he obtained and states that there is
anterior ST-segment depression concerning for ischemia, but no ST elevation.
• You look at the tracing and note ST depression in leads V2 and V3. You wonder whether this could actu-
ally be a STEMI, and what would be the best way to confirm your suspicion…

A 60-year-old man presents with retrosternal chest pain…

• The patient reports that he’s had pain for 2 days that has been constant and never goes away.
CASE 2

• He has no dyspnea, diaphoresis, or radiation of the pain. Additionally, there is no increase in the pain
with exertion.
• You obtain an ECG and note ST-segment elevation in the inferior and lateral leads.
• Given the patient’s history of present illness, you are not convinced that he has STEMI and wonder what
the best next step is…

A 32-year-old woman with chest pain presents…
• She was triaged as a low-acuity patient, given her age and the fact that she has no past medical prob-
lems.
CASE 3

• Your discussion with the patient reveals that she developed pain about 30 minutes prior. The pain was
associated with diaphoresis and vomiting, but those symptoms have resolved. Her pain has improved
but is still present.
• You obtain an ECG and note ST-segment depression and T-wave inversion in leads I and aVL.
• You wonder what would be the most appropriate next step for this young woman…

n Introduction Practice discusses the prehospital and ED diagnosis

Acute coronary syndromes (ACS) include unstable
angina, non–ST-segment elevation acute coronary
syndrome (NSTE-ACS), and ST-segment elevation
myocardial infarction (STEMI).1 Over 200,000
STEMIs present to emergency departments (EDs)
in the United States annually, and most recent
data indicate that the incidence of STEMI is 7.3
per 10,000 adult ED visits.2 The diagnosis and
management of STEMI in the prehospital setting
and the ED is a time-sensitive emergency. Failure
to recognize acute myocardial infarction (AMI) is
dangerous for the patient, as the risk-adjusted
mortality ratio for nonhospitalized patients is 1.9
compared to patients who were hospitalized.3 This
point is highlighted by the fact that many patients
with STEMI do not start seeking healthcare until 1.5
to 2 hours into the process.4 Even more concerning,
a large proportion of patients with STEMI—40% in
one observational study—do not initiate their care
by calling emergency medical services (EMS)5 even
though there is good evidence that arrival to the ED
by ambulance allows for earlier delivery of ultimate
reperfusion.5-7 This issue of Emergency Medicine
and treatment of STEMI, emphasizing the value
of serial ECGs, recognizing subtle STEMI patterns,
and focusing attention on special populations in an
effort to help eliminate gaps in patient care that may
contribute to poor outcomes.
n Critical Appraisal of the Literature
Ovid MEDLINE® and PubMed were searched for
articles relating to STEMI, from 2009 to December
2020. Initial search terms included STEMI + treat-
ment, STEMI + therapies, STEMI + special popula-
tions, and STEMI + disposition. The Cochrane Data-
base of Systematic Reviews from 2009 to December
2019 was also searched for STEMI + controversies.
Each search was performed through the Florida
State University library. Due to the large volume of
articles, a decision was made to focus on system-
atic reviews and evidence-based guidelines, with a
secondary review of their key references. The overall
quality of the literature driving recommendations for
STEMI is high, with a number of prospective studies
with clear outcome measures identified.

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n Etiology and Pathophysiology ture and a platelet-rich thrombus develop, leading to
ACS includes STEMI and NSTE-ACS. NSTE-ACS can decreased blood flow and ischemia. Figure 2 depicts
be further characterized into non–ST-segment eleva- coronary artery anatomy.
tion myocardial infarction (NSTEMI) and unstable an- Within minutes of the onset of infarction, there
gina. Although this review focuses on STEMI, it is im- will be alterations in the electrical potential of the car-
portant to note that NSTE-ACS accounts for over 70% diac myocytes, which can be seen on electrocardio-
of all ACS diagnoses.8 The most common underlying gram (ECG) as ST-segment elevation.11 The location
pathology that leads to STEMI is the presence of an of the coronary occlusion will produce ST-segment
atherosclerotic plaque within the coronary artery.9 elevation on the ECG in a predictable pattern cor-
This is described as type 1 myocardial infarction (MI) responding to the affected artery and the anatomical
and is illustrated in Figure 1. Plaques that have been location of injury. (See Figure 3.) For example, oc-
demonstrated to be more prone to causing ACS have clusion of the right coronary artery (RCA) will produce
a thin fibrous cap, a large lipid pool, and are vulner- a predictable ST-segment elevation pattern in leads
able to disruption.9 Disruption of the plaque leads to II, III, and aVF, the inferior part of the heart. Early
exposure to circulating platelets, platelet adhesion,
activation, and aggregation.10 In ACS, plaque rup-
Figure 2. Coronary Artery Anatomy
Figure 1. Type 1 Myocardial Infarction Pulmonary
artery
Aorta
Left coronary
artery
Superior
vena cava Circumflex
branch
Right
atrium
Plaque rupture/erosion To left
Right ventricle
with occlusive thrombus ventricle
Right Anterior
coronary interventricular
artery
artery
Left
Inferior ventricle
Plaque rupture/erosion with vena cava
nonocclusive thrombus Posterior
Marginal
interventricular
branch
artery

Republished with permission of Elsevier Science & Technology Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM.
Journals, from Fourth Universal Definition of Myocardial Infarction Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e;
(2018). Thygesen K, Alpert JS, Jaffe AS, et al. Volume 40, Issue 3, 2019. 2019. www.accessemergencymedicine.com Copyright © The McGraw-
Permission conveyed through Copyright Clearance Center, Inc. Hill Companies, Inc. Used with permission.

Figure 3. Predicted Distribution of ST-Segment Elevation Relative to Occluded Artery

Abbreviations: Cx, circumflex branch of left coronary artery; LAD, left anterior descending artery; RCA, right coronary artery.
Image courtesy of Marshall Frank, DO, MPH
www.ebmedicine.net

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changes can be seen prior to the development of ST- EMS dispatch can coach the patient in self-adminis-
segment elevation. An example of this can be seen in tration of aspirin prior to arrival of EMS personnel.13
lead aVL. ST-segment depression or T-wave inversion However, EMS dispatchers have been noted to over-
in that lead may represent early reciprocal changes of triage, which could lead to assignment of resources to
an inferior wall MI.12 incidents not requiring advanced level of care, leaving
portions of a community without resources. In a 2006
retrospective study that analyzed 104 cardiac-related
n Differential Diagnosis emergency calls in a single suburban community’s EMS
The differential diagnosis of ST-segment elevation on system, the positive predictive value of the dispatch
the ECG ranges from benign causes such as normal protocol correctly identifying a cardiac emergency was
variants or early repolarization, to potentially life- 28.6%.14
threatening causes such as acute coronary occlusion. Once EMS personnel arrive, patients with pos-
(See Table 1.) The emergency clinician should be sible ACS should have an ECG within 10 minutes.
able to differentiate the various causes based on Prehospital identification of STEMI allows for early
symptomatology and ECG patterns. catheterization laboratory activation and can reduce
first medical contact-to-balloon time. Paramedics are
able to identify STEMI with a sensitivity ranging from
n Prehospital Care 71% to 97% and specificity from 91% to 100%. For
The care and management of the patient with chest the patient with an ECG diagnostic of STEMI, the
pain begins when the prehospital system is activated. goal is transport to a facility capable of performing
In many systems, specially trained emergency medical emergent cardiac catheterization.
services (EMS) dispatchers will ascertain the patient’s Transport modality varies based on the EMS sys-
location and send advanced life support-capable tem. Some systems may have multiple percutaneous
resources to aid in identifying potential ACS patients coronary intervention (PCI)-capable facilities within a
and initiate treatment. Using a standardized protocol, short transport time, while others may require heli-
copter EMS transport to get to an appropriate facility
in a timely manner. Some EMS systems that are not
Table 1. Differential Diagnosis of able to get a patient to a PCI-capable facility within
ST-Segment Elevation 90 minutes may be permitted to use protocols for
administration of prehospital fibrinolytics in STEMI.
Cause of ST-Segment Electrocardiogram and/or Clinical Pharmacologic treatment of STEMI patients
Elevation Finding
focuses on administration of aspirin. Although field
ST-segment elevation • Chest pain, dyspnea, diaphoresis, or interventions have advanced greatly, no medication
myocardial infarction other anginal complaints
used in the prehospital setting for STEMI rivals aspirin
• ST-segment elevation in anatomically
contiguous leads in efficacy, with a number needed to treat of 42.15
• Reciprocal electrocardiogram changes For the patient with normal blood pressure who is
Pericarditis • Pleuritic pain; may improve with sitting up in pain, nitroglycerin can be administered sublingually
or become worse when lying down in the prehospital setting at a dose of 0.4 mg every 5
• Diffuse ST-segment elevation with minutes until pain is relieved (max 3 doses). There is
concave morphology a theoretical concern for causing hypotension in the
• No ST-segment depression or reciprocal
changes
setting of STEMI with right ventricular involvement,
due to reduction in preload. Inferior STEMI may
Myocarditis • ST-segment changes may resemble
acute ischemia
involve the right coronary artery, and 33% to 50%
involve the right ventricle.4,16 Guidelines recommend
Electrolyte • Tall, symmetric, peaked T waves
derangement • May mimic acute ischemia that nitrates be avoided in this setting.4
(hyperkalemia) The goals of prehospital management of STEMI
Left bundle branch • Appropriate discordant ST-segment are early recognition, administration of aspirin, and
block pattern elevation typically seen in V1-V3 timely transport to a PCI-capable facility for reperfu-
Brugada syndrome • ST-segment elevation >2 mm in >1 of sion. As with all patients, hemodynamic abnormality,
V1-V3 leads followed by negative T wave hypoxia, dysrhythmias, and other potentially life-
(Type 1) threatening conditions will be addressed. The prac-
Hypothermia (Osborn • Positive deflection at J wave, commonly tice of bypassing non-PCI capable facilities to get
wave) in precordial leads the STEMI patient to a PCI-capable facility is safe,
• Typically seen when core temperature
and is recommended if the first medical contact-to-
<30°C
balloon time is <90 minutes and transport time is
Early repolarization • Asymptomatic, young age
• Notching at J point
<30 minutes.17

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n Emergency Department Evaluation
The diagnosis of STEMI is made by ECG, combined
with the patient’s history and physical examination
findings. The goal of emergency care for patients
suspected of having a STEMI is to obtain an ECG
within 10 minutes from first medical contact, regard-
less of whether this occurs in the prehospital setting
or in the ED.1
History
The classic presentation of STEMI is chest pain or
discomfort that is located on the left side, right side,
or retrosternally. The pain may radiate to the arm,
the back, or the jaw. As suggested by a prospective
review, historical factors that increase the likelihood
of ACS include radiation to the shoulder, radiation to
both arms, increased pain with exertion, and radiation
to the left arm.18 Other signs and symptoms include
(but are not limited to) diaphoresis, vomiting, weak-
ness, and dyspnea.19
Although the history will not make the diagnosis
of STEMI, it may give the emergency clinician reason
to suspect ACS in a patient who is not presenting
with chest pain. In a study involving over 20,000 pa-
tients with ACS, it was found that 8.4% did not have
chest pain. The most common non–chest pain signs
and symptoms were dyspnea, diaphoresis, nausea,
and syncope.20
Special attention should be paid to the patient
presenting with chest pain and diaphoresis. In a
2016 study of over 12,000 patients with ACS, these
features were found to have the highest likelihood
ratio and positive predictive value for STEMI.21 Also
deserving of mention is the presence of radiation
of chest pain. Although classic teaching describes
radiation to the left arm or the jaw, radiation of pain
to both arms has been shown to be 96% specific,
though only 11% sensitive.22 Noting previously
worrisome signs or symptoms in the patient who is
asymptomatic on arrival to the ED or who had an
ECG consistent with a STEMI in the field but has since
normalized will aid in identifying patients who may
benefit from early intervention.23 Likewise, the past
medical history in a patient with ST elevation on the
ECG will aid in determining causes of ST elevation
not due to ACS; for example, the end-stage renal
patient with hyperkalemia. (See Table 1, page 4.)
The history should include past medical history,
medications, medication compliance, and allergies.
Medications and treatment provided in the prehos-
pital field as well as information about the last meal
should also be obtained.
Physical Examination
In a stable patient with an ECG diagnostic of STEMI,
the physical examination will be rather limited. Vital
signs should be monitored, with close attention paid
to the heart rate and blood pressure. In acute MI
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treated with thrombolytic therapy, the incidence of
atrioventricular block is 7%, so the emergency clini-
cian should be prepared to manage bradycardia if it
occurs.24 Cardiogenic shock complicates 5% to 10%
of AMI cases.25 Measurement of blood pressure and
evaluation of other signs of systemic disease and
inadequate tissue perfusion (cool skin, altered mental
status, diaphoresis) will guide the identification of
cardiogenic shock.
n Diagnostic Studies
Imaging
A radiograph of the chest may be obtained to help
guide decision-making, but it must be used in the
correct clinical context (eg, to assess for pneumonia
or pneumothorax). In the setting of suspected aortic
dissection, chest x-ray is not a definitive study and has
a reported sensitivity for aortic dissection of 67%.26 If
there is a high clinical suspicion for aortic dissection,
a computed tomography angiogram (CTA) would be
indicated. However, this decision must be driven by
high clinical suspicion (eg, STEMI plus new neurologic
deficit), as it will delay reperfusion therapy.
For a patient in whom STEMI is suspected but not
entirely certain, an echocardiogram may be indicated.
Echocardiography is a noninvasive way to assess for
regional wall motion abnormalities (RWMA) or other
pathologic findings, and it can help confirm a diag-
nosis. It should be noted, however, that RWMA can
be seen in focal myocarditis, prior infarct, and cardio-
myopathies, in addition to acute ischemia. Echocar-
diography for AMI is highly sensitive but has a low
specificity. In a prospective study analyzing the utility
of echocardiography in 180 ED visits for acute chest
pain, RWMA was present in 93% of patients with AMI
and in 43% of patients without AMI.27
Laboratory Testing
In the setting of STEMI, laboratory testing is of limited
utility. Although high-sensitivity (hs) cardiac troponin
(cTn) assays measure cTn concentrations that are
5-fold to 100-fold lower than conventional assays and
can detect AMI early, it is our opinion that a patient
presenting with signs and symptoms of ACS and ST
elevation on ECG should be managed as a STEMI
regardless of the hs-cTn level.28 The measurement of
hemoglobin and hematocrit are also of limited utility.
Although the prevalence of anemia on admission in
the setting of ACS is between 10% and 43%, the find-
ing of ST elevation, even in confirmed severe anemia,
should not delay cardiac catheterization.29 Screening
for drugs of abuse is also not indicated in the setting
of STEMI, as this can delay definitive treatment un-
necessarily.
Finally, it is our opinion that the only laboratory
study that might have impact on disposition to the
cardiac catheterization laboratory is the serum potas-
5 © 2021 EB MEDICINE. ALL RIGHTS RESERVED.
sium level. As can be seen in Figure 4, hyperkalemia dial Infarction (2018), notes the following criteria as
can mimic STEMI. When there is high suspicion for being suggestive of AMI:1
hyperkalemia and there is access to rapid point-of-
care measurement of the serum potassium level, this New ST elevation at the J point in 2 contiguous leads,
should be considered prior to cardiac catheterization. with the cut-point of ≥1 mm in all leads other than leads
Nonetheless, serum potassium measurement should V2 and V3, where the following cut-points apply:
not delay cardiac catheterization laboratory activation. • ≥2 mm in men aged ≥40 years
• ≥2.5 mm in men aged <40 years
Electrocardiogram • ≥1.5 mm in women of any age
When interpreting the ECG for evaluation of
STEMI, the measurements and location of points In addition to these diagnostic criteria, the 2018
of measurements must be consistent. The J point definition of MI discusses the use of lead aVR, the
is the point where the QRS complex ends and the use of posterior leads, and the diagnostic findings in
ST segment begins.1 (Figure 5, arrow #2.) The J left bundle branch block (LBBB) pattern and paced
point is used to determine the magnitude of ST- rhythms.1
segment elevation, and is compared to an isoelec-
tric portion of the tracing. The measurement should
Figure 5. Identification of the J Point
be taken at the onset of the QRS complex.1 (Figure
5, arrow #1.) Although some clinicians advocate
for the TP segment (the isoelectric interval between
the end of the T wave and the onset of the P wave)
to be used as the isoelectric segment for compari-
son, it is specifically recommended in guidelines to
utilize the QRS onset as the reference point for J
point determination.1

The expert consensus of the European Society of
Cardiology (ESC), the American College of Cardiol-
Republished with permission of Elsevier Science & Technology
ogy Foundation (ACCF), American Heart Association Journals, from Fourth Universal Definition of Myocardial Infarction
(AHA), and World Heart Federation (WHF) Task Force, (2018). Thygesen K, Alpert JS, Jaffe AS, et al. Volume 40, Issue 3, 2019.
known as the Fourth Universal Definition of Myocar- Permission conveyed through Copyright Clearance Center, Inc.

Figure 4. Electrocardiogram of ST-Segment Elevation Caused by Hyperkalemia

Image courtesy of Marshall Frank, DO, MPH.

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Lead aVR
In a patient with hemodynamic abnormality or com-
promise, ST-segment elevation in aVR associated
with ≥1 mm of ST depression in multiple leads may
suggest left main coronary artery (LMCA) stenosis
or occlusion.4 (See Figure 6.) Other causes of this
ECG finding may include triple vessel disease, diffuse
subendocardial ischemia, and tachycardia-related
widespread (multiple leads) depression with recipro-
cal STE in aVR.
Nonetheless, ST elevation in aVR is not specific
for LMCA, and the patient’s clinical condition must be
taken into consideration.30 In a 2019 study, Harhash
et al found that only 10% of patients with ST depres-
sion in multiple leads and ST elevation in aVR had an
acute thrombotic coronary occlusion.31
Obtaining posterior leads (V7, V8, and V9) increas-
es the ability to detect posterior STEMI.36 Posterior
leads are acquired by moving standard leads V4, V5,
and V6 to the patient’s left-side back. Lead V7 should
be placed at the level of lead V6 at the posterior axil-
lary line, lead V8 at the tip of the scapula, and lead
V9 halfway between lead V8 and the left paraspinal
muscles. (See Figure 7.)
ST elevation of ≥0.5 mm in any posterior lead is
recommended as the cut-off point. An ST elevation of
≥1 mm has increased specificity and is recommended
as the cut-off point in men aged <40 years.1 Fig-
ure 8, page 8, shows an ECG with typical posterior
STEMI findings in lead V2.

Posterior Leads
Posterior STEMI (also called inferobasal STEMI) is
rare, occurring in approximately 3% of acute MIs.32 Figure 7. Posterior Lead Placement
Left circumflex artery occlusion should be considered Scapula
when evaluating a patient with concern for ACS and
an initial ECG that is considered nondiagnostic. There
is an underrepresentation of STEMI from circumflex
artery occlusion and an overrepresentation of NSTEMI
from circumflex artery occlusion, due to posterior
leads not being obtained.33 Pattern recognition in
these cases is key. Posterior STEMI will present as ST
depression in leads V1, V2, or V3 with an associated
positive T wave in the standard 12-lead ECG.1,34
According to ESC guidelines, these patients should
be managed as for STEMI.35 When an ECG appears
V7 V8 V9
to have anterior ischemia, posterior (inferobasal)
STEMI should be considered.

Figure 6. Electrocardiogram Showing ST-Segment Elevation in aVR With Widespread ST

Depressions in a Patient with a Left Main Coronary Artery Stenosis

This ECG demonstrates an example of a patient with 90%-95% stenosis of the distal left main coronary artery. Note the ST-segment elevation in aVR
and ST-segment depression in multiple leads.
Image courtesy of Marshall Frank, DO, MPH.
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Left Bundle Branch Block and Paced Rhythms
In the United States, it is estimated that each
year, 5000 to 10,000 patients with LBBB will have
a STEMI.37 In the setting of an LBBB pattern, ST
elevation of ≥1 mm that is concordant with the QRS
complex is an indicator of STEMI. In patients with
right ventricular paced rhythms, similar findings can
be used.1 According to the 2017 ESC guidelines,
patients who have symptoms that are consistent
with ongoing myocardial ischemia and LBBB should
be managed similarly to STEMI patients, regardless
of whether the LBBB is known to be present
previously.35
Three independent criteria that aid in the diagnosis
of STEMI in the presence of LBBB were published in
1996 by Sgarbossa et al.38 The original 3 criteria are:
(1) concordant ST elevation ≥1 mm in leads with a
positive QRS complex; (2) concordant ST depression
≥1 mm in leads V1-V3; and (3) excessive discordant
ST elevation ≥5 mm in leads with a negative QRS
complex. Although these criteria are mentioned in
the Fourth Universal Definition of MI,1 there are no
specific recommendations within the 2013 ACCF/AHA
guidelines4 for use in management decisions.
The use of the Sgarbossa criteria can reduce false
activation of the cardiac catheterization laboratory
because of its high specificity and positive predictive
value.39 In a meta-analysis involving over 1600
patients, a Sgarbossa score of ≥3 performed with a
specificity of 98% and sensitivity of 20%.40 Similarly,
in patients with a Sgarbossa score of ≥5, the criteria
performed with a 100% specificity and a 14%
sensitivity.37 Figure 9 shows the points assigned to
Figure 8. ECG of Posterior STEMI
V7
V8
V9
Electrocardiogram (ECG) shows a typical posterior STEMI finding in
lead V2. Posterior leads were obtained in the same tracing, showing ST
elevation consistent with posterior STEMI.
Image courtesy of Marshall Frank, DO, MPH.
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JANUARY 2021 • www.ebmedicine.net 8
each portion of the Sgarbossa criteria.
The criterion that lacks adequate specificity is
the one on the far right of the figure. This criterion
is ST elevation ≥5 mm discordant with the QRS
complex. This criterion alone gives 2 points. It has
been proposed that replacement of absolute ST
elevation ≥5 mm with a ratio of ST/S-wave amplitude
outperforms the third part of Sgarbossa criteria. Smith
et al used an ST/S ratio of <-0.25 as a replacement for
the absolute ST elevation of ≥5 mm. In other words,
if the discordant ST-segment deviation is >25% of the
amplitude of the QRS, ischemia should be suspected.
This revised rule was found to be significantly more
accurate than the third Sgarbossa criterion.41 Figure
10 demonstrates an example of how to calculate the
revised rule.
An online tool for the Sgarbossa criteria
is available at:
www.mdcalc.com/sgarbossas-criteria-mi-
left-bundle-branch-block
Figure 9. Sgarbossa Criteria
Reprinted from American Heart Journal. Volume 166, Issue 4. Qiangjun
Cai, Nilay Mehta, Elena B. Sgarbossa, et al. The left bundle-branch
block puzzle in the 2013 ST-elevation myocardial infarction guideline:
From falsely declaring emergency to denying reperfusion in a high-risk
population. Are the Sgarbossa Criteria ready for prime time? Pages
409-413. Copyright 2013 with permission from Elsevier.
Figure 10. Modified Sgarbossa Rule
Reprinted from Annals of Emergency Medicine. Stephen W. Smith,
Kenneth W. Dodd, Timothy D. Henry, et al. Diagnosis of ST-elevation
myocardial infarction in the presence of left bundle branch block with
the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Volume
60, Issue 6. Pages 766-776. Copyright 2012 with permission from
Elsevier.
©2021 EB MEDICINE
 Figure 11 is an ECG obtained from a patient
who presented with chest pressure and diaphoresis.
The patient was known to have LBBB. The ECG
demonstrates Sgarbossa criteria with concordant ST-
segment elevation in lead V5. This patient had been
prescribed dual antiplatelet therapy, but had stopped
taking clopidogrel and subsequently developed
stenosis of a previously placed coronary artery stent.
It is important to evaluate every ECG with LBBB
or ventricular pacing for Sgarbossa criteria. One
proposed method to simplify the Sgarbossa criteria
in real-time clinical practice is to start by looking at
each lead for concordance of the QRS complex and
the ST segment. Each lead should be discordant or
isoelectric. If there is concordance, stop and evaluate
for Sgarbossa criteria further. Is there concordant
ST-segment elevation in any lead? If yes, this meets
Sgarbossa criteria. Is there ST-segment concordant
ST-segment depression in leads V1-V3? If yes, this
meets criteria. Is there >5 mm of discordant ST-
segment elevation in any lead with a negative QRS?
Finally, is there ST/S ratio of <-0.25? If yes, strongly
suspect ACS in the appropriate clinical setting.
Serial Electrocardiograms
For a patient with suspected ACS, obtaining serial
ECGs is important if the initial ECG is nondiagnostic.
Dynamic ECG changes are seen in AMI, and the
Figure 11. ECG of Concordant ST-Segment Elevation in Left Bundle Branch Block
Electrocardiogram (ECG) of a patient with known left bundle branch block who presented with chest pressure and diaphoresis.
Image courtesy of Marshall Frank, DO, MPH.
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recording of serial ECGs with fixed electrode
positions, at 15- to 30-minute intervals for the first
1 to 2 hours, is recommended.1 A 2018 prehospital
study reported that 8% of all STEMIs were identified
only on repeat ECG.42
Reciprocal Changes
An important part of the ECG interpretation is looking
for reciprocal changes. Reciprocal changes can be
thought of as ST-segment depression that mirrors
the ST-segment elevation on an ECG with STEMI.
The mnemonic “PAILS” is commonly taught as a
way to recall where one should expect reciprocal
changes. (See Table 2.) When considering the PAILS
mnemonic, envision that lead aVL (a lateral lead) is
almost completely opposite that of lead III (an inferior
lead). Thus, one would expect reciprocal ST-segment
changes in that lead from an inferior STEMI. In fact,
in 1993, Birnbaum et al found that most patients with
inferior STEMI had reciprocal changes in aVL.43
Table 2. PAILS Mnemonic for Reciprocal
Changes
• Posterior STEMI → anterior reciprocal changes
• Anterior STEMI → inferior reciprocal changes
• Inferior STEMI → lateral reciprocal changes
• Lateral STEMI → septal or inferior reciprocal changes
• Septal STEMI → posterior reciprocal changes
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9 © 2021 EB MEDICINE. ALL RIGHTS RESERVED.
 An ECG with ST-segment elevation and reciprocal
changes can help diagnose STEMI. For example, the
presence of reciprocal changes helps to differentiate
true STEMI from STEMI mimics such as pericarditis.
(See the “Pericarditis” section following). In addition to
aiding in the diagnosis of STEMI versus other causes
of ST-segment elevation, reciprocal changes can aid
in prognostication. Reciprocal change in STEMI has
also been shown to indicate a significantly larger
myocardial area at risk and may identify patients with
greater potential for salvage with revascularization.44
Differentiating Pericarditis From STEMI
The ECG of a patient presenting with acute pericar-
ditis may demonstrate diffuse ST-segment elevation
and PR-segment depression that must be differenti-
ated from STEMI in the clinical setting. The ECG may
evolve through 4 phases.45,46 Phase I demonstrates
diffuse ST-segment elevation and PR-segment de-
pression. As this phase progresses, the ST and PR
segments normalize (phase II), followed by T-wave
inversion (phase III), and finally, normalization of the
T waves (phase IV).46 Phase I changes are observed
in >80% of patients with pericarditis and must be dif-
ferentiated from AMI.47
Table 3 lists features that may help differentiate
pericarditis from STEMI. The morphology of the ST
segment in STEMI is often dome-shaped (convex).
Conversely, the ST-segment elevation in pericarditis
is classically concave. In STEMI, there is regional ST-
segment elevation following an arterial distribution,
while in pericarditis, the ST-segment elevation is rath-
er diffuse.45,46 With the exception of lead aVR, there
should be no ST-segment depression or reciprocal
changes seen in pericarditis.45 (See the “Reciprocal
Changes” section, pages 9-10) Evaluation of leads II
and III may also aid in differentiation. Although it has
been suggested that ST-segment elevation in lead
II that is greater than the elevation in lead III is more
Table 3. Findings Differentiating
Pericarditis From STEMI
ECG or Clinical Finding STEMI Pericarditis
ST-segment elevation Convex (dome- Concave upward
morphology shaped)
Regional ST-segment Yes No, diffuse
elevation
Reciprocal changes Yes No
Pain changes with respiration No Yes
Pain changes with position No Yes, worse when
supine
Friction rub Unlikely Yes
Abbreviations: ECG, electrocardiogram; STEMI, ST-segment elevation
myocardial infarction.
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JANUARY 2021 • www.ebmedicine.net 10
likely to be pericarditis than STEMI, a 2012 retrospec-
tive study of 283 patients with a diagnosis of STEMI
or pericarditis showed that this rule does not have a
level of diagnostic accuracy that is reliable for clinical
decision-making.48
n Treatment
Initial Therapies
Oxygen
Oxygen is no longer recommended routinely for
nonhypoxic patients with a STEMI because it may
increase coronary vascular resistance.49 A 2018 meta-
analysis of 7700 patients with acute MI, half receiv-
ing oxygen supplementation and half not receiving
it, showed no benefit to oxygen-treated patients
in all-cause mortality, recurrent ischemia, recurrent
infarction, heart failure, or development of arrhyth-
mias.50 A 2017 Swedish randomized clinical trial of
6629 patients with suspected MI and oxygen satura-
tion of ≥90% found that routine use of supplemental
oxygen in these patients was not found to reduce
1-year all-cause mortality.51 In fact, some studies have
shown potential harm, with larger infarct size, recur-
rent infarction, and dysrhythmias.52 The 2013 ACCF/
AHA STEMI guidelines recommend oxygen therapy
for only patients who are hypoxemic, with oxygen
saturation <90%.4 If oxygen is indicated, it should be
administered at 2 to 4 L/min via nasal cannula. The
rate should be increased or changed to a face mask
as needed.44
Opioids
Morphine, used judiciously, was once considered
standard therapy for pain relief in ACS. By decreas-
ing both pain and anxiety, it was thought to reduce
myocyte metabolic demand and decrease tissue
injury in ischemia. However, the safety of morphine in
ACS has never been established. The 2005 retrospec-
tive nonrandomized CRUSADE trial of 17,000 patients
evaluated patients with NSTE-ACS who were given
morphine. Use of any morphine, alone or in combi-
nation with nitroglycerin, was associated with higher
mortality, even after risk adjustment.53 A 2015 retro-
spective cardiac magnetic resonance imaging (MRI)
study of PCI-reperfused STEMI patients who received
intravenous (IV) morphine showed larger infarct size
compared to those who did not receive IV morphine.
This was not, however, proven to be causative.54
In addition, there is now pharmacokinetic evidence
that the use of opioids delays the absorption of P2Y12
inhibitors that are commonly given for ACS. A pair
of small trials assessing ticagrelor and clopidogrel
showed decreased platelet inhibition when IV
morphine was also given.55,56 In light of both the
benefits and potential harms, the 2017 ACEP Clinical
Policy recommends that clinical judgment be used in
deciding whether to give STEMI patients morphine
©2021 EB MEDICINE
for pain control while awaiting PCI.57 Nonetheless, the
2013 ACCF/AHA guidelines consider morphine to be
the drug of choice for pain relief for STEMI patients.4
Treatment modalities aimed at resolution of myocardial
ischemia (eg, aspirin, nitroglycerin) should be initiated
prior to considering use of IV morphine. If clinical
judgment dictates that morphine be given (ie, the
patient’s pain is refractory to nitroglycerin), morphine
should be administered 4 to 8 mg IV initially, with
lower doses for elderly patients.44
Antiplatelet Therapy
Aspirin
Aspirin has the greatest benefit for reduction of
morbidity and mortality when it is administered early in
STEMI. The most effective dose of aspirin has not been
prospectively established with PCI, but it is generally
accepted that the loading dose of non–enteric-
coated aspirin be chewed, and that it will take effect
within 60 minutes. The 2013 ACCF/AHA guidelines
recommend aspirin 162 mg to 325 mg orally before
PCI.4 There is theoretical concern for greater bleeding
side effects with higher-dose regimens of aspirin. The
2015 TRANSLATE-ACS paper studied 10,200 patients
with MI who had undergone PCI and were prescribed
dual-antiplatelet therapy, with oral aspirin doses of
325 mg (high dose) or 81 mg (low dose). The use of
high-dose aspirin was associated with rates of major
adverse cardiovascular events similar to low-dose
aspirin and, predictably, came with more risk for minor
bleeding events; however, bleeding events requiring
hospitalization were similar in both groups.58 Based on
consensus, an 81-mg oral aspirin maintenance dose is
recommended over higher doses.
P2Y12 Inhibitors
The P2Y12 inhibitors—including clopidogrel, pra-
sugrel, and ticagrelor—bind adenosine phosphate
platelet receptors to inhibit platelet activation and ag-
gregation. The selection of medication is based upon
the use of fibrinolysis versus PCI. A loading dose of
one of these P2Y12 inhibitors is recommended by the
2013 ACCF/AHA guidelines before or at the time of
PCI.4 However, specific drug selection is based upon
multiple patient-specific factors.
It is known that the level of platelet inhibition by
clopidogrel can vary by patient weight, presence of
diabetes, hepatic metabolism, and concurrent use
of proton-pump inhibitors. However, none of these
factors have shown detrimental effects in patients
treated with clopidogrel.4
Prasugrel inhibits platelet aggregation more ef-
fectively than clopidogrel, but its use comes with a
higher bleeding risk in STEMI. Prasugrel is contraindi-
cated in patients with a history of stroke or transient
ischemic attack and did not show benefit in patients
older than 75 years.59 A 2018 trial of 89,000 patients
in the United Kingdom undergoing PCI for STEMI
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who were given prasugrel showed an overall lower
30-day and 1-year mortality than patients receiving
either clopidogrel or ticagrelor.60
Ticagrelor was compared to clopidogrel in a
study of 18,000 patients with ACS, about one-third of
whom had STEMI. Patients receiving ticagrelor and
PCI had fewer stent thromboses and a lower total
death rate than those given clopidogrel, but this was
balanced against an increase in stroke and intracranial
hemorrhage.61,62
In summary, the use of all 3 of these P2Y12 inhibitors
are class I, level of evidence B recommendations.44 Data
suggest that there is an increased risk for bleeding with
prasugrel and ticagrelor compared to clopidogrel.63 The
decision regarding which P2Y12 inhibitor to use must
be based on patient history, weight, age, allergies,
drug interactions, cost, and dosing. European
Society of Cardiology guidelines state that P2Y12
inhibitors should be given as soon as possible or at
the time of PCI.35 Based on this, it is advisable to
have established institutional protocols and to discuss
therapy with the treating interventional cardiologist.
The oral loading dose for clopidogrel is 600 mg;
prasugrel is 60 mg; and ticagrelor is 180 mg.
Nitroglycerin
Nitroglycerin reduces left ventricular preload and
increases coronary artery blood flow; however, there
is no evidence that its use actually reduces myocardial
injury in STEMI. The 2013 ACCF/AHA guidelines do
note that nitroglycerin may be beneficial in patients
with STEMI and hypertension or STEMI and heart
failure and should be considered in these instances.4
Nitroglycerin is commonly given as 0.4 mg sublingual
doses because it can be given rapidly without IV
access. However, the absorption is variable, and it
can be difficult to titrate effects, even with customary
subsequent additional doses at 5-minute intervals.
An IV infusion of nitroglycerin may be started at 10
mcg/min and titrated up every 3 to 5 minutes to
symptomatic improvement.44,62,64
Beta Blockers
Beta blockers reduce myocardial oxygen demand by
decreasing heart rate, inotropy, and blood pressure.
The 2013 ACCF/AHA STEMI guidelines recommend
beta blockers for all patients with STEMI within the
first 24 hours of treatment, barring contraindications,
and regardless of PCI, fibrinolysis, or neither.4 Beta
blockers do not necessarily need to be started in
the ED. The initial studies on beta blockers were
conducted in the 1980s, prior to routine use of
reperfusion therapies, statins, and P2Y12 inhibitors,
but a 1985 meta-analysis showed a 25% reduction
in mortality at 1 year across several beta blocker
types.65 Since the proliferation of rapid primary PCI,
observational studies have shown a decreased benefit
to beta blocker usage. A meta-analysis including
11 © 2021 EB MEDICINE. ALL RIGHTS RESERVED.
40,873 STEMI patients and a cohort study of registry
data including 91,895 STEMI patients did not show
mortality differences between patients undergoing
PCI who did and did not receive beta blockers after
PCI for AMI.66,67
Reperfusion Therapies
Restoration of blood flow through an occluded
coronary artery is the mainstay of STEMI therapy.
Fibrinolysis and PCI are the 2 rapid treatment options
for STEMI treatment that are readily available to
patients after ED arrival. While PCI is preferred
over fibrinolysis, not all hospitals are capable of
performing this on-site or have a catheterization lab
available and equipped 24 hours a day.
Percutaneous Coronary Intervention
When PCI is readily available, the 2013 ACCF/
AHA guidelines recommend that primary PCI be
performed in STEMI patients with symptoms <12
hours in duration. Between 12 and 24 hours, PCI
is reasonable if there is clinical or ECG evidence
of ongoing ischemia. PCI is further recommended
for patients with cardiogenic shock or severe acute
heart failure, regardless of time of STEMI onset.4
Primary PCI has higher rates of infarct artery patency
and lower rates of recurrent ischemia, reinfarction,
intracranial hemorrhage, and death, compared to
lytics.64 Potential complications of PCI include artery
access site problems, contrast reactions, reperfusion
events, and other technical issues.
Thrombolytics
Although randomized clinical trials have shown that
primary PCI is superior to fibrinolysis in reducing
mortality, reinfarction, and stroke, it may not be avail-
able as an immediate reperfusion option. Fibrinolysis
must be considered when patients present to a center
without a PCI program, in places that do not have
24-hour catheterization laboratory coverage, or when
other delays to getting a patient to a catheterization
laboratory exist. There is a time-dependent reduction
in morbidity and mortality in patients with STEMI who
receive fibrinolytic therapy within 12 hours of symp-
tom onset.44 Although the benefit of fibrinolysis >12
hours after symptom onset has not been established,
fibrinolysis should be considered in a symptomatic
patient presenting with hemodynamic instability or a
large amount of myocardium at risk.44 For example, in
a patient presenting with persistent symptoms over 12
hours and cardiogenic shock, the emergency clinician
may determine that fibrinolytic therapy is indicated.
There are 4 fibrinolytic agents currently available:
tenecteplase, reteplase, alteplase, and streptokinase.
The first 3 are fibrin-specific; streptokinase is not.
Because of a significant reduction in mortality when
treating with a fibrin-specific fibrinolytic agent (ie,
accelerated tissue plasminogen activator [tPA])
JANUARY 2021 • www.ebmedicine.net 12
versus a non–fibrin-specific agent (streptokinase),
a fibrin-specific agent is preferred.44,67,68 Table 4
lists the available fibrinolytic agents along with their
dosages and patency rates. It should be noted that
streptokinase is no longer available in the United
States. Additionally, because it is highly antigenic,
streptokinase is absolutely contraindicated within 6
months of previous exposure, due to a potential for
serious allergic reaction.44
The 2013 ACCF/AHA guidelines recommend fi-
brinolytics for STEMI patients with ischemic symptom
onset within the prior 12 hours and when PCI is not
available within 120 minutes of first medical contact.
Fibrinolysis should also be considered between 12
and 24 hours in STEMI patients with ongoing signs
of ischemia.4 Any ED with the potential to receive
STEMI patients should have a streamlined protocol
for the administration of fibrinolytics that includes an
evaluation for these contraindications. Even a well-
equipped, 24-hour PCI center could have unforeseen
delays to catheterization laboratory transfer.
Patients aged >75 years are at increased risk for
intracranial hemorrhage, and there is some evidence
that half-dose fibrinolytic with tenecteplase reduces
the incidence.69 The 2017 ACEP Clinical Policy rec-
ommends reduced-dose fibrinolysis for any patient
aged >75 years, and it further recommends consid-
eration of fibrinolysis in any situation where door-
to-device time is anticipated to be longer than 120
minutes.57 Any decision for fibrinolysis will include
consideration of relative contraindications, age, time
to PCI, and patient comorbidities.
Table 4. Agents for Fibrinolysis44,68
Agent Dosage Patency Ratea
Tenecteplase Weight: 85%
(TNK-tPA) • <60 kg: 30 mg IV bolus
• 60-69 kg: 35 mg IV bolus
• 70-79 kg: 40 mg IV bolus
• 80-89 kg: 45 mg IV bolus
• ≥90 kg: 50 mg IV bolus
Reteplase (rPA) • 2 IV boluses of 10 units given 84%
30 min apart
Alteplase (tPA) Weight ≤67 kg: 73%-84%
• First: 15 mg IV bolus
• Second: 0.75 mg/kg IV over
30 min (max 50 mg)
• Third: 0.5 mg/kg IV over 60
min (max 35 mg)
Weight >67 kg:
• First: 15 mg IV bolus
• Second: 50 mg IV over 30 min
• Third: 35 mg IV over 60 min
Streptokinaseb • 1.5 million units IV over 60 min 60%-68%
a
90-minute time to myocardial infarction (TIMI) risk score 2 or 3 flow.
b
Not available in the United States.
Abbreviation: IV, intravenous.
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©2021 EB MEDICINE
Reperfusion Dysrhythmias
The most common reperfusion dysrhythmias are
premature ventricular contractions, sustained or
nonsustained ventricular tachycardia, accelerated
idioventricular rhythm (AIVR), atrial fibrillation, and
ventricular fibrillation.70 Special attention should be
paid to AIVR. This dysrhythmia is usually seen during
AMI reperfusion (following PCI or thrombolysis).71
(See Figure 12.) AIVR has an appearance similar to
ventricular escape, but the rate is faster, >50 beats/
min (versus 20 to 40 beats/min for ventricular es-
cape). AIVR is generally well-tolerated and self-lim-
ited, typically resolving when the sinus rate exceeds
the ventricular focus.71 Management of AIVR with an
antidysrhythmic may cause a hemodynamic collapse
and should be avoided.71
Heparin and Anticoagulation Therapy
For STEMI patients with planned primary PCI, unfrac-
tionated heparin is recommended by the 2013 ACCF/
AHA guidelines: 70 to 100 units/kg IV bolus without
GP IIb/IIIa receptor antagonist, or 50 to 70 units/kg IV
bolus if given with a GP IIb/IIIa receptor antagonist.
Additional boluses are recommended as needed to
maintain therapeutic activated clotting time levels.
Bivalirudin, given prior to PCI as a 0.75 mg/kg IV
bolus followed by an infusion at 1.75 mg/kg/hr is
additionally recommended, with or without prior un-
fractionated heparin. In patients who are at high risk
for bleeding, the ACCF/AHA guidelines recommend
bivalirudin, without heparin.
STEMI patients who primarily receive fibrinolytic
therapy should receive anticoagulant therapy for a
minimum of 48 hours. Unfractionated heparin as a
weight-based bolus and a subsequent infusion is
recommended by the 2013 ACCF/AHA guidelines.
Figure 12. Electrocardiogram of Accelerated Idioventricular Rhythm
Electrocardiogram of a 42-year-old man 30 minutes after receiving fibrinolytics for an acute myocardial infarction.
Republished with permission of John Wiley & Sons - Books. ECGs for the Emergency Physician 2. Amal Mattu, William Brady. © 2008. Permission
conveyed through Copyright Clearance Center, Inc.
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Acceptable alternative agents include enoxaparin and
fondaparinux. (See Table 5.)
Transfer of STEMI Patients to a PCI Center
The 2017 ACEP Clinical Policy recommends transfer
of STEMI patients to a PCI center as soon as possible
to reduce major adverse cardiac events. The primary
focus is on developing streamlined systems to trans-
fer STEMI patients directly to a PCI-capable facility.
For STEMI patients presenting to a non-PCI center,
transfer to a PCI center is recommended if door-to-
device time can be achieved in 120 minutes or less.57
If not, fibrinolysis should be considered. Transfer to a
PCI-capable center is recommended once fibrinolysis
is initiated.72 Angiography can then be performed at
the receiving hospital as soon as feasible; preferably
within 24 hours, but not within the first 2 to 3 hours
Table 5. Anticoagulation Therapy for
STEMI Patients Receiving Fibrinolytic
Therapy44
Medication Dose
Unfractionated • Bolus: 60 units/kg IV (max 4000 units)
heparin • Infusion: 12 units/kg/hr (max 1000
units/hr)
Enoxaparin • Age <75 years: 30 mg IV bolus followed
in 15 min by 1 mg/kg subcut every 12 hr
• Age ≥75 years: no IV bolus;
0.75 mg/kg subcut every 12 hr
(max 75 mg for first 2 doses)
Fondaparinux* • 2.5 mg IV followed the next day by
2.5 mg subcut daily
*Contraindicated if creatinine clearance <30 mL/min.
Abbreviation: IV, intravenous; STEMI, ST-segment elevation myocardial
infarction; subcut, subcutaneous.
13 © 2021 EB MEDICINE. ALL RIGHTS RESERVED.
after fibrinolytics were given.4 Additionally, the 2013
ACCF/AHA guidelines recommend that any STEMI
patient with acute severe heart failure or cardiogenic
shock be transferred immediately to a PCI-capable
center, regardless of time from MI onset.4
n Special Circumstances and Populations
Gender Differences
The approach to the male and female STEMI patient
should be similar. However, women are less likely to
have central chest pain. This is considered to be a con-
tributing factor in the observation that cardiovascular
disease mortality has remained higher in women than
in men since the 1980s.73 Risk factors for acute MI in
women are similar to those for men and include smok-
ing, hypertension, dyslipidemia, diabetes, and obe-
sity.74 Having institution-specific standardized STEMI
treatment protocols may help eliminate these dispari-
ties. A retrospective review of one of these protocols
found there was no difference in pretreatment medi-
Risk Management Pitfalls for Patients in the
Emergency Department With STEMI
1. “The patient with chest pain was young, so
I didn’t get an ECG.” Typically, youth equates
to better health. However, even young patients
can have risk factors for, and subsequent
development of, coronary artery disease. Many
patient populations have poor access to care
for common diseases such as hypertension and
diabetes, and they may be discovered upon
their first presentation for STEMI or ACS. Other
young patients may have undiscovered genetic
predispositions to coronary disease, such as
familial hypercholesterolemia.
2. “The patient had nausea and diaphoresis, but
he didn’t have chest pain, so I didn’t get an
ECG.” While classic presentations of STEMI with
chest pain and diaphoresis and/or shortness
of breath and nausea usually trigger at least a
screening ECG, many patients will present with
only one or a few of these symptoms. An ECG
is a painless, noninvasive, and low-cost test. It
should be ordered liberally.
3. “The patient had shortness of breath and
cough without chest pain, so an ECG was not
obtained in triage.” Most EMS and emergency
centers have protocols and triage systems in
place to obtain an ECG liberally and early in
patient care. If not, these should be instituted and
adherence assured. In most systems, an ECG will
JANUARY 2021 • www.ebmedicine.net 14
cations, but it still found women to be less likely to
receive statin and antiplatelet therapy at discharge.74
In this decade, reduction in gender-disparate mortality
has occurred for the first time, and has been attributed
to an increased awareness of cardiovascular disease in
women and adherence to evidence-based treatment
for cardiovascular disease.73
Elderly Patients
Elderly patients make up a large proportion of ACS
patients, and they present more often with symp-
toms other than chest pain. Common symptoms in
elderly patients with ACS include dyspnea, diapho-
resis, nausea and vomiting, and syncope.75 STEMI
recognition by ECG can be complicated in elderly
patients, as there is a higher likelihood of left ven-
tricular hypertrophy, prior MI, conduction abnor-
malities, and underlying rhythm abnormalities such
as atrial fibrillation.76 Also, elderly patients more
often have relative and absolute contraindications
to reperfusion therapy. Even though reperfusion el-
be delayed with very atypical ACS presentations.
It is best to have broad indications for obtaining
an ECG.
4. “I saw LBBB on ECG, but didn’t think I could
identify STEMI in these patients.” Most
emergency medical providers with basic ECG
interpretation training—EMTs, paramedics,
advanced practice providers, and physicians—
will recognize typical ST elevation in typical
distributions. Subtle ST elevation can be
missed, as can ST elevation with complicating
blocks or rhythms, such as right bundle branch
block, LBBB, fast atrial fibrillation, or even sinus
tachycardia. If a presentation is concerning,
multiple clinicians should review the 12-lead ECG.
Using the Sgarbossa criteria will aid in STEMI
diagnosis in these patients.
5. “The EMS system in my community does
not activate the catheterization lab from
the field.” It is clear that earlier catheterization
laboratory activation allows for earlier definitive
intervention. Yet, barriers still exist to in-field
catheterization laboratory activation. EMS
systems need to have competent and consistent
training in STEMI recognition, and they need a
system to transmit ECGs to receiving hospitals.
Local EMS systems need to be integrated into the
cardiac care system of each of their destination
©2021 EB MEDICINE
igibility declines with age, elderly patients who are
reperfusion candidates are less likely to ultimately
receive treatment.77 One study found that age >75
years was a characteristic of those less likely to re-
ceive reperfusion.78 Various explanations have been
offered for this age-correlated under-treatment, but
it most likely relates to less-typical STEMI presenta-
tion, more complex comorbidities, and more fac-
tors involved in the decision for reperfusion, such
as baseline functionality and independence.
PCI and fibrinolysis in the elderly should be ap-
proached in a manner similar to the general popula-
tion. Age itself should not be a reason to withhold
reperfusion therapy, but comorbidities, quality of
life, and personal preferences in goals of care may
be more important in the decision-making process.75
Additionally, do-not-resuscitate orders, physicians’
orders for life-sustaining treatment, and advance
directives need to be taken into consideration with
reperfusion strategies; however, none of these neces-
sarily preclude intervention.
centers. Each receiving hospital, in turn, needs
to have protocols in place for rapid transfer of
the STEMI patient directly to their catheterization
laboratory.
6. “I didn’t get another ECG, since the first one
looked normal.” If a patient with coronary artery
occlusion is reached early enough, ECG findings
may be very subtle or not yet even present. ST
elevation could develop over the next minutes
or hours. If a presentation or initial ECG is
concerning, 12-lead ECGs should be repeated
every 10 to 30 minutes to observe for developing
ischemic changes, or until symptoms have
resolved or care is transferred.
7. “I identified STEMI on an ECG with LBBB,
but couldn’t get the cardiologist to take the
patient to the catheterization lab.” Protocols
should be in place for both EMS systems and
emergency care centers for rapid and consistent
care once ST elevation is identified. EMS systems,
emergency centers, and cardiac care teams will
be aware of the protocols of the other, and,
optimally, even integrated into a single system.
8. “I saw STEMI on the ECG, but did not
recognize that the patient had aortic
dissection.” STEMI is not the only etiology of ST
elevation on ECG, and training and experience
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Cocaine-Associated STEMI
Patients with cocaine-associated STEMI are gener-
ally managed similarly to other STEMI patients, with
an even stronger emphasis on PCI. Cocaine causes
systemic and coronary vascular changes and causes
alteration in platelet function and coagulation. There
are case reports involving acute coronary artery
thrombosis after cocaine use.79 Case reports show
higher rates of intracranial hemorrhage, making PCI
preferred over fibrinolysis.80 Therapy recommenda-
tions come from only observational studies, case
series, and animal studies. The 2008 AHA scientific
statement on the management of cocaine-associated
chest pain and MI has been used to direct care.80
Benzodiazepines can be used initially to relieve chest
pain and provide a level of sedation to decrease
heart rate and blood pressure. Beta blockers are not
recommended in the acute setting after cocaine use
because of theoretical coronary vasoconstriction due
to unopposed alpha-receptor stimulation. The data
available, however, are inconsistent, with some stud-
are necessary to identify other causes. Evaluation
should continue until a definitive diagnosis and
treatment plan is confidently reached.
9. “I identified STEMI, but a serum troponin
resulted negative before the patient went
to the catheterization lab. Based on the
troponin, I canceled the catheterization
lab activation.” STEMI is an ECG diagnosis.
Definitive care is dependent upon this and the
patient presentation. While biomarkers may be
useful in confirmation of diagnosis later on and
tracking patient response to treatment, waiting
for them to return or turn positive would delay
intervention.
10. “The patient had cardiogenic shock, but I did
not use vasopressors because I was afraid of
worsening the ischemia.” Goals for treating the
most critical STEMI patients include definitive
revascularization and maximizing coronary
perfusion until this can be achieved. Fluids and
vasopressors should be used to get the patient to
definitive care. Management of cardiogenic shock
should be initiated in the field, continued and
escalated as needed by the emergency center
team, and refined pre- and post-intervention by
the cardiac care team.
15 © 2021 EB MEDICINE. ALL RIGHTS RESERVED.
ies showing improvement and some showing worsen-
ing of coronary hemodynamics. If administration of a
beta blocker is indicated, consider labetalol, due to
its combined alpha- and beta-blocking effects.79
Out-of-Hospital Cardiac Arrest
Some 75% to 85% of STEMI patients who have been
resuscitated from ventricular fibrillation/pulseless
ventricular tachycardia in out-of-hospital cardiac arrest
have coronary artery disease, with 65% of these hav-
ing acute coronary lesions.81 Patients with sustained
return of spontaneous circulation and STEMI or new
LBBB on ECG have an even higher rate of coronary
artery disease, 70% to 90%, with acute coronary le-
sions in up to 80% cases.81 These acute lesions may,
of course, be amenable to PCI, and current guidelines
recommend early catheterization/reperfusion for
these postarrest patients. Early access to a cardiac
catheterization laboratory for these patients is as-
sociated with a 2-fold to 3-fold higher functionally
favorable survival rate over patients who did not have
access to a catheterization laboratory.
It is known that patients with refractory ventricular
fibrillation/pulseless ventricular tachycardia (defined as
>15 minutes of standard resuscitation or 3 unsuccessful
shocks) have a high prevalence of significant coronary
artery disease. These critical patients can benefit from
extracorporeal membrane oxygenation (ECMO) to
support perfusion and to temporize until PCI, and EMS
systems can consider transporting these patients di-
rectly to centers equipped with both capabilities. Early
use of PCI and ECMO have shown a 2-fold to 4-fold
increase in survival, albeit in observational studies.81
n Controversies and Cutting Edge
Managing STEMI During the COVID-19
Pandemic
The complexity of diagnosis and management of mul-
tiple pathologic processes, including STEMI, has been
increased during the SARS-CoV-2 (COVID-19) pandemic.
In a recent consensus statement from the Society for
Cardiovascular Angiography and Interventions, the
American College of Cardiology, and the American Col-
lege of Emergency Physicians, an emphasis was made
that primary PCI within 90 minutes of first medical contact
should remain the standard of care for STEMI patients
during the COVID-19 pandemic.82
COVID-19 patients have been shown to present
with STEMI mimics such as focal myocarditis or stress
cardiomyopathy. In certain circumstances, a more de-
tailed evaluation in the ED (eg, echocardiography to
assess for wall motion abnormality) may be indicated
prior to transfer to the cardiac catheterization labo-
ratory. As a result, during the COVID-19 pandemic,
there may be longer door-to-balloon times.82
JANUARY 2021 • www.ebmedicine.net 16
PCI for STEMI of 12- to 24-Hour Duration
Subacute ischemia may not be marked by chest pain
alone, but could be more subtle, with persistent atyp-
ical symptoms such as dyspnea or nausea. The 2013
ACCF/AHA guidelines recommend PCI in patients
with cardiogenic shock or evidence of severe acute
heart failure, regardless of time of onset of STEMI.4
PCI in these cases will have to be balanced against
the patient’s own stability to undergo PCI. Interven-
tional aggressiveness will vary depending upon a
center’s capabilities and experience, support services,
and even individual physicians’ ability to perform PCI
on critically ill patients.
Transfer of STEMI Patients to a PCI Center
STEMI patients with onset of ischemic symptoms
within the previous 12 hours are candidates for
transfer to a PCI center if the transfer can be accom-
plished within 2 hours.44 The emergency clinician will
need to take into account not just travel time, but
also dispatch and arrival of a transport service, patient
packaging for transport, and catheterization laborato-
ry readiness at the destination facility. The travel time
itself can change hour-by-hour, depending on road
traffic and weather conditions. One should strongly
consider the use of aeromedical transport to save
out-of-hospital time and facilitate reaching the goal of
120 minutes for primary PCI.
PCI for the Elderly and Patients with Severe
Comorbidities
While PCI and fibrinolysis in patients with advanced
age should be approached in a manner similar to the
general population, their comorbidities and goals
of care need to be considered before aggressive
procedures are undertaken. The goal of reperfusion is
not just to extend life, but also to improve the qual-
ity of life, with reduction in cardiac symptoms and
improvement in exercise tolerance and functional
status. When possible, patients and families should
be included in the decision-making process and this,
in turn, should be communicated clearly to consul-
tants and relayed in the chart. Similarly, patients with
severe comorbidities and near end-of-life conditions
should have their goals of care considered. No single
condition fully precludes intervention. These situa-
tions can be time-consuming for the emergency clini-
cian, but frank discussions need to be held with the
patient, family, and consultants.
n Disposition
All STEMI patients should be admitted after either
fibrinolysis or PCI. Recommendations are for all pa-
tients to ultimately be treated at a PCI center, either
primary or as a transfer. Admission to the hospital
allows for observation of reperfusion arrhythmias,
management of comorbidities, and optimization of
care after discharge.
©2021 EB MEDICINE
 Case Conclusions
The 74-year-old woman with chest pain who was delivered to your ED by EMS…
The thought of anterior ischemia in this patient made you concerned for the presence of posterior STEMI.
You noticed ST depression in leads V2 and V3, with a prominent R wave and upright T wave. Based on this,
CASE 1

you obtained posterior leads, V7, V8, and V9. The posterior tracing (V7, V8, V9) showed ST elevation of 1 mm
in leads V7 and V8. You promptly activated your cardiac catheterization lab and spoke with interventional
cardiology. The patient had been given aspirin in the field. You administered nitroglycerin and prepared the
patient for transfer to the catheterization lab. About an hour later, the interventional cardiologist called and
informed you that the patient had a 99% circumflex artery occlusion that required a stent. The patient was
now in the ICU and doing very well. You successfully diagnosed an isolated posterior (inferobasilar) STEMI.

The 60-year-old man who presented with retrosternal chest pain…

Based on this patient’s presentation, you were not convinced that he had ACS, despite ST elevation noted
on the ECG. You noted that there was no reciprocal ST depression found anywhere on the ECG tracing.
You also noted that all ST elevation was in a concave, upward pattern and was rather diffuse. You asked the
patient to lie supine, and he stated that the pain got worse. Based on the fact that the patient had con-
CASE 2

stant chest pain not associated with diaphoresis, vomiting, or radiation, along with your evaluation of the
ECG, you decided to not activate the cardiac catheterization lab. Instead, you discussed the case with the
interventional cardiologist, and said you were more concerned that the patient had pericarditis rather than
STEMI. The cardiologist agreed with your assessment. You recommended a formal echocardiogram be per-
formed in the ED, and she agreed. You obtained the study, which showed no wall motion abnormality, but
did show a moderate pericardial effusion, thus confirming your suspicion of pericarditis.

The 32-year-old woman who presented with chest pain…

You evaluated the ECG of this young patient with no past medical problems. The charge nurse stated
that the patient was “just anxious” and could wait in the waiting room to be evaluated for this chest pain.
However, you were concerned about her chest pain being associated with diaphoresis and vomiting. After
discussion with the patient, you determined that she had a family history of early MI, and that her pain
radiated to both arms. The ECG, although showing ST depression in leads I and aVL, was not diagnostic of
STEMI; however, based on your clinical concern, you asked for the patient to be placed in the critical care
room and have serial ECGs obtained every 10 minutes. Additionally, because of your concern for develop-
ing STEMI, you asked that defibrillator pads be placed. You administered 324 mg of aspirin orally and 0.4
CASE 3

mg of nitroglycerin subligually. The second ECG was obtained, and it showed >1 mm of ST elevation in
leads II and aVF. You activated the cardiac catheterization lab and discussed your findings with the inter-
ventional cardiologist. The cardiologist could not see the ECG in real-time and was reluctant to take her
for catheterization because of her age. After you described the ECG changes and the patient’s symptoms,
she agreed to take her. You went to reassure the patient and discuss the plan, but as you walked into the
room, she became unresponsive, and you noted ventricular fibrillation on the monitor. You quickly charged
the defibrillator and delivered a single shock. The patient was in VF for a matter of seconds, and regained
a pulse and consciousness after defibrillation. The patient was quickly taken to the cardiac catheterization
laboratory. A short time later, the cardiologist called to say she found a 100% occlusion of the RCA and was
able to place a stent, with excellent subsequent flow.

n Summary and location of measurement of the ST segment.

Early consideration and recognition of STEMI are
arguably the most important aspects of treatment. A
patient’s history, initial presentation, and initial ECG
interpretation will guide the treating team to rapid PCI
or fibrinolysis at the most appropriate treating center.
When diagnosing and treating patients with suspicion
for STEMI, the following points must be followed:
• Have a low threshold for obtaining an initial ECG
and serial ECGs; the initial ECG should be ob-
tained within 10 minutes of first medical contact.
• For diagnostic purposes, know the measurements
• Obtain supplemental leads (eg, posterior leads)
when the circumstances warrant.
• Consider STEMI mimics and manage, if present.
• Recognize STEMI in LBBB and paced rhythms,
and use the revised Sgarbossa criteria to evaluate.
• Be aware of the current evidence on initial medi-
cations and treatments of STEMI in the ED.
• Support streamlined EMS/ED protocols for PCI
referral, administration of fibrinolytics, timely
transfer if necessary, and management of patient
disposition.

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 Clinical Pathway for Management of STEMI
in the Emergency Department

Patient presents with signs or symptoms of Obtain 12-lead ECG within 10 minutes of patient contact
acute coronary syndromes (Class I, Level B)

YES ECG diagnostic of STEMI?

NO

• Perform history and physical examination

Evaluate for other forms of ACS or other causes of chest pain
• Treat/manage hemodynamic instability

• Obtain IV access, monitor hemodynamics, place defibrillator pads Obtain serial ECGs as clinically indicated (ie, persistent
on patient symptoms, return of symptoms, high pretest probability)
• Activate cardiac catheterization team or initiate transfer to PCI-
capable facility
• Start medical management:
l
Aspirin, 162-325 mg orally (Class I, Level B)
l
Nitroglycerin, 0.4 mg sublingually every 5 min x 3 doses
l
Heparin, 50-70 units/kg IV bolus (Class I, Level C)
l
P2Y12 inhibitor (as soon as possible or at time of PCI)
n
Clopidogrel, 600 mg orally (Class I, Level B) or
n
Prasugrel, 60 mg orally (Class I, Level B) or
n
Ticagrelor, 180 mg orally (Class I, Level B)

At PCI-capable facility? YES Perform primary PCI within 90 minutes of first medical contact
(Class I, Level B)
NO

If patient is transferred, can PCI be performed within 120 minutes? YES Transfer to a PCI-capable facility (Class I, Level B)

NO

Abbreviations: ACS, acute coronary syndromes; ECG, electrocardiogram;

Perform fibrinolysis within 30 minutes of arrival (Class I, Level B) IV, intravenous; PCI, percutaneous coronary intervention; STEMI, ST-
segment elevation myocardial infarction.

Class of Evidence Definitions

Each action in the clinical pathways section of Emergency Medicine Practice receives a score based on the following definitions.

Class I Class II
• Always acceptable, safe • Safe, acceptable Class III Indeterminate
• Definitely useful • Probably useful • May be acceptable • Continuing area of research
• Proven in both efficacy and effectiveness • Possibly useful • No recommendations until further
Level of Evidence: • Considered optional or alternative research
Level of Evidence: • Generally higher levels of evidence treatments
• One or more large prospective studies • Nonrandomized or retrospective stud- Level of Evidence:
are present (with rare exceptions) ies: historic, cohort, or case control Level of Evidence: • Evidence not available
• High-quality meta-analyses studies • Generally lower or intermediate levels • Higher studies in progress
• Study results consistently positive and • Less robust randomized controlled trials of evidence • Results inconsistent, contradictory
compelling • Results consistently positive • Case series, animal studies, • Results not compelling
consensus panels
• Occasionally positive results

This clinical pathway is intended to supplement, rather than substitute for, 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 © 2021 EB Medicine. www.ebmedicine.net. No part of this publication may be reproduced in any format without written consent of EB Medicine.

JANUARY 2021 • www.ebmedicine.net 18 ©2021 EB MEDICINE

n References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, random-
ized, and blinded trial should carry more weight than
a case report.
To help the reader judge the strength of each refer-
ence, pertinent information about the study, such as the
type of study and the number of patients in the study is
included in bold type following the references, where
available. The most informative references cited in this
paper, as determined by the authors, are noted by an
asterisk (*) next to the number of the reference.
1.* Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal defini-
tion of myocardial infarction (2018). Eur Heart J. 2019;40(3):237-
269. (Guideline) DOI: 10.1093/eurheartj/ehy462
2. Ward MJ, Kripalani S, Zhu Y, et al. Incidence of emergency
department visits for ST-elevation myocardial infarction in
a recent six-year period in the United States. Am J Cardiol.
2015;115(2):167-170. (Cross-sectional analysis of database;
1.5 million ED visits)
3. Pope JH, Aufderheide TP, Ruthazer R, et al. Missed diagnoses
of acute cardiac ischemia in the emergency department. N Engl
J Med. 2000;342(16):1163-1170.
4.* O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA
guideline for the management of ST-elevation myocardial
infarction: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice
Guidelines. Circulation. 2013;127(4):e362-e425. (Evidence-
based guideline) DOI: 10.1161/CIR.0b013e3182742c84
5. Mathews R, Peterson ED, Li S, et al. Use of emergency medical
service transport among patients with ST-segment–elevation
myocardial infarction. Circulation. 2011;124(2):154-163.
(Observational analysis; 37,634 patients)
6. Brown AL, Mann NC, Daya M, et al. Demographic, belief, and
situational factors influencing the decision to utilize emergency
medical services among chest pain patients. Circulation.
2000;102(2):173-178. (Retrospective study and survey; 875
and 962, respectively)
7. Canto JG, Zalenski RJ, Ornato JP, et al. Use of emergency
medical services in acute myocardial infarction and subsequent
quality of care. Circulation. 2002;106(24):3018-3023.
(Retrospective; 3805 patients)
8.* Anderson JL, Adams CD, Antman EM, et al. ACC/AHA 2007
guidelines for the management of patients with unstable
angina/non–ST-elevation myocardial infarction. Circulation.
2007;116(7). (Guideline)
DOI: 10.1161/CIRCULATIONAHA.107.181940
9. Chang H, Min JK, Rao SV, et al. Non-ST-segment elevation
acute coronary syndromes: targeted imaging to refine upstream
risk stratification. Circ Cardiovasc Imaging. 2012;5(4):536-546.
(Review)
10. Hollander J, Diercks D. Acute coronary syndrome: acute
myocardial infarction and unstable angina. In: Tintinalli J, ed.
Emergency Medicine: A Comprehensive Study Guide. 7th ed.
New York, NY: McGraw-Hill; 2011:369-385. (Textbook chapter)
11. Hudson K, McGrath N, Brady W. The electrocardiogram in the
evaluation and management of acute coronary syndrome. In:
Mattu A, ed. Cardiovascular Emergencies. Dallas, TX: American
College of Emergency Physicians; 2015:11-35. (Textbook)
12. Hassen GW, Talebi S, Fernaine G, et al. Lead aVL on
electrocardiogram: emerging as important lead in early
GROUP SUBSCRIPTIONS: groups@ebmedicine.net
diagnosis of myocardial infarction? Am J Emerg Med.
2014;32(7):785-788. (Review)
13. Barron T, Clawson J, Scott G, et al. Aspirin administration by
emergency medical dispatchers using a protocol-driven aspirin
diagnostic and instruction tool. Emerg Med J. 2012;30(7):572-
578. (Retrospective; 44,141 calls)
14. Reilly MJ. Accuracy of a priority medical dispatch system in
dispatching cardiac emergencies in a suburban community.
Prehosp Disaster Med. 2006;21(2):77-81. (Retrospective; 104
calls)
15. ISIS-2 (Second International Study of Infarct Survival)
Collaborative Group. Randomized trial of intravenous
streptokinase, oral aspirin, both, or neither among 17,187 cases
of suspected acute myocardial infarction: ISIS-2. J Am Coll
Cardiol. 1988;12(6):A3-A13. (Randomized, placebo-controlled;
17,187 patients)
16. Kinch JW, Ryan TJ. Right ventricular infarction. N Eng J Med.
1994;330(17):1211-1217. (Review)
17. Weisberg S, Tennyson J. Cardiovascular emergencies. In:
Cooney D, ed. Cooney’s EMS Medicine. 1st ed. New York, NY:
McGraw-Hill; 2016:264-271. (Textbook chapter)
18. Goodacre S, Locker T, Morris F, et al. How useful are clinical
features in the diagnosis of acute, undifferentiated chest pain?
Acad Emerg Med. 2002;9(3):203-208. (Prospective; 893
patients)
19. Panju AA, Hemmelgarn BR, Guyatt GH, et al. The rational
clinical examination. Is this patient having a myocardial
infarction? JAMA. 1998;280(14):1256-1263. (Review)
20. Brieger D, Eagle KA, Goodman SG, et al. Acute coronary
syndromes without chest pain, an underdiagnosed and
undertreated high-risk group. Chest. 2004;126(2):461-469.
(Prospective observational; 20,881 patients)
21. Gokhroo RK, Ranwa BL, Kishor K, et al. Sweating: a specific
predictor of ST-segment elevation myocardial infarction
among the symptoms of acute coronary syndrome: Sweating
In Myocardial Infarction (SWIMI) Study Group. Clin Cariol.
2016;39(2):90-95. (Prospective; 12,913 patients)
22. Fanaroff AC, Rymer JA, Goldstein SA, et al. Does this patient
with chest pain have acute coronary syndrome? JAMA.
2015;314(18):1955. (Review)
23. Meisel SR, Dagan Y, Blondheim DS, et al. Transient ST-elevation
myocardial infarction: clinical course with intense medical
therapy and early invasive approach, and comparison with
persistent ST-elevation myocardial infarction. Am Heart J.
2008;155(5):848-854. (Prospective; 69 patients)
24. Meine TJ, Al-Khatib SM, Alexander JH, et al. Incidence,
predictors, and outcomes of high-degree atrioventricular
block complicating acute myocardial infarction treated with
thrombolytic therapy. Am Heart J. 2005;149(4):670-674. (Meta-
analysis; 75,993 patients)
25. Vahdatpour C, Collins D, Goldberg S. Cardiogenic shock. J Am
Heart Assoc. 2019;8(8):e011991. (Review)
26. Kodolitsch Yv, Nienaber CA, Dieckmann C, et al. Chest
radiography for the diagnosis of acute aortic syndrome. Am J
Med. 2004;116(2):73-77. (Retrospective; 216 patients)
27. Sabia P, Afrookteh A, Touchstone DA, et al. Value of regional
wall motion abnormality in the emergency room diagnosis
of acute myocardial infarction. A prospective study using
two-dimensional echocardiography. Circulation. 1991;84(3
Suppl):I85-I92. (Prospective; 180 patients)
28. Vasile VC, Jaffe AS. High-sensitivity cardiac troponin for the
diagnosis of patients with acute coronary syndromes. Curr
Cardiol Rep. 2017;19(10):92. (Review)
29. Stucchi M, Cantoni S, Piccinelli E, et al. Anemia and acute
coronary syndrome: current perspectives. Vasc Health Risk
Manag. 2018;14:109-118. (Review)
19 © 2021 EB MEDICINE. ALL RIGHTS RESERVED.
30. Kosuge M, Kimura K, Ishikawa T, et al. Predictors of left main
or three-vessel disease in patients who have acute coronary
syndromes with non–ST-segment elevation. Am J Cardiol.
2005;95(11):1366-1369. (Retrospective; 310 patients)
31. Harhash AA, Huang JJ, Reddy S, et al. AVR ST segment
elevation: acute STEMI or not? Incidence of an acute coronary
occlusion. Am J Med. 2019;132(5):622-630. (Retrospective
chart review; 99 ECGs)
32. Oraii S, Maleki M, Tavakolian AA, et al. Prevalence
and outcome of ST-segment elevation in posterior
electrocardiographic leads during acute myocardial infarction. J
Electrocardiol. 1999;32(3):275-278. (Prospective; 138 patients)
33. Wong C-K, White HD. Patients with circumflex occlusions miss
out on reperfusion. Curr Opin Cardiol. 2012;27(4):327-330.
(Review)
34. Levis JT. ECG diagnosis: isolated posterior wall myocardial
infarction. Permanente J. 2015;19(4):e143-e144. (Review)
35.* Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for
the management of acute myocardial infarction in patients
presenting with ST-segment elevation: the Task Force for
the Management of Acute Myocardial Infarction in Patients
Presenting With ST-Segment Elevation of the European
Society of Cardiology (ESC). Eur Heart J. 2018;39(2):119-177.
(Evidence-based guideline) DOI: 10.1093/eurheartj/ehx393
36. Matetzky S, Freimark D, Feinberg MS, et al. Acute myocardial
infarction with isolated ST-segment elevation in posterior
chest leads V7–9. J Am Coll Cardiol. 1999;34(3):748-753.
(Retrospective; 486 patients)
37. Jain S, Ting HT, Bell M, et al. Utility of left bundle branch block
as a diagnostic criterion for acute myocardial infarction. Am J
Cardiol. 2011;107(8):1111-1116. (Retrospective; 892 patients)
38. Sgarbossa EB, Pinski SL, Barbagelata A, et al.
Electrocardiographic diagnosis of evolving acute myocardial
infarction in the presence of left bundle-branch block. N Eng J
Med. 1996;334(8):481-487. (Case control; 131 patients)
39. Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch
block puzzle in the 2013 ST-elevation myocardial infarction
guideline: From falsely declaring emergency to denying
reperfusion in a high-risk population. Are the Sgarbossa Criteria
ready for prime time? Am Heart J. 2013;166(3):409-413.
(Review)
40.* Tabas JA, Rodriguez RM, Seligman HK, et al.
Electrocardiographic criteria for detecting acute myocardial
infarction in patients with left bundle branch block: a meta-
analysis. Ann Emerg Med. 2008;52(4):329-336. (Systematic
review and meta-analysis; 11 studies, 2100 patients)
DOI: 10.1016/j.annemergmed.2007.12.006
41. Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-elevation
myocardial infarction in the presence of left bundle branch
block with the ST-elevation to S-wave ratio in a modified
Sgarbossa rule. Ann Emerg Med. 2012;60(6):766-776.
(Retrospective; 162 ECGs)
42. Tanguay A, Lebon J, Lau L, et al. Detection of STEMI using
prehospital serial 12-lead electrocardiograms. Prehosp Emerg
Care. 2018;22(4):419-426. (Retrospective; 728 patients)
43. Birnbaum Y, Sclarovsky S, Mager A, et al. ST segment
depression in aVL: a sensitive marker for acute inferior
myocardial infarction. Eur Heart J. 1993;14(1):4-7.
(Retrospective; 107 patients)
44. Kidambi A, Mather AN, Uddin A, et al. Reciprocal ECG
change in reperfused ST-elevation myocardial infarction is
associated with myocardial salvage and area at risk assessed by
cardiovascular magnetic resonance. Heart. 2013;99(22):1658-
1662. (Prospective; 35 patients)
45. Abrahamian FM. ACS Mimic: non-AMI causes of ST-
segment elevation. In: Mattu AT, Tabas JA; Barish RA, ed.
Electrocardiography in Emergency Medicine. Dallas, TX:
JANUARY 2021 • www.ebmedicine.net 20
American College of Emergency Physicians; 2007:119-132.
(Textbook)
46. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl
J Med. 2004;351(21):2195-2202. (Review)
47. Khandaker MH, Espinosa RE, Nishimura RA, et al. Pericardial
disease: diagnosis and management. Mayo Clin Proc.
2010;85(6):572-593. (Review)
48. Henning D, Moeller CM, Fjaeldstad A, et al. Evaluating the
utility of ST elevation in lead II > lead III in differentiating
pericardial disease from STEMI. Scand J Trauma Resus Emerg
Med. 2012;20(Suppl 2):P20. (Retrospective; 283 patients)
49. McNulty PH, King N, Scott S, et al. Effects of supplemental
oxygen administration on coronary blood flow in patients
undergoing cardiac catheterization. Am J Physiol Heart Circ
Physiol. 2005;288(3):H1057-H1062. (Case-controlled; 18
patients)
50. Abuzaid A, Fabrizio C, Felpel K, et al. Oxygen therapy in
patients with acute myocardial infarction: a systemic review
and meta-analysis. Am J Cardiol. 2018;131(6):693-701. (Meta-
analysis; 7 studies, 7702 patients)
51. Hofmann R, James SK, Jernberg T, et al. Oxygen therapy
in suspected acute myocardial infarction. N Eng J Med.
2017;377(13):1240-1249. (Registry-based, randomized,
prospective trial; 6629 patients)
52. Stub D, Smith K, Bernard S, et al. Air versus oxygen in
ST-segment-elevation myocardial infarction. Circulation.
2015;131(24):2143-2150. (Multicenter prospective
randomized trial; 470 patients)
53. Meine TJ, Roe MT, Chen AY, et al. Association of intravenous
morphine use and outcomes in acute coronary syndromes:
Results from the CRUSADE quality improvement initiative. Am
Heart J. 2005;149(6):1043-1049. (Retrospective observational;
57,039 patients)
54. de Waha S, Eitel I, Desch S, et al. Intravenous morphine
administration and reperfusion success in ST-elevation
myocardial infarction: insights from cardiac magnetic resonance
imaging. Clin Res Cardiol. 2015;104(9):727-734. (Prospective
observation study; 276 patients)
55. Kubica J, Adamski P, Ostrowska M, et al. Morphine delays
and attenuates ticagrelor exposure and action in patients with
myocardial infarction: the randomized, double-blind, placebo-
controlled impression trial. Eur Heart J. 2016;37(3):245-252.
(Randomized double-blind single-center study; 70 patients)
56. Hobl E-L, Stimpfl T, Ebner J, et al. Morphine decreases
clopidogrel concentrations and effects: a randomized,
double-blind, placebo-controlled trial. J Am Coll Cardiol.
2014;63(7):630-635. (Randomized double-blind placebo-
controlled trial; 24 patients)
57. American College of Emergency Physicians Clinical Policies
Subcommittee on Reperfusion Therapy for Acute STEMI,
Promes SB, Glauser JM, et al. Clinical Policy: emergency
department management of patients needing reperfusion
therapy for acute ST-segment elevation myocardial infarction.
Ann Emerg Med. 2017;70(5):724-739. (Clinical Policy)
DOI: 10.1016/j.annemergmed.2017.09.035
58. Xian Y, Wang TY, McCoy LA, et al. Association of discharge
aspirin dose with outcomes after acute myocardial infarction.
Circulation. 2015;132(3):174-181. (Retrospective observational
study; 228 hospitals, 10,213 patients)
59. Montalescot G, Wiviott SD, Braunwald E, et al. Prasugrel
compared with clopidogrel in patients undergoing
percutaneous coronary intervention for ST-elevation myocardial
infarction (triton-timi 38): double-blind, randomised controlled
trial. Lancet. 2009;373(9665):723-731. (Double-blind,
randomized controlled trial; 707 sites from 30 countries,
3534 patients)
60. Olier I, Sirker A, Hildick-Smith DJR, et al. Association of
©2021 EB MEDICINE
 different antiplatelet therapies with mortality after primary
percutaneous coronary intervention. Heart. 2018;104(20):1683-
1690. (Retrospective cohort study; 89,000 patients)
61. Steg PG, James S, Harrington RA, et al. Ticagrelor versus
clopidogrel in patients with ST-elevation acute coronary
syndromes intended for reperfusion with primary percutaneous
coronary intervention. Circulation. 2010;122(21):2131-2141.
(Trial subgroup analysis; 7544 patients)
62. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus
clopidogrel in patients with acute coronary syndromes. N Eng
J Med. 2009;361(11):1045-1057. (Double-blind, randomized
trial; 18,624 patients)
63. Koski R, Kennedy B. Comparative review of oral P2Y(12)
inhibitors. 2018;43(6):352-357. (Review)
64. ACC/AHA guidelines for the management of patients with ST-
elevation myocardial infarction. Circulation. 2004;110(9). (AHA
practice guidelines)
65. Yusuf S, Peto R, Lewis J, et al. Beta blockade during and after
myocardial infarction: an overview of the randomized trials.
Prog Cardiovasc Dis. 1985;27(5):335-371. (Multistudy review)
66. Huang B-T, Huang F-Y, Zuo Z-L, et al. Meta-analysis of relation
between oral -blocker therapy and outcomes in patients with
acute myocardial infarction who underwent percutaneous
coronary intervention. Am J Cardiol. 2015;115(11):1529-1538.
(Meta-analysis; 10 studies; 40,873 patients)
67. Dondo TB, Hall M, West RM, et al. -blockers and mortality
after acute myocardial infarction in patients without heart failure
or ventricular dysfunction. J Am Coll Cardiol. 2017;69(22):2710-
2720. (Retrospective cohort study; 91,895 patients)
68. GUSTO Investigators. An international randomized trial
comparing four thrombolytic strategies for acute myocardial
infarction. N Engl J Med. 1993;329(10):673-682. (Prospective
randomized; 41,021 patients)
69. Armstrong PW, Gershlick AH, Goldstein P, et al. Fibrinolysis
or primary PCI in ST-segment elevation myocardial infarction.
N Eng J Med. 2013;368(15):1379-1387. (Randomized,
prospective trial; 1892 patients)
70. Tatli E, Alicik G, Buturak A, et al. Arrhythmias following
revascularization procedures in the course of acute myocardial
infarction: are they indicators of reperfusion or ongoing
ischemia? Scientific World Journal. 2013;2013:160380.
(Retrospective; 151 patients)
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71. Gildea TH, Levis JT. ECG diagnosis: accelerated idioventricular
rhythm. Perm J. 2018;22:17-173. (Review)
72. O’Connor RE, Al Ali AS, Brady WJ, et al. Part 9: acute coronary
syndromes. Circulation. 2015;132(18 suppl 2):S483-S500.
(Clinical guidelines update)
73. Mehta LS, Beckie TM, DeVon HA, et al. Acute myocardial
infarction in women. Circulation. 2016;133(9):916-947. (AHA
statement)
74. Wei J, Mehta PK, Grey E, et al. Sex-based differences in quality
of care and outcomes in a health system using a standardized
STEMI protocol. Am Heart J. 2017;191:30-36. (Retrospective
cohort study; 4918 patients)
75. Engberding N, Wenger NK. Acute coronary syndromes in the
elderly. F1000 Research. 2017;6:1791. (Review)
76. Wenger N. “STEMI at Elderly Age: Expert Analysis.“ 2016.
Available at: https://www.acc.org/latest-in-cardiology/
articles/2016/08/26/08/47/stemi-at-elderly-age. Accessed
December 10, 2020. (ACC expert anaylsis)
77. Alexander KP, Newby LK, Armstrong PW, et al. Acute coronary
care in the elderly, part II. Circulation. 2007;115(19):2570-2589.
(AHA scientific statement)
78. Eagle KA, Goodman SG, Avezum Á, et al. Practice variation and
missed opportunities for reperfusion in ST-segment-elevation
myocardial infarction: findings from the global registry of acute
coronary events (GRACE). Lancet. 2002;359(9304):373-377.
(Prospective registry study; 9251 patients)
79. Finkel JB, Marhefka GD. Rethinking cocaine-associated
chest pain and acute coronary syndromes. Mayo Clin Proc.
2011;86(12):1198-1207. (Review)
80. McCord J, Jneid H, Hollander JE, et al. Management of
cocaine-associated chest pain and myocardial infarction.
Circulation. 2008;117(14):1897-1907. (AHA scientific
statement)
81. Yannopoulos D, Bartos JA, Aufderheide TP, et al. The
evolving role of the cardiac catheterization laboratory in the
management of patients with out-of-hospital cardiac arrest:
a scientific statement from the American Heart Association.
Circulation. 2019;139(12). (AHA scientific statement)
82. Mahmud E, Dauerman HL, Welt FG, et al. Management of
acute myocardial infarction during the COVID-19 pandemic.
J Am Coll Cardiol. 2020;76(11):1375-1384. (Multiple-society
position statement)
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n CME Questions
Current subscribers receive CME credit
absolutely free by completing the
following test. Each issue includes 4 AMA
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smartphone or visit www.ebmedicine.net/E0121
1. Within how many minutes after first medical
contact should an electrocardiogram (ECG)
be obtained and interpreted in a patient
presenting with suspected myocardial
infarction (MI)?
a. 10 minutes
b. 30 minutes
c. 90 minutes
d. 120 minutes
2. With regard to prehospital ECGs, which of the
following is most correct? unable to aid to determine presence of AMI.
a. Prehospital ECGs are expensive and
unnecessary.
b. Prehospital ECGs reduce the time to
diagnosis and treatment.
c. Prehospital ECGs are not necessary for
suspected acute coronary syndomes.
d. Most EMS systems in the United States
cannot obtain ECGs.
3. A patient presenting with chest pain and ____
has the highest likelihood ratio and positive
predictive value for ST-segment elevation
myocardial infarction (STEMI)?
a. Dyspnea
b. Epigastric pain
c. Emesis
d. Diaphoresis
4. ST-segment elevation in aVR with ST
depression in multiple leads may be:
a. Left main coronary artery disease
b. A normal variant
c. A problem of pulmonary etiology
d. Toxicologic overdose
JANUARY 2021 • www.ebmedicine.net 22
5. Isolated ST depression of ≥0.5 mm in leads
V1-V3 may indicate occlusion of the:
a. Left anterior descending artery
b. Left marginal artery
c. Left circumflex coronary artery
d. Left main coronary artery
6. Your 70-year-old patient presents with chest
pain and an ECG with ST-segment depression
of 1 mm in leads V2 and V3. If posterior leads
(V7-V9) are obtained, what cut-off point of ST
elevation is recommended?
a. 1 mm
b. 1.5 mm
c. 2 mm
d. 0.5 mm
7. In a patient with left bundle branch block:
a. ST-segment elevation ≥1 mm discordant
with the QRS complex in any lead may be an
indicator of acute myocardial ischemia (AMI).
b. ST-segment elevation ≥1 mm concordant
with the QRS complex in any lead may be an
indicator of AMI.
c. ST-segment depression ≥1 mm discordant
with the QRS complex in any lead may be an
indicator of AMI.
d. ST-segment elevation, whether concordant
or discordant with the QRS complex, is
8. A patient presents with retrosternal chest pain
for 20 minutes, with vomiting and diaphoresis.
The ECG is nondiagnostic, but you note
hyperacute T waves. Which of the following is
the best option for evaluation of this patient?
a. Management of dyspepsia
b. CT imaging of the abdomen and pelvis
c. Obtaining serial ECGs
d. Administration of opioid analgesia
9. All of the following are indicated in the
management of STEMI EXCEPT:
a. Supplemental oxygen in a patient with SpO2
of 94%
b. Aspirin in a patient without allergy
c. Nitroglycerin for a patient with active chest
pain
d. Heparin in a patient without contraindication
10. Patients whose ischemic symptoms have
been present ≤12 hours may be candidates
for transfer to a percutaneous coronary
intervention (PCI)-capable center if transfer
can be accomplished within:
a. 30 minutes
b. 90 minutes
c. 120 minutes
©2021 EB MEDICINE

In upcoming issues of
Emergency Medicine Practice
JANUARY 2021 | VOLUME 23 | ISSUE 1
Emergency Medicine Practice
Evidence-Based Education • Practical Application
LEARNING OBJECTIVES:
• What are the key aspects of
ECG and patient history that
will help identify STEMI in the
prehospital and ED settings?
• What are common STEMI
mimics and how can you
differentiate them?
• What is the latest evidence on
the therapies for management
of STEMI in the ED?
Authors
Marshall Frank, DO, MPH, FACEP
Assistant Professor of Emergency Medicine,
Florida State University College of Medicine;
Medical Director, Sarasota County Fire
Department, Sarasota, FL
Carson Sanders, BS, NRP, CCEMT-P
Assistant Chief-EMS, Sarasota County Fire
Department, Sarasota, FL
Bryan P. Berry, MD, BCEM, FACEP
Associate Clinical Faculty of Emergency
Medicine, Florida State University College
of Medicine; Emergency Medicine Physician,
Sarasota Memorial Hospital, Sarasota, FL
Peer Reviewers
James Morris, MD, MPH
Program Director, Emergency Medicine
Residency, Texas Tech University Health Sciences
Center, Lubbock, TX
Douglas L. Robinson, DO, MS
Medical and Aeromedical Director, Military
Intelligence Battalion, 75th Ranger Regiment,
FBGA; Emergency Medicine Physician, Piedmont
Regional Medical Center, Columbus, GA
Andrew Schmidt, DO, MPH
Assistant Professor, Department of Emergency
Medicine, University of Florida-Jacksonville,
Jacksonville, FL
This issue is eligible for 4 CME credits. See page 23.
• Community-Acquired Pneumonia
• Atrial Fibrillation and Flutter
• Acute Urinary Retention
• Chemical Inhalations
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Evaluation and Management
of ST-Segment Elevation
Myocardial Infarction in the
Emergency Department
n Abstract
The identification and management of ST-segment elevation
myocardial infarction (STEMI) continues to evolve. Early diagnosis
of STEMI and expeditious time to reperfusion therapy is the focus
of management. The diagnosis of STEMI is commonly made in the
prehospital setting, which can aid in timely definitive management.
This article describes the evaluation and management of STEMI in
the prehospital and emergency department settings.
For online access, scan with an enabled device:
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CME Objectives: Upon completion of this activity, you should be able
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The Emergency Medicine Practice Editorial Board
EDITOR-IN-CHIEF
Andy Jagoda, MD, FACEP
Professor and Chair Emeritus, Department
of Emergency Medicine; Director, Center
for Emergency Medicine Education and
Research, Icahn School of Medicine at
Mount Sinai, New York, NY
ASSOCIATE EDITOR-IN-CHIEF
Kaushal Shah, MD, FACEP
Vice Chair for Education, Department of
Emergency Medicine, Weill Cornell School
of Medicine, New York, NY
EDITORIAL BOARD
Saadia Akhtar, MD, FACEP
Associate Professor, Department of
Emergency Medicine, Associate Dean for
Graduate Medical Education, Program
Director, Emergency Medicine Residency,
Mount Sinai Beth Israel, New York, NY
William J. Brady, MD
Professor of Emergency Medicine and
Medicine; Medical Director, Emergency
Management, UVA Medical Center;
Operational Medical Director, Albemarle
County Fire Rescue, Charlottesville, VA
Calvin A. Brown III, MD
Director of Physician Compliance,
Credentialing and Urgent Care Services,
Department of Emergency Medicine,
Brigham and Women's Hospital, Boston,
MA
Peter DeBlieux, MD Emergency Medicine, Harvard Medical
Professor of Clinical Medicine, Louisiana
State University School of Medicine; Chief
Experience Officer, University Medical
Center, New Orleans, LA
Deborah Diercks, MD, MS, FACEP,
FACC
Professor and Chair, Department of
Emergency Medicine, University of Texas
Southwestern Medical Center, Dallas, TX
Daniel J. Egan, MD
Program Director, Harvard Affiliated
Emergency Medicine Residency, Boston,
MA
Marie-Carmelle Elie, MD
Associate Professor, Department of
Emergency Medicine & Critical Care
Medicine, University of Florida College of
Medicine, Gainesville, FL
Nicholas Genes, MD, PhD
Associate Professor, Department of
Emergency Medicine, Icahn School of
Medicine at Mount Sinai, New York, NY
Michael A. Gibbs, MD, FACEP
Professor and Chair, Department of
Emergency Medicine, Carolinas Medical
Center, University of North Carolina School
of Medicine, Chapel Hill, NC
Steven A. Godwin, MD, FACEP
Professor and Chair, Department of
Emergency Medicine, Assistant Dean,
Simulation Education, University of Florida
COM-Jacksonville, Jacksonville, FL
Joseph Habboushe, MD MBA
Assistant Professor of Emergency Medicine,
NYU/Langone and Bellevue Medical
Centers, New York, NY; CEO, MD Aware
LLC
Eric Legome, MD
Chair, Emergency Medicine, Mount Sinai
West & Mount Sinai St. Luke's; Vice Chair,
Academic Affairs for Emergency Medicine,
Mount Sinai Health System, Icahn School of
Medicine at Mount Sinai, New York, NY
Keith A. Marill, MD, MS
Associate Professor, Department of
School, Massachusetts General Hospital,
Boston, MA
Angela M. Mills, MD, FACEP
Professor and Chair, Department of
Emergency Medicine, Columbia University
Vagelos College of Physicians & Surgeons,
New York, NY
Charles V. Pollack Jr., MA, MD,
FACEP, FAAEM, FAHA, FACC, FESC
Clinician-Scientist, Department of
Emergency Medicine, University of
Mississippi School of Medicine, Jackson MS
Ali S. Raja, MD, MBA, MPH
Executive Vice Chair, Emergency Medicine,
Massachusetts General Hospital; Associate
Professor of Emergency Medicine and
Radiology, Harvard Medical School, Boston,
MA
Robert L. Rogers, MD, FACEP,
FAAEM, FACP
Assistant Professor of Emergency Medicine,
The University of Maryland School of
Medicine, Baltimore, MD
Alfred Sacchetti, MD, FACEP
Assistant Clinical Professor, Department of
Emergency Medicine, Thomas Jefferson
University, Philadelphia, PA
Robert Schiller, MD
Chair, Department of Family Medicine,
Beth Israel Medical Center; Senior Faculty,
Family Medicine and Community Health,
Icahn School of Medicine at Mount Sinai,
New York, NY
Scott Silvers, MD, FACEP
Associate Professor of Emergency Medicine,
Chair of Facilities and Planning, Mayo Clinic,
Jacksonville, FL
Corey M. Slovis, MD, FACP, FACEP
Professor and Chair, Department of
Emergency Medicine, Vanderbilt University
Medical Center, Nashville, TN
Ron M. Walls, MD
Professor and COO, Department of
Emergency Medicine, Brigham and
Women's Hospital, Harvard Medical School,
Boston, MA
CRITICAL CARE EDITORS
William A. Knight IV, MD, FACEP,
FNCS
Associate Professor of Emergency Medicine
and Neurosurgery, Medical Director, EM
Advanced Practice Provider Program;
Associate Medical Director, Neuroscience
ICU, University of Cincinnati, Cincinnati, OH
Scott D. Weingart, MD, FCCM
Professor of Emergency Medicine; Chief,
EM Critical Care, Stony Brook Medicine,
Stony Brook, NY
RESEARCH EDITORS
Aimee Mishler, PharmD, BCPS
Emergency Medicine Pharmacist, Program
Director, PGY2 EM Pharmacy Residency,
Valleywise Health, Phoenix, AZ
Joseph D. Toscano, MD
Chief, Department of Emergency Medicine,
San Ramon Regional Medical Center, San
Ramon, CA
INTERNATIONAL EDITORS
Peter Cameron, MD
Academic Director, The Alfred Emergency
and Trauma Centre, Monash University,
Melbourne, Australia
Andrea Duca, MD
Attending Emergency Physician, Ospedale
Papa Giovanni XXIII, Bergamo, Italy
Suzanne Y.G. Peeters, MD
Attending Emergency Physician, Flevo
Teaching Hospital, Almere, The Netherlands
Edgardo Menendez, MD, FIFEM
Professor in Medicine and Emergency
Medicine; Director of EM, Churruca Hospital
of Buenos Aires University, Buenos Aires,
Argentina
Dhanadol Rojanasarntikul, MD
Attending Physician, Emergency Medicine,
King Chulalongkorn Memorial Hospital;
Faculty of Medicine, Chulalongkorn
University, Thailand
Stephen H. Thomas, MD, MPH
Professor & Chair, Emergency Medicine,
Hamad Medical Corp., Weill Cornell
Medical College, Qatar; Emergency
Physician-in-Chief, Hamad General Hospital,
Doha, Qatar
Edin Zelihic, MD
Head, Department of Emergency Medicine,
Leopoldina Hospital, Schweinfurt, Germany

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 Points & Pearls
QUICK READ
JANUARY 2021 | VOLUME 23 | ISSUE 1
Points
• The location of the coronary occlusion will
produce ST-segment elevation in a predictable
pattern on ECG. (See Figure 3.)
• The goals of prehospital management of STEMI
are early recognition, administration of aspirin,
and timely transport to a PCI-capable facility for
reperfusion.
• Patients with suspected ACS should have an ECG
performed within 10 minutes of the first medical
contact, and serial ECGs should be performed
liberally to monitor for changes.
• Bypassing non-PCI capable facilities to get the
STEMI patient to a PCI-capable facility is safe,
and is recommended if the first medical contact-
to-balloon time is <90 minutes and transport
time is <30 minutes.17
• Echocardiography is a noninvasive way to assess
for regional wall motion abnormalities or other
pathologic findings, and it can help confirm a
diagnosis.
• A patient presenting with signs and symptoms of
ACS and ST elevation on ECG should be man-
aged as a STEMI regardless of the hs-cTn level.28
• Obtaining posterior leads (V7, V8, and V9) increas-
es the ability to detect posterior (inferobasal)
STEMI.37 (See Figure 7.)
• In the setting of an LBBB pattern, ST elevation of
≥1 mm that is concordant with the QRS complex
is an indicator of STEMI. In patients with right
ventricular paced rhythms, similar findings can be
used.1
• An ECG with ST-segment elevation and recipro-
cal changes can help diagnose STEMI; the pres-
ence of reciprocal changes helps to differentiate
true STEMI from STEMI mimics such as pericardi-
tis. (See Table 3.)
• The ECG of a patient presenting with acute peri-
carditis may demonstrate diffuse ST-segment el-
evation and PR-segment depression that must be
differentiated from STEMI in the clinical setting.
• Based on consensus, an 81-mg maintenance as-
pirin dose is recommended over higher doses.59
• The choice of P2Y12 inhibitor (clopidogrel,
JANUARY 2021 • www.ebmedicine.net 28
Evaluation and Management
of STEMI in the
Emergency Department
Pearls
• Evaluate every ECG with LBBB or ventricular
pacing for Sgarbossa criteria. (See Figures 9
and 10.)
• Fibrinolysis must be considered when
patients present to a center without a PCI
program, in places that do not have 24-hour
cath lab coverage, or when other delays to
getting a patient to a cath lab exist. See
Table 4.
• It is specifically recommended in guidelines
to utilize the QRS onset as the reference
point for J point determination.1
(See Figure 5.)
• Oxygen is no longer routinely recommended
for nonhypoxic patients with a STEMI
because it may increase coronary vascular
resistance.50
• The 2017 ACEP Clinical Policy recommends
clinical judgment be used in deciding
whether to give STEMI patients morphine
for pain control while awaiting PCI.58
ticagrelor, or prasugrel) will depend on patient
history, allergies, drug interactions, cost, and
dosing.45
• Primary PCI has higher rates of infarct artery
patency and lower rates of recurrent ischemia,
reinfarction, intracranial hemorrhage, and death,
compared to lytics.65
• STEMI patients who primarily receive fibrinolytic
therapy should receive anticoagulant therapy for
a minimum of 48 hours.
• Any ED with the potential to receive STEMI
patients should have a streamlined protocol for
the administration of fibrinolytics that includes an
evaluation for contraindications.
• The 2017 ACEP Clinical Policy recommends
transfer of STEMI patients to a PCI center as
soon as possible to reduce major adverse
cardiac events.58
©2021 EB MEDICINE
 Calculated
Decisions
POWERED BY

Clinical Decision Support for Emergency Medicine Practice Subscribers

Sgarbossa Criteria for Myocardial

Infarction in Left Bundle Branch Block
The Sgarbossa criteria score is used to diagnose acute myocardial
Click the thumbnail above infarction in patients with prior left bundle branch block.
to access the calculator.

About the Score

It is often difficult to identify a myocardial infarc-
tion (MI) in patients with existing left bundle branch
block (LBBB). Approximately 1 in 200 patients with
MI have LBBB. The use of the Sgarbossa criteria is
a well-accepted approach for determining which
patients with LBBB are having an MI.
A Sgarbossa score of ≥ 3 is 90% specific for MI,
but is not sensitive (36% sensitivity). Therefore, a
score ≥ 3 should be acted upon, but a lower score
cannot be used to rule out MI. Clinicians should
maintain a high index of suspicion if the patient’s
clinical presentation is consistent with MI.
Evidence Appraisal
Sgarbossa et al developed and validated the Sgar-
bossa criteria in 1996, based on a set of electrocar-
diographic criteria for the diagnosis of acute MI in
patients with chest pain and LBBB. The Sgarbossa
criteria cannot rule out MI in patients with existing
LBBB. Smith et al modified the Sgarbossa criteria by
adjusting the component of excessively discordant
ST-segment elevation (Smith 2012). This modifica-
tion has been referenced by Dr. Sgarbossa (Cai
CALCULATOR REVIEW AUTHOR
Graham Walker, MD
Department of Emergency Medicine, Kaiser San
Francisco Medical Center, San Francisco, CA
2013) and should be included in the Sgarbossa
criteria.
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Elena Sgarbossa, MD
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References
Primary Reference
• Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardio-
graphic diagnosis of evolving acute myocardial infarction
in the presence of left bundle-branch block. N Engl J Med.
1996;334(8):481-487.
DOI: 10.1056/NEJM199602223340801
Validation Reference
• Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-ele-
vation myocardial infarction in the presence of left bundle
branch block with the ST-elevation to S-wave ratio in a modi-
fied Sgarbossa rule. Ann Emerg Med. 2012;60(6):766-776.
DOI: 10.1016/j.annemergmed.2012.07.119
Additional Reference
• Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch
block puzzle in the 2013 ST-elevation myocardial infarction
guideline: from falsely declaring emergency to denying re-
perfusion in a high-risk population. Are the Sgarbossa Criteria
ready for prime time? Am Heart J. 2013;166(3):409-413.
DOI: 10.1016/j.ahj.2013.03.032
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