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HYPERTENSIVE EMERGENCIES
305
emergent lowering of blood pressure and heart rate
to limit vascular shear forces and dissection pro-
gression. Goal blood pressure should be a systolic
blood pressure of 100–120, or lower if tolerated.
First line antihypertensives in this setting are either
propranolol or labetalol. In patients who cannot tol-
erate beta-blockade, verapamil or diltiazem may be
employed. In patients with an intact mental status and
no signs of renal dysfunction, sodium nitroprusside
may be employed to achieve further blood pressure
decrease.
10
Congestive heart failure
Congestive heart failure can result primarily from
an acute cardiac insult, but it can also result from a
rapid increase in afterload from a cholinergic surge.
In this setting of acute onset of CHF, therapy should
be directed toward acute afterload and preload reduc-
tion. This is best accomplished with nitroglycerin
or ACE inhibitors, and ultimately with furosemide.
By decreasing preload and afterload, there will be a
decrease in cardiac wall stress and oxygen consump-
tion, and allow for systemic perfusion.
Disposition
All patients with a hypertensive emergency should be
admitted to the hospital, with the majority sent to the
intensive care unit for careful hemodynamic moni-
toring and titration of antihypertensive therapy. An
arterial line may be useful for second-to-second pres-
sure management, particularly in patients with labile
blood pressures.
Section IV: Decision making
Look for evidence of hypertensive emergency target •
organ damage.
Do not lower blood pressure in the ED simply •
because the blood pressure is elevated.
If end-organ damage is found, blood pressure •
should be lowered within the fi rst 1–2 hours by
20–30%.
Choice of blood pressure-lowering agent should •
be directed toward the specifi c clinical needs of the
patient (Table 21-2).
and include headache and facial fl ushing in up to 25%
of patients.
5,6,8,9
Nitroprusside once was routine therapy in hyper-
tensive emergencies; however, the agent has fallen
into disfavor recently. It is advantageous because it
acts rapidly, within 1–2 minutes, and has a half-life of
4 minutes. Despite this favorable profi le, nitroprusside
decreases cerebral blood fl ow while increasing intrac-
erebral pressure. Nitoprusside is also contraindicated
in the setting of cardiac ischemia as it can cause a
coronary steal phenomenon exacerbating the isch-
emia. Nitroprusside can only be used for a maximum
of 48 hours secondary to production of thiocyanate
as a byproduct of its metabolism. Logistically it also
poses both storage and handling issues, as it is light
sensitive and rapidly degrades. Since the agent crosses
the placenta, it should not be used in patients who are
pregnant.
1,5,6,8,9
Clevidipine is a new dihydropyridine calcium chan-
nel blocker that may be useful in the treatment of
hypertensive emergency. The drug has an onset of
action of 2–4 minutes and a half life of 5–15 min-
utes. Like esmolol, clevidipine is rapidly hydrolyzed
by plasma esterases, and therefore may be particularly
helpful in patients with renal and hepatic dysfunction.
As with other calcium channel blockers, it is not indi-
cated in patients who suffer from severe aortic steno-
sis or for patients in congestive heart failure (CHF). It
may have a niche in treating hypertensive emergencies
in patients who cannot tolerate beta-blockade.
8
Hydralazine is a popular drug for rapid blood pres-
sure lowering, but with the exception of pregnancy, is
probably best avoided in the management of hyper-
tensive crises. Hydralazine works within 10 minutes,
but its blood pressure effects may persist for greater
than 12 hours.
5
This prolonged activity relates to the
rate of acetylation of hydralazine; 50% of the popula-
tion acetylates slowly.
9
In addition, hydralazine should
never be used in aortic dissection, as it increases vas-
cular shear forces.
Special cases
Aortic dissection
In the specifi c case of aortic dissection, goals for
blood pressure reduction differ from other hyperten-
sive emergencies. Rather than a 20–25% reduction
in blood pressure over the fi rst 2 hours, the goal is
CHAPTER 21
306
Edmunds E, Landray MJ, Li-Saw-Hee FL, et al. 7
Dyslipidaemia in patients with malignant-phase hyper-
tension. QJM. 2001;94(6): 327–332.
Marik PE, Varon J. Hypertensive crises: Challenges and 8
management. Chest. 2007;131:1949–1962.
Tintanelli J, Gabor K, Stapczynski S. 9 Emergency Medicine:
A Comprehensive Study Guide. New York: McGraw Hill
Book Company; 2003.
Kaplan NM, Rose BD. Hypertensive emergencies: 10
Malignant hypertension and hypertensive encephal-
opathy. In: Bakris GL, ed. UpToDate. Waltham, MA:
UpToDate; 2008. Available at: www.UpToDate.com.
Accessed June 8, 2010.
Wolfson AB, Linden CH, Rosen CL, Shaider J. In: 11
Harwood Nuss, ed. Clinical Practice of Emergency
Medicine. Philadelphia: Lippincott Williams and
Wilkins; 2005.
References
Mcgowan C. Hypertensive emergencies. In: Hemphill 1
RR, ed. Emedicine, Boston: Emedicine; 2007:1–5.
Varon J. Diagnosis and management of labile blood pres-2
sure during acute cerebrovascular accidents and other
hypertensive crises. Am J Emerg Med. 2007;25:949–959.
Fleming J, Meredith C, Henry J. Detection of hyperten-3
sion in the emergency department. Emerg Med J. 2005;22:
636–640.
Kitiyakara C, Guzman NJ. Malignant hypertension and 4
hyp ertensive emergencies. J Am Soc Nephrol. 1998;9:
133–142.
Varon J, Marik PE. Clinical review: The management of 5
hypertensive crises. Crit Care. 2003;7(5):374–84.
Varon J and Marik PE. The diagnosis and management 6
of hypertensive crises[see comment]. Chest. 2000;118(1):
214–227.
Table 21-2. Pharmacological Management for Hypertensive Emergencies
Drug Dosage Reference Avoid in
Labetalol 20 mg IV push over 2 minutes followed by 40–80 mg
at 10-minute intervals for max of 300 mg
Cocaine ingestion, bradycardia,
bronchospasm, heart failure
Esmolol Initial bolus: 80 mg (~1 mg/kg) over 30 seconds,
followed by a 150 mcg/kg/minute infusion
See Labetalol
(can be used in renal/liver patients)
Fenoldopan Initial: 0.1–0.3 mcg/kg/minute. May be increased in
increments of 0.05–0.1 mcg/kg/minute every 15 minutes
Elevated intraocular pressure
Nitroprusside Initial: 0.3–0.5 mcg/kg/minute; increase in increments
of 0.5 mcg/kg/minute. Usual dose: 3 mcg/kg/minute
Elevated ICP, pregnancy
Nicardipine Initial: 5 mg/hour increased by 2.5 mg/hour every
15 minutes to a maximum of 15 mg/hour
Aortic stenosis
Clevidipine Initial: 1–2 mg/hour CHF, severe AS, impaired lipid metabolism
SECTION FIVE
Cardiac Testing
309
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.
The electrocardiogram
in acute coronary syndromes
Laura Oh
1
& William J. Brady
2
1
Department of Emergency Medicine, University of Virginia School of Medicine,
Charlottesville, VA, USA
2
Vice Chair, Department of Emergency Medicine, Professor of Emergency Medicine
and Medicine, University of Virginia Health System, Charlottesville, VA, USA
22
Section I: Case presentation
A 43-year-old man presented to the emergency depart-
ment (ED) with chest pain. He had noted progressive
chest discomfort over the prior several days with exer-
tion. Now, the chest pain had come at rest approxi-
mately 30 minutes prior to presentation, and resolved
soon after presentation. He also complained of dysp-
nea and mild nausea. The past medical history was sig-
nifi cant for hypertension, tobacco use, and a parental
history of coronary disease. The physical examination
was unremarkable. The patient received an aspirin.
The initial 12-lead EKG was minimally abnormal with
nonspecifi c ST-segment–T-wave changes. The fi rst tro-
ponin level was normal.
The patient was admitted to an ED-based chest pain
center for serial biomarkers and further observation.
The patient remained pain free during the initial 4 hours
of observation; the second troponin level was still nor-
mal. However, he then developed recurrent chest pain
accompanied by diaphoresis. The electrocardiogram
(EKG) (Figure 22-1) demonstrated an inverted T wave
in lead aVl. Despite nitrates and morphine, the chest
discomfort continued. With the recurrent chest pain
accompanied by a new, although minimal, alteration of
the EKG, the management strategy changed to hospital
admission.
While awaiting an inpatient bed, the patient’s pain
worsened. ST-segment trend monitoring revealed
progressive change in the ST-segments of the inferior
leads. Ultimately, signifi cant ST-segment elevation
was noted in the leads II, III, and aVf, consistent with
an inferior ST-segment elevation myocardial infarc-
tion (STEMI) (Figure 22-2).
The patient received thrombolytics, with resolution of
the chest pain and normalization of the ST-segments.
Repeat biomarker testing was positive, indicating
acute myocardial infarction (MI).
Section II: Case discussion
with a similar history to the opening of this case: chest
pain that sounds like an acute coronary syndrome,
maybe a couple of risk factors, perhaps a past history
of ischemic cardiac disease, an EKG that is nondiag-
nostic, and a set of cardiac biomarkers that is normal.
What is a safe protocol for these kinds of patients?
Dr Richard Harrigan: At our institution, we do not
have a chest pain center, so we have to make the deci-
sion of whether to admit these patients, or send them
home. We do have a prolonged ED rule-out protocol
that involves two sets of cardiac biomarkers and two
EKGs. The problem of potentially putting this patient
into that protocol would be that his pretest probabil-
ity for cardiac disease seems rather high. He is not
that old, but he has risk factors, a story consistent
CHAPTER 22
310
typical anginal symptoms; these latter patients should
be considered for admission.
Dr Shamai Grossman: I think the problem here is
that we often don’t differentiate between what is
with possible myocardial ischemia, and it seems likely
that he has presented in-between episodes of isch-
emia. I favor the application of the two sampling rule-
out over 6 hours after presentation more in a patient
with an atypical presentation than in the patient with
Figure 22.1 Normal sinus rhythm (NSR) with “reciprocal” ST-segment depression with T wave inversion in leads I and
AVL—a potential early warning sign of inferior wall ST-segment elevation myocardial infarction.
Figure 22.2 Progressive ST-segment elevation in the inferior leads consistent with inferior wall ST-segment elevation
myocardial infarction.
THE ELECTROCARDIOGRAM IN ACUTE CORONARY SYNDROMES
311
event rate, and can be safely discharged from the
ED with appropriate follow-up. A patient who has a
higher pretest probability can still be put into an ED
chest pain or observation unit if a risk-stratifi cation
study can be done at the end of marker sampling,
regardless of the ED rule-out protocol. Higher risk
patients likely should be admitted to the hospital or,
at least, be referred to a cardiologist for evaluation
that day.
PR: How do you defi ne “unstable angina”? What is it
about the history that allows us to say that this patient
is no longer having stable angina, or has developed an
unstable event?
SG: Traditionally, unstable angina had two mean-
ings: the fi rst, new onset angina that was considered
unstable because it was new in onset, and the second
is “crescendo angina,” or angina that is progressing
over a number of days, ultimately ending in infarc-
tion. Where that terminology becomes problematic
is the scenario where a patient presents with a single
episode of chest pain, and we decide to call it “chest
pain, rule out myocardial infarction”; we obtain serial
biomarkers, and then decide that perhaps the process
is complete and negative. The problem with that is,
if it is truly unstable angina, then you are putting a
patient who has an unstable lesion on a treadmill, and
you may end up with an infarction during the testing
study, or a progression of the disease. The historical
management of the patient with unstable angina was
that patient needs admission to the hospital, needs to
be “cooled down” with heparin, ultimately with a
plan to have more diagnostic testing when the patient
is no longer symptomatic. Here, more diagnostic test-
ing would be either a risk stratifi cation study, such as
a stress test with nuclear scan, to defi ne if signifi cant
coronary obstructive lesions are present, or going to
the catheterization laboratory to defi ne and treat the
coronary artery pathologies and related obstruction.
PR: We are constantly told that a common error
that we make in emergency medicine is missing
myocardial infarction, and I do not believe it. I do
not think we are missing STEMIs, perhaps what we
are missing are some of the MIs that are very hard
to defi ne, the non-ST-segment elevation myocardial
infarctions (NSTEMIs), the right ventricular infarc-
tion, the posterior MI, and the MI in the face of
bundle branch block. When would you do special
classically called a “rule-out myocardial infarction,”
and what was traditionally called “unstable angina.”
Unstable angina suggests you are not done with your
workup when you’ve decided the patient is not hav-
ing a myocardial infarction. You clearly need to do
more investigations. Having ruled out myocardial
infarction is not going to be useful if the patient has
unstable angina. In that sense, observation units do
not always fi ll the appropriate role for all chest pain
that is possibly cardiac ischemia. If you want to know
if a specifi c event was a myocardial infarction, then,
obtaining serial biomarkers 6 hours apart is reason-
able. If you want to know whether the recurrent
events the patient is having every day were actually
ischemic in nature, then a chest pain unit may not be
the best idea for the patient, and hospital admission
may still be the most appropriate strategy.
PR: The diffi cult problem that can lead to missed
diagnosis of myocardial infarction in the emergency
department is not the STEMI presentation, but rather
patients like this one in our case today—they are hav-
ing unstable angina, yet an objective test is not always
positive or diagnostic in this presentation.
Dr William Brady: When a patient presents to the
ED with chest pain or with an anginal equivalent;
who looks ill, diaphoretic, or pale; and has obvious
ST-segment elevation on the electrocardiogram; I do
not think that anyone questions the diagnosis, nor fails
to understand the time sensitivity of the treatment. On
the other side of the spectrum is the group of patients
who have non-ST elevation acute coronary syndrome
presentations. In this situation, you must ask yourself
which diagnostic strategy are you following: ruling
out an MI, ruling out acute coronary syndrome, or
ruling out asymptomatic coronary obstructive lesion?
For some patients, you may need all three strategies.
Early on, in the fi rst minutes of presentation to the
ED, you are ruling out STEMI, then you progress into
ruling out acute coronary syndrome, at least one that
is marker-positive with an evolving EKG. After that,
with continued stability of the patient, you are evolv-
ing into “Is this an ischemic coronary syndrome with
obstructive coronary lesions?”
I believe that in patients with atypical presentations
who have an EKG that is normal, minimally abnor-
mal, or unchanged; negative serial biomarkers; and a
stable ED course; you have safely completed the ED
evaluation. These patients have a very low 30-day
CHAPTER 22
312
occluded epicardial artery responsible for their syn-
drome. Interestingly and unfortunately, none of these
patients had percutaneous coronary interventions
(PCIs) or urgent reperfusion therapy within 6 hours.
These patients had higher cardiovascular complica-
tions and mortality rates compared to patients with-
out obstruction of an epicardial artery.
PR: Carrying on with our case, the patient has a nor-
mal set of biomarkers, but then becomes symptomatic
again. What is the next most appropriate diagnostic
step?
RH: Recurrent chest discomfort: here you almost
have to restart the evaluation, which is a challenge
to the culture in the ED where we seem to think that,
if we’ve done the work, we’ve done the EKG, and
we’ve done the initial set of cardiac markers, that
we’re done; we fi nd it hard to reset the clock and
begin again with new EKGs and reevaluation. I do
not know exactly where that mindset comes from. In
this case, ST-segment trend monitoring was revealing
in this patient; if you do not have that technology
available, the poor man’s ST-segment trend moni-
toring is the serial EKG. When you have a patient
with either recurrent or ongoing chest pain, such a
scenario should trigger a response similar to that of
a new patient reevaluation, including a repeat EKG.
The most important thing you can do is to get another
EKG at that time.
SG: This situation is exactly why we do serial EKGs. I
fi nd repeating an EKG is far more valuable than extra
EKG leads, particularly when your data do not quite
provide an answer. If the patient has a classic story
for unstable angina, and the initial EKG is not reveal-
ing, then repeat it. Now, when you obtain a cardiol-
ogy consultation, you can demonstrate serial changes:
normal to nonspecifi c to worrisome ST-segments.
With this information, you have now proven that
the patient not only should be admitted to the hos-
pital, but directly to the catheterization laboratory to
address an unstable plaque.
RH: It’s easy data; it’s free, noninvasive, and easy
to obtain. One additional closing thought: from an
electrocardiographic point of view, I fi nd it interest-
ing that in our case the fi rst EKG abnormality this
patient showed us was the change in lead aVL. This
fi nding can be an early warning of impending inferior
wall STEMI.
additional lead testing on a patient who comes in
with a history like our man today with nonspecifi c
changes on the EKG?
RH: I would not have been tempted to do special
lead testing on this patient as he presented. He does
lie in a group that we have termed “prone to classic
angina”: not elderly, not female, not diabetic, and
so he should present with classic symptoms, and
indeed, he does. Whereas his EKG does not show
ischemia initially, at that time he was not having
ongoing symptoms, so that is not surprising. There
is no proven benefi t to additional lead EKGs in any
certain subpopulation in terms of decreasing mortal-
ity. However, I would be tempted to add leads when
I have ongoing ischemic symptoms without any fi nd-
ings on the 12-lead EKG. If I have ongoing symp-
toms of ischemia, but the presentation is not one of
STEMI, but rather in the right precordial leads, and
I see some degree of ST-segment depression, maybe
a taller-than-expected R wave, signaling that this
may be a posterior myocardial infarction, then, in
this instance, the addition of leads V8 and V9 would
allow you to visualize the ST-segment elevations you
are looking for to diagnose a posterior wall infarc-
tion. Lastly, in patients who present with ongoing
ischemic symptoms who have diffi cult to interpret
inferior changes (i.e., borderline ST-segment eleva-
tion or ST-segment elevations that are subtle with
more atypical characteristics), right-sided V leads
may demonstrate ST-segment elevation suggesting a
right ventricular infarction.
WB: A review looked at ST-segment depression in
the right precordial leads. The current standard
approach for patients who present with ST-segment
depression syndromes, either with or without a posi-
tive marker, is not to provide a fi brinolytic agent, but
perhaps take them to the catheterization laboratory
within 24 hours. While this approach is appropriate
in patients with NSTEMI, patients with acute poste-
rior wall infarction should not be managed with this
strategy of delayed coronary angiography. We need to
get out of the idea of looking exclusively for anatomic
segment infarctions, meaning anterior wall, inferior
wall, or lateral wall. Instead, we need to get into the
mindset of looking for an occluded artery syndrome.
This review considered patients who presented with
right precordial ST-segment depression, and notes
that more than a quarter of these patients have an
THE ELECTROCARDIOGRAM IN ACUTE CORONARY SYNDROMES
313
or catastrophic causes, of acute chest pain that are
both life-threatening in outcome and time-sensitive in
management.
4
In 2007, the Joint Task Force of the European
Society of Cardiology, American College of Cardiology
Foundation, the American Heart Association, and the
World Health Federation (ESC/ACC/AHA/WHF)
redefi ned myocardial infarction as evidence of myo-
cardial necrosis in a clinical setting consistent with
myocardial ischemia. In addition to serum biomark-
ers and pathologic evidence on autopsy, EKG changes
(e.g., new ST-segment–T-wave changes, new left bun-
dle branch block, and pathological Q waves) are rec-
ognized as central criteria in the diagnosis of MI.
5
The initially normal or minimally abnormal EKG
The single EKG is more powerful diagnostically at
ruling in than ruling out myocardial infarction. The
EKG is a highly specifi c test (at least 94%, thus its
power in the rule-in approach), but it is also highly
insensitive (25–50%, hence its inability to conclusively
rule-out).
6
Fifty percent of patients who are ultimately
diagnosed with MI will have a nondiagnostic initial
EKG. A frequent pitfall of EKG interpretation and
application is to assume that the initially normal EKG
is equivalent to a nonspecifi c EKG; further, neither
of these entities can be used to exclude the diagnosis
of MI by themselves (i.e., to the exclusion of other
clinical data). In the adult ED population, 1–4% of
patients with an absolutely normal EKG have a fi nal
diagnosis of AMI; patients with nonspecifi c EKG
fi ndings (e.g., T-wave fl attening or subtle ST-segment
deviations [⬍0.5 mm]) experience AMI in 4–8% of
cases.
7
Thus, the EKG cannot be used by itself to rule
out MI, yet the EKG, when used in the context of
other clinical data, can be useful as negative evidence
to answer the question: is the patient having an MI?
In a 2001 study by Welch et al. examining prog-
nostic value of a normal or nonspecifi c initial EKG
in AMI, patients with an initially normal EKG have a
41% lower risk of in-hospital death. The 30-day mor-
tality rate, however, is still substantial; the patients
with AMI and normal or nonspecifi cally abnormal
initial EKGs experience a composite rate of mortal-
ity and life-threatening adverse event of 19.2% and
27.5% respectively, compared with the 34.9% rate
experienced by patients with AMI and initially diag-
nostic EKG.
8
Section III: Concepts
Historical background of the electrocardiogram
The electrocardiogram (EKG) is one of the most
widely applied and cost-effective tests in emergency
medicine. Dutch scientist Willem Einthoven (1860–
1927) is credited with the discovery of the EKG, as
well as its ability to graphically record the electri-
cal activity of the heart.
1
In 1895, Einthoven him-
self questioned whether efforts to fully interpret the
EKG should be abandoned, given the uncertainty of
the recording; yet, by 1908, Einthoven had success-
fully interpreted the EKG in the clinical setting, for
which he eventually won the 1924 Nobel Prize.
2
In
the presentation speech of Einthoven’s Nobel Prize,
it was noted that Einthoven had developed a tool of
“the greatest clinical signifi cance: that different forms
of heart disease reveal themselves characteristically
in the electrocardiogram.”
2
Today, 100 years after
Einthoven’s initial EKG interpretations, the EKG
continues to play a pivotal role in the management
of the patient with suspected cardiovascular disease,
guiding not only diagnosis, but also the treatment and
disposition.
Defi nition of acute coronary syndrome
In the ED, the most frequent reason for obtaining an
EKG is chest pain. According to a 2007 Centers for
Disease Control report, 120 million patients are seen
annually in the ED, with 5.4% of these patients pre-
senting with chest pain.
3
Approximately 1 million of
these patients will develop an acute myocardial infarc-
tion (AMI). Although only a minority of patients will
have pain of cardiac origin, the priority for a patient
presenting with chest pain suspected of acute coronary
syndrome (ACS) is identifi cation of ST-segment eleva-
tion myocardial infarction. The term acute coronary
syndrome is used to describe a spectrum of myocardial
injury syndromes inclusive of unstable angina (UA),
non-ST elevation myocardial infarction, and ST eleva-
tion myocardial infarction. In UA, the EKG is consis-
tent with reversible ischemia and the biomarkers are
normal. In NSTEMI, the EKG may initially be indis-
tinguishable from UA, but biomarkers will be elevated
in a “typical rise and fall pattern.” In STEMI, the
EKG will show ST elevation and biomarker elevation.
AMI and UA (along with aortic dissection, pulmonary
embolism, tension pneumothorax, and esophageal
rupture) represent two of the six priority diagnoses,
CHAPTER 22
314
Several ACS risk stratifi cation algorithms have been
developed to aid the clinician, such as the Thrombolysis
in Myocardial Infarction (TIMI) risk score, Global
Registry of Acute Events (GRACE) score, Goldman
Criteria, Sanchis score, and the Vancouver Chest
Pain Rule.
12–17
One of the clinical questions that the
ED physician seeks to answer in evaluating patients
with suspected ACS is determining which patients
can be safely discharged from the ED. Unfortunately,
the fi rst four algorithms above were not designed for
this purpose; they are primarily used for risk stratifi -
cation in admitted patients, and cannot be applied to
determine if discharge of an ED patient is appropri-
ate. The Vancouver Rule is unique in that it identifi es
with 98.8% sensitivity very low-risk patients who are
able to be discharged early from the ED; these include
patients under 40 who have a normal EKG and no
prior history of ischemic chest pain, those over 40 and
low-risk pain characteristics (no radiation of pain, no
increase with deep breath or palpation) with an initial
CK-MB under three, and those over 40 and low-risk
pain characteristics with a CK-MB over three but no
change in EKG or CK-MB 2 hours after arrival.
16
The
Vancouver rule, however, has yet to be prospectively
validated.
New algorithms, serial biomarker rule-out proto-
cols, and chest pain units all hold promise as means to
decrease the 2% diagnostic error rate in AMI. Twenty-
fi ve percent of the patients who are mistakenly dis-
charged, however, are sent home likely because of a
more fundamental error—an error in the interpreta-
tion of the EKG itself.
14
EKG changes refl ecting non-ST-segment elevation
syndromes: T-wave inversion, ST-segment
depression, and the U wave
T-wave inversion
Repolarization is more sensitive to ischemia than depo-
larization; therefore, ST-segments and T waves are the
portions of the EKG primarily affected when there is
an increased myocardial demand for oxygen.
18,19
The
myocardium normally depolarizes from endocardium
to epicardium, and repolarizes in the opposite direc-
tion. When there is extensive ischemia, it causes a delay
in the repolarization so that the direction of repolar-
ization reverses, resulting in a T-wave inversion.
20
In a
normal EKG, the T wave is upright in most leads and
inverted in lead aVR. Normal T-wave inversions may
Roughly 2% of patients who present to the ED with
AMI are incorrectly discharged, and these patients do
less well than their admitted counterparts. A study by
Pope et al. examined the incidence and clinical out-
come of failure to hospitalize patients with acute car-
diac ischemia. Nonhospitalized patients with MI have
a 30-day risk of death that is 1.9 times that of hos-
pitalized MI patients, and nonhospitalized patients
with UA have a 30-day risk of death that is 1.7 times
that of hospitalized UA patients.
9
The missed MI also
accounts for a signifi cant portion of malpractice dol-
lars in the United States.
4
The EKG and risk stratifi cation
The EKG is best used with Bayesian principles in
mind: the interpretation of the EKG is a biologic test,
and the result depends on the patient’s pretest prob-
ability of disease.
10
In a patient with a 90% pretest
probability of infarction, a negative EKG would only
decrease posttest probability of infarction to 80%.
4
A
patient with a 10% pretest probability and the same
negative EKG would have a different management
plan. This Bayesian approach is best summed in the
following statement: interpret the EKG within the
context of the clinical presentation.
Pretest probability is either derived by the clinician’s
individual judgment or by clinical decision rules.
Assigning a patient’s pretest probability of disease
based on experience is no easy task. In a 2004 study
by Miller et al., ED physicians were asked to predict
based on history, physical, and EKG whether chest
pain in 17,737 patients was cardiac or noncardiac in
nature; 2.8% of patients whom physicians believed
to have noncardiac chest pain experience an adverse
event.
11
Up to one-third of patients with ACS do not
experience chest pain, and atypical features often used
by clinicians to exclude the diagnosis of ACS (repro-
ducible chest wall pain, pleuritic pain) carry odds
ratios (0.6 for each) that cannot exclude the diagno-
sis reliably.
8
According to Pope et al., preconceptions
about heart disease in women and nonwhite popu-
lations and atypical presentation likely contribute to
misdiagnosis of ACS. Women less than 55 years old
have an odds ratio of 6.7 for inappropriate discharge,
while nonwhite persons have an odds ratio of 4.5.
Patients with an initial normal or nondiagnostic EKG
have an odds ratio of 7.7.
9