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NON-ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
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38
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
ST-segment elevation
myocardial infarction
David F. M. Brown
Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital,
Associate Professor, Harvard Medical School, Boston, Massachusetts, USA
3
Section I: Case presentation
A 45-year-old man developed chest tightness and nau-
sea while watching TV. He also complained of jaw and
left arm pain, but no back pain. EMS was called after
the symptoms did not resolve over 30 minutes. Field
vital signs were: heart rate 75 beats/min, blood pres-
sure 100/66 mmHg, respirations 16 breaths/min, oxy-
gen saturation 95%. The skin was diaphoretic with
clear lungs, along with regular heart sounds without a
murmur, a benign abdomen, and equal pulses. A fi eld
electrocardiogram (EKG) revealed evidence of acute
inferolateral ST-segment elevation myocardial infarc-
tion (STEMI). The patient was then brought to the
emergency department (ED). He arrived with ongoing
chest pain, and continued diaphoresis.
The past medical history was notable for hyperten-
sion, for which he took lisinopril. He had no prior
history of chest pain. He did not smoke nor use rec-
reational drugs. His father had a coronary bypass
surgery at age 50.
The ED vital signs were: heart rate 78 beats/min, blood
pressure 110/60 mmHg, respirations 12 breaths/min,
and oxygen saturation 99% on 2 liters of oxygen by
nasal canula. The skin was moist and there was no
jugular vein distention. The breath sounds were clear.
The heart sounds were regular with a crisp S1 and S2.
There were no murmurs. The extremities were with-
out edema. The pulses were brisk. The neurological
examination was normal. An EKG was unchanged
from the fi eld tracing.
Section II: Case discussion
Dr Richard Harrigan: We stress the EMS presentation
with acute myocardial infarctions (MIs) or patients
with chest pain. With prolonged ED waiting times
because of the backup in the waiting room or prob-
lems with triage, EDs need a protocol to obtain an
emergent EKG for anyone who presents with chest
pain, including those patients who arrive on their
own (i.e., not via an ambulance). Without this, there
is potential for critical delays in treatment.
Dr Peter Rosen: We had a patient present with chest
pain. An EKG was taken and read by an ED attend-
ing. The EKG was not immediately diagnostic, and
the patient was evaluated for a noncardiac cause.
Subsequently, the patient developed more chest pain.
A different attending was now responsible for that
patient and said, “Let me see the patient’s EKG.” He
had not seen the original one, and he wanted to see
if there were changes on it. At that moment, a tech
brought an EKG to be read and the attending thought
he was reading the second EKG on the patient with
chest pain, but was actually reading the fi rst EKG on
an entirely different patient. The error that was made
was that the attending, who was very busy, didn’t
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
39
we do have prehospital EKG, but not prehospital lysis
in place. EMS often show-up with a prehospital EKG,
but we rarely get a call ahead of time to discuss.
DB: There are a number of papers that show prehos-
pital EKGs, either interpreted by trained paramedics
or sent to the receiving ED, are as accurate as those
performed in EDs and interpreted by physicians, or
at least close to as accurate. When we fi rst went to
paramedic performance of the EKG about a decade
ago, the initial interpretations were somewhat spotty.
However, with training and experience, the accu-
racy level has become very acceptable with rare false
positives.
PR: My concern is that patients can be complex and
at times not evolving MIs, but looking like they are,
and this makes the problem somewhat harder when
you can’t get an answer until the patient is in the
catheterization laboratory. To me, this emphasizes the
need for early and easy access to the catheterization
laboratory.
Let me ask you another question. We know that
inferior wall MIs have better outcomes then anterior
wall MIs. Do you think that we are unnecessarily rep-
erfusing inferior wall MIs? Do you think they would
do just as well if they were left alone?
SG: Ultimately, the anterior wall MI patients are far
more likely to end up as cardiac cripples (with ejec-
tion fractions [EF] in the 15–20% range) if they are
left without some form of reperfusion. For this rea-
son, the fi brinolysis or primary intervention window
is often extended beyond 6 hours for this group of
patients. Inferior wall MI patients without concomi-
tant right ventricle or posterior wall involvement will
not only be more likely to survive their MI, but sur-
vive with minimal damage to their myocardium (EF
of 40–45%). Nevertheless, there is some mortality
benefi t in reperfusing inferior wall MIs if they arrive
within the 6-hour window. For this reason, one must
weigh very carefully reperfusion in this population
versus the adage of “do no harm.”
PR: When would you do right-sided leads looking for
a right ventricular infarction, and when would you add
posterior leads looking for a posterior MI in the face
of an EKG that was suggestive of inferior wall MI?
WB: The EKG in our case shows an extensive STEMI
involving the lateral and inferior walls, with the
check the name of the patient against the name on
the EKG. I could see how that would happen when
you are busy, and you ask for a tracing and someone
hands you one. You immediately assume it’s the one
you asked for rather than a separate one.
Dr William Brady: Thus, as with all diagnostic inves-
tigations, the confi rmation of the patient’s identity is
a vital portion of the study interpretation.
Dr David Brown: Our policy is that an immediate
EKG is done based on triage symptoms and handed
to an attending, and that attending has to sign the
tracing, stating “no STEMI.” While that might avoid
an error in recognition that this wasn’t the patient’s
initial tracing, it would not identify an initial tracing
for a separate patient. While it is understandable how
such errors occur during busy times, there is no sub-
stitute for compulsive attention to the name on the
tracing as part of interpretation.
PR: Hopefully this was a one-time error, but it seems
to me that it is the kind of error that is easy to repeat.
Perhaps, if we can computerize our patient care a
bit better, then maybe the EKG will automatically
appear rather than having to go hunt for the paper.
On another note, not every state has a selective desti-
nation policy for potential acute MI patients, and not
every EMS system has the ability to obtain 12-lead
EKGs in the fi eld.
Dr Shamai Grossman: Boston pioneered a selective
destination policy for potential MI patients several
years ago, and has successfully cut critical minutes
away in treating STEMI patients by bringing them only
to EDs with 24-hour catheterization laboratories.
WB: Prehospital diagnosis and prehospital notifi cation
prior to arrival using the 12-lead EKG can potentially
shave as much as 20 to 30 minutes off the patient’s
total door-to-reperfusion therapy time just by having
the hospital involved and ready to move quickly.
RH: In Philadelphia, there are fi ve university hos-
pitals all very close to each other, all percutaneous
coronary intervention (PCI) capable, and many have
arrangements with the smaller hospitals where they
will, upon receiving a patient, fax an EKG to the
University Hospital and activate the system there.
The interventionalist will come into the catheteriza-
tion laboratory in parallel with the patient arriving
from the outside hospital. In the city of Philadelphia,
CHAPTER 3
40
DB: This patient doesn’t need any additional leads
to push toward a treatment algorithm, and most
U.S. hospitals have a treatment algorithm in place in
advance of these patients’ arrival. If you’re at a place
where either fi brinolysis onsite or transfer for PCI are
options, then the extent of the MI might push you
to think about transferring the patient. Nevertheless,
there are also features here that favor fi brinolytic
therapy; namely, the short duration of symptoms.
That’s the one situation where fi brinolysis might be
considered the preferred therapy.
PR: We are all giving aspirin in the fi eld, but do you
feel that there is a need to start beta-blockers or nitrates
in the fi eld, or do you think this a case where faster
transport to the defi nitive care site is really the optimal
strategy?
RH: I favor “do less and get them there faster.” This
is colored by the environment I work in, which is an
inner city where the transport times are much shorter
then in a rural environment. Growing evidence about
the risks of IV beta-blocker therapy lead me toward
not asking prehospital personnel to make a decision
about this therapy. IV beta-blockers must be given with
extreme caution, even in patients who are hyperten-
sive and don’t have heart block or signs of cardiogenic
shock. Prehospital aspirin is very appropriate. Nitrates
have been given in the prehospital setting for a long
time, and usually without ill effect; the caveat with
nitrates being to be alert for a right ventricular infarc-
tion, where nitrates could cause hypotension. If the
prehospital people are taking an appropriate history,
checking blood pressures for hypotension, and know
their patient is not taking medications such as sildenafi l,
then nitrates remain appropriate in the prehospital set-
ting. Nevertheless, in contrast to aspirin, administering
nitrates early has not been shown to alter mortality.
PR: The patient is now in your ED, and you have
access to a catheterization laboratory. What medica-
tions would you start in the ED before you send the
patient to the laboratory? Should you anticoagulate
this patient with heparin or with platelet inhibitors?
WB: Aspirin is the key medication; if it hasn’t been
administered in the prehospital setting, I would make
sure the patient receives aspirin.
SG: I favor four baby aspirin in lieu of enteric-coated
aspirin, since baby aspirin has the most rapid absorption.
ST-segment elevation so extensive that it provides
us with a diagnosis. If you are working in a system
that primarily uses fi brinolysis, I would go ahead
and start that process. If you work in a system that
uses an invasive laboratory either at your institution
or a neighboring institution, I would activate your
team and move towards treatment. At this point, the
patient’s blood pressure is adequate, although at the
low end of normal, at 100/66 mmHg.
With respect to a right-sided EKG, remember that
between one-quarter and one-third of inferior wall
STEMIs involve the right ventricle (RV) and exhibit
RV infarction. Do you need to specifi cally diagnosis
it in an EKG? Not necessarily. I think you need to be
aware of this possibility, and be cautious with vaso-
dilatating medication like nitrates and morphine in
inferior myocardial infarction patients, and perhaps
be a little more aggressive with IV fl uid. Placing a sin-
gle lead on the right chest RV4 would be very appro-
priate. However, I would not delay time to lysis or
to the cathetererization laboratory to perform these
additional leads.
Posterior leads would be interesting, but again we
already do have a diagnosis of an extensive MI here
involving the lateral and inferior walls. This EKG
already does show ST-segment depression in V1 and
V2, so there could be a posterior wall as well. Unless
I had some time on my hands waiting for the drugs to
be mixed or for the patient to go to the catheter labo-
ratory, I would not do posterior leads as how would
it alter treatment? It may help you defi ne a more ill
patient with a greater degree of risk, yet this is already
a high-risk EKG. Of the 12 leads, it looks like all but
one have some form of ST-segment deviation. In a
patient with a nondiagnostic 12-lead EKG, meaning
that the ST-segments are not signifi cantly abnormal
other than V1 and V2, I would defi nitely perform a
posterior lead analysis to look for the rare isolated
posterior wall STEMI, which I think would alter your
approach to treatment. That last scenario is where
the real “added value” of the posterior lead analysis
is found, in the detection of the “isolated” posterior
wall infarction.
PR: If you knew that the patient had inferior and
posterior involvement, would you be more inclined
to transfer the patient to a facility with a catheteriza-
tion laboratory instead of starting fi brinolysis in your
own ED?
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
41
to facilities that don’t have interventional catheteriza-
tion capability at their facility. I’m not sure that’s a
good thing, since we know that only a small percent-
age of patients with STEMI who are transferred from
one institution to another have a door-to-balloon
time of less than 90 minutes. Many of these commu-
nity hospital patients are being transferred despite the
fact that fi brinolytic therapy might be the preferred
treatment.
SG: When would you transfer this patient from a
community ED to a hospital with catheterization
laboratory?
DB: A delayed presentation, an extensive MI, and the
relative availability of PCI would all come into play in
my decision. I think its incumbent on the community
emergency physician to have some sense of door-to-
balloon times of the receiving hospital if we select that
therapy as our mainstay of treatment.
PR: Has the argument fi nally been resolved as to
whether one worsens outcome if you both thrombol-
yse and subsequently PCI?
RH: The trials that looked at giving a dose of fi brin-
olytic agent in addition to follow up with PCI have
not shown an improved outcome with both. There
is a role for rescue PCI, but that’s not the same thing
as coming at the patient with a plan to both lyse and
follow up with a PCI.
SG: Early data suggested that salvage angioplasty had
a worsened outcome when compared to primary PCI.
However, more recent data suggest that if a patient
does not reperfuse with fi brinolytics (i.e., the patient
has ongoing symptoms, EKG changes or hemody-
namic instability), then that patient’s outcome with
salvage angioplasty is as good as one in whom pri-
mary PCI was instituted.
PR: Is there a standard fi brinolytic agent used univer-
sally now? There was a vicious debate between the use
of streptokinase and tPA based on the cost of the rela-
tive drugs; people argued that tPA worked better than
streptokinase.
WB: Today, most EDs use either t-PA, TNK, or, less
often, rPA. I believe that although t-PA is more expen-
sive than streptokinase, it has an incremental mortality
benefi t, particularly in early presenters who are both
young and have anterior wall infarction. For all comers
Most of the large studies used either 160 mg or 325 mg.
Since there are few complications with the higher dose,
that is what I would use.
WB: I would probably administer nitroglycerin
whether it be sublingual or topical. At this point, I
would probably hold off on any IV nitro, not because
I have any concern about it, but because it will not
lower mortality. Beta-blockers can wait until a later
time during the fi rst hospital day. Unless the patient
had melenic stool by history or a positive hemaoccult
test, I would use heparin, preferably unfractionated,
with a bolus and drip, although I would have no prob-
lem in using low molecular weight heparin. This is one
of the patient groups that benefi ts from a glycoprotein
inhibitor. Nevertheless, I would not delay time to take
the patient to the catheter laboratory to administer this
medication. Lastly, I don’t believe clopidogrel has a lot
to offer this patient acutely in the ED, although I’m
sure the patient will probably end up on this agent.
PR: Is morphine appropriate for the treatment of MI
pain?
WB: If you look at several large databases, retro-
spective analysis has demonstrated that patients who
receive morphine in a nonhospital setting actually
don’t fare so well compared to patients who receive
the drug while in the hospital. In the ED, we need
to be cautious with the administration of morphine,
realizing that it is a very potent vasodilatator, and can
alter perfusion. In this patient, who has a reasonable
chance of having a right ventricular wall infarction, we
need to be even more cautious. Morphine is not only
a pain medication, but also an anxiolytic. Therefore,
in patients who are experiencing an acute coronary
syndrome (ACS) event, a small dose of intravenous
morphine, mainly as an anxiolytic, may still have a
role. I continue to use morphine in selected individuals
with potential ACS—but I do so cautiously.
PR: Besides a preference for fi brinolysis in a patient
who has a short time period of symptoms, are there
other indications that would make one want to fi brin-
olyse this patient rather than send him to the catheter-
ization laboratory?
DB: The guidelines were written to encourage fi brin-
olytic therapy in those patients with early presenta-
tion. Having said that, the pendulum has swung in
favor of primary PCI even for patients who present
CHAPTER 3
42
recurrent disease, or complications of the two different
kinds of stents, and what should we be looking for?
RH: The argument can be made that, in a given
patient at any given time, it doesn’t matter. We should
assume that a patient who has had a recent procedure
with any kind of stent could have stent occlusion, or
potentially dislodgment or propagation.
DB: The trend in our institution has moved toward
bare-metal stents for PCI with acute MI, with the
thinking that they are less likely to thrombose.
SG: Although the data are inconclusive, the GRACE
registry fi nds that although acute MI survival appears
similar in the fi rst 6 months following discharge,
thereafter mortality is greater in patients treated with
drug-eluting stents due to an increased risk of late
reinfarction. This suggests that in this patient popula-
tion, late stent thrombosis is more likely with drug-
eluting stents.
PR: I would stress that from an ED perspective,
whatever the procedure, if the patient is having new
symptoms and EKG changes, it is prudent to assume
you are dealing with a new thrombosis and treat the
patient accordingly. It seems as though we are seeing
fewer STEMIs and more non-ST-segment myocardial
infarctions. I don’t know if that’s because of better
pre-infarction care, or if we are just getting people to
the hospital earlier with their unstable angina?
WB: We are seeing fewer STEMIs in our region. This
is likely related to much more aggressive control of
risk factors, such as blood sugar, high blood pressure,
serum lipids, cessation of smoking, etc.
PR: Years ago, the time from the onset of symptoms
to coming to the ED averaged over three hours.
SG: Sadly, despite major public education initiatives,
the lag time from symptom onset to arrival in the ED
has not changed signifi cantly in acute MI patients.
Denial remains very powerful despite a growing public
awareness of the disease.
Case resolution
The patient was recognized in the fi eld to have an
acute inferoposterior MI. This information was com-
municated to the emergency physician who, with a
single page, activated the entire catheterization team.
with STEMI, the data is less compelling. Many insti-
tutions have moved away from streptokinase because
of the data and in part because of other issues, and
have moved towards either rPA or tNK. tNK admin-
istered as a single dose, or rPA, which has two boluses
without an infusion, have the benefi t of having much
simpler administration regimens—thus minimizing
the potential for error and improving the effi ciency of
administration.
SG: Despite these small advantages, streptokinase
remains the thromblytic agent of choice in Europe
because of a very signifi cant cost differential.
PR: Must the use of streptokinase be limited to one
time only?
SG: Streptokinase is a protein produced by beta-hemo-
lytic streptococcus. Because streptokinase is a bacterial
product, one can develop immunity to it. Therefore,
streptokinase should not be re-dosed after four days
from the fi rst administration, as it may not be as effec-
tive, and it can also cause an allergic reaction. In addi-
tion, streptokinase is contraindicated in patients who
have had a strep throat in the prior 6 months.
PR: If this patient had signs of pump failure, given the
extensiveness of the infarction as it appears on this
EKG, would you consider primary surgical interven-
tion for this patient instead of PCI or thrombolysis?
DB: That would depend on what we learned at angiog-
raphy. In all likelihood, if this patient were taken to
the catheterization laboratory, he would have a single
vessel infarction that would be amenable to catheter-
directed therapy and stent placement. He might need
to be supported through the MI with intra-aortic bal-
loon placement. The indications for emergency coro-
nary artery bypass graft surgery (CABG) are limited to
left main disease, left main thrombosis (which is not
likely given this EKG), unexpected signifi cant three-
vessel disease, or complications of the procedure to
place a stent (such as a coronary artery dissection or
a coronary artery rupture). An unexpected rare aortic
dissection complicated by retrograde fl ap propaga-
tion and occlusion of the right coronary artery would
also require emergency surgery.
PR: This patient was treated with PCI, and received
a metal stent. I believe that most cardiologists have
moved toward drug-eluting stents. Are there differ-
ences in what we can expect to see in the ED in terms of
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
43
and of those who reach the hospital, at least 5–6%
will still die within the following 30 days.
1
A STEMI is strictly defi ned as a rise above the upper
limit of normal and subsequent fall of cardiac bio-
markers specifi c for myocardial necrosis (troponin or
CK-MB) in a patient who also has new or presumed
new ST-segment elevation in two or more contiguous
leads. In practice for the emergency physician, who
will not have the trending of cardiac biomarkers avail-
able in real time, the defi nition is generally considered
to be a history consistent with ACS, and the elec-
trocardiographic criteria as above. The defi nition of
ST-segment elevation is ⬎0.1 mV.
1
Contiguous leads
are defi ned as V1-6 in the chest leads, while in the
frontal plane, contiguity is defi ned as the lead sequence
aVL, I, inverted aVR, II, aVF, and III. Patients who
meet the clinical criteria for a STEMI and have either
a left bundle branch block not known to be old, or
electrocardiographic evidence of an isolated true pos-
terior MI, are also considered, for treatment algorithm
purposes, to have a STEMI.
The pathophysiology of a STEMI begins when an ath-
erosclerotic plaque within a coronary artery becomes
unstable due to plaque rupture or hemorrhage into the
plaque; the degree of stenosis caused by atheroscle-
rotic plaque need not be critical prior to the plaque
becoming unstable. Plaque rupture or hemorrhage
results in an infl ammatory cascade that causes plate-
let adherence and subsequence activation. Activated
platelets express glycoprotein (GP) 2b-3a receptors on
their surface and are then cross-linked by fi brinogen,
which is a bivalent molecule with binding sites on each
end that are specifi c for the GP 2b-3a receptor. The
resultant platelet-fi brinogen web is further stabilized
by thrombin, which cross-links and modifi es fi brino-
gen to fi brin. As the platelet-fi brin aggregation grows,
it traps circulating red and white blood cells, and a
thrombus forms. At the same time, the infl ammatory
process leads to the release of vasoactive mediators,
which may cause local vasospasm, further compromis-
ing coronary blood fl ow. If this process results in com-
plete occlusion of the epicardial coronary artery at the
site of plaque rupture, a STEMI occurs.
Clinical presentation
Patients with a STEMI classically present with ongo-
ing discomfort in the substernal (precordial) region of
the chest. This discomfort may be described as pain,
In the ED, the patient received IV normal saline
1000 cc bolus, and the blood pressure increased to
120/80 mmHg. He was given IV unfractionated hepa-
rin 5000 unit bolus, and was started on an infusion of
1000 units/hr. He was given clopidogrel 600 mg p.o.,
and transferred to the cardiac catheterization labo-
ratory. Coronary angiography revealed a proximal
RCA thrombotic occlusion that was easily opened,
and a bare-metal stent was placed without complica-
tions, resulting in TIMI grade 3 fl ow down the vessel.
The patient was transferred to the critical care unit,
and had an uncomplicated hospital course. The peak
troponin level was 6.2. A cardiac ECHO on hospital
day three showed an inferior hypokinesis with an EF
of 52%. He was discharged on aspirin, clopidogrel,
simvastatin, and metoprolol on hospital day four, and
was doing well at 30-day follow up.
Section III: Concepts
Epidemiology and pathophysiology
ST-segment elevation myocardial infarction (STEMI)
is at one end of the spectrum of ACS, which occurs as a
result of coronary artery disease. Coronary artery dis-
ease continues to be the leading cause of death in the
United States, despite marked advances in its preven-
tion, diagnosis, and treatment over the past 60 years.
The advances in the treatment of ACS and particularly
of STEMI began with the use of cardiac monitoring
and the development of external cardiac defi brillators
in the 1950s, and progressed to widespread utiliza-
tion of external cardiac massage and admission of
ACS patients within cardiac care units in the 1960s.
Pharmacologic developments in the management
of STEMI began with the use of aspirin and beta-
blockers, and have advanced to include more sophis-
ticated antiplatelet and anticoagulant agents. In the
1980s, the widespread use of fi brinolytic therapy ush-
ered in the reperfusion era of STEMI therapy. Also in
the 1980s, coronary angiography was fi rst performed
in the setting of acute STEMI, demonstrating occlu-
sion of the infarct-related epicardial coronary artery;
subsequently, a variety of mechanical interventions to
open the artery were developed. These advances have
contributed to an overall decline in the age-adjusted
mortality of ischemic heart disease by reducing the
case fatality rate of STEMI. Nonetheless, there are
approximately 500,000 STEMIs annually in the US
CHAPTER 3
44
compromise, or shock. Jugular venous distention,
rales, and a third heart sound (S3) suggest congestive
heart failure. If altered mental status and hypotension
are additionally present, cardiogenic shock is likely.
Emergency department diagnosis
The differential diagnosis of chest discomfort and the
associated symptoms described above are broad but,
in the case of a STEMI, the diagnosis hinges on the
fi ndings on a 12-lead electrocardiogram (EKG). An
EKG should be obtained immediately in the evaluation
of any patient with chest discomfort or a suspected
STEMI as the treatment (see below) is extremely time-
sensitive. The initial EKG fi nding in patients with a
STEMI is peaked hyperacute T waves in the distribu-
tion supplied by the infarct-related artery (IRA). These
are uncommonly seen in isolation by the clinician
because, while T waves will become tall and sharply
peaked within minutes of IRA occlusion, within min-
utes thereafter ST-segment elevation will become evi-
dent as well (Figure 3-1). In order to be diagnostic, the
pressure, or tightness and may have started at rest or
during exertion. It may also be located in the left or
right anterior chest and may radiate to the shoulder,
neck, jaw, arm, or back. There may be associated
symptoms of dyspnea, nausea, vomiting, diaphore-
sis, weakness, dizziness, or fatigue. Note that patients
may present atypically, with chest discomfort that is
sharp, stabbing, pleuritic, or palpable. Occasionally
there may be no discomfort at all, and the patient
may present only with one or several of the associ-
ated symptoms. Other atypical presentations may
include isolated discomfort in the back, neck, jaw, or
arm; upper abdominal pain or burning; indigestion;
and generalized weakness. Elderly patients, women,
non-Caucasians, and diabetics are particularly likely
to have atypical presenting symptoms.
The physical examination is frequently unrevealing
in patients with a STEMI. The heart rate may be rapid,
slow, or normal. A 4th heart sound (S4) may occasion-
ally be present, and the skin may be diaphoretic. Most
other fi ndings relate to complications of a STEMI. Vital
signs may show evidence of dysrhythmia, respiratory
Figure 3.1 12-lead EKG shows hyperacute T waves in
leads V2-V5 and ST elevations in leads I, avL, and V1-V5
consistent with acute anterolateral STEMI. Note also there
is sinus node dysfunction with a ventricular escape rhythm
for the fi rst three beats, then normal sinus rhythm for the
next two beats, and then a junctional escape rhythm for
the rest of the tracing. Reproduced with the permission of
David F. M. Brown, M.D.