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ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
45
If there are also ST elevations in leads V5, V6, I, and
aVL, the location of the LAD occlusion is likely to
be proximal to the fi rst diagonal branch, resulting in
an anterolateral MI (see Figure 3-1). Inferior infarc-
tions (Figure 3-2) are characterized by ST elevations
in leads II, III, and aVF, and are most commonly
due to occlusion of the right coronary artery (RCA).
With inferior MI, reciprocal ST depressions may also
be present in leads I and aVL. Inferior MIs may be
complicated by concomitant right ventricular (RV)
infarction, which can be evident on right-sided EKG
leads, particularly in RV4 and RV5. Inferior MIs
may also be associated with posterior wall involve-
ment, which is seen on an EKG as ST depressions in
leads V1-V3, and often, early R wave progression
with tall R waves in V1-V3 (Figure 3-2). Posterior
MIs in isolation are the rarest of transmural MIs,
and the most easily misdiagnosed. This is because
the EKG will generally show ST depressions in V1,
V2, V3 and sometimes V4 and V5, often with tall R
waves in V1-V3, but without evidence of ST eleva-
tions. Such fi ndings may be mistakenly attributed to
non-transmural anterior wall ischemia. Clues to the
diagnosis of isolated posterior wall infarction are
the horizontal (rather than sloping) nature of the ST
depressions, prominent R waves, and tall upright T
waves in leads V1-V3.
ST-segment elevation must be at least one millimeter
above the baseline, which generally is measured at
the T-P segment. Most typically, the ST elevation in
patients with a STEMI will be convex or domed; less
commonly it may be straight or even rarely concave
in appearance. Concave ST-segment elevations are
more characteristic of conditions other than a STEMI,
including pericarditis, benign early repolarization, left
bundle branch block, left ventricular hypertrophy or
aneurysm, paced ventricular rhythms, Prinzmetal’s
(variant) angina, hyperkalemia, hypothermia with
Osborne waves, intracranial hemorrhage, Brugada’s
syndrome, and a normal variant.
In addition to the clinical history, another impor-
tant feature that helps distinguish a STEMI from other
conditions is the dynamic nature of the ST-segment
abnormalities seen with a STEMI. The importance,
therefore, of serial EKGs in patients with a suspected
STEMI cannot be underscored enough. The EKG
leads involved with the ST elevations generally corre-
spond to anatomic location of the myocardial infarc-
tion, and the associated vessel. Anterior myocardial
infarctions generally exhibit an ST elevation in leads
V1-V4, while an ST elevation in leads V1-V2 is more
specifi cally indicative of involvement of the septum.
These infarctions are caused by acute occlusion of
the left anterior descending (LAD) coronary artery.
Figure 3.2 12-lead EKG shows ST elevation in leads II, III, and avF, as well as ST depressions in leads V1-V3 consistent with
acute inferoposterior STEMI. Note also the reciprocal ST depressions in leads I and avL. Reproduced with the permission of
David F. M. Brown, M.D.
CHAPTER 3
46
are detectable 4–10 hours after the onset of myo-
cardial cell death. In addition to troponins, creatine
phosphokinase MB fraction and myoglobins are also
frequently used.
Despite their limitations in the early stages of
STEMI, cardiac biomarkers should nonetheless be
sent along with a chemistry panel, complete blood
count, and coagulation studies for ED laboratory
analysis.
Imaging studies are also generally unhelpful in the
diagnoses of a STEMI. Chest radiography is usually
normal or unchanged from baseline. Nonetheless, it
is indicated as it may help exclude other causes of
chest pain, including pneumothorax, pneumonia,
Boerhaave’s syndrome, and, to a lesser degree, aortic
dissection. In addition, the chest fi lm can be valuable
when a STEMI is complicated by congestive heart
failure.
Treatment
After attending to the ABCs, the primary focus of
treatment of a STEMI within 12-24 hours of symp-
tom onset is urgent rapid revascularization of the IRA.
This may be accomplished either with intravenous
fi brinolytic therapy or with catheter-directed primary
percutaneous coronary intervention (PCI). Although
Occasionally, isolated posterior wall MI will pres-
ent with a nondiagnostic 12-lead EKG, and the diag-
nosis can only be confi rmed when extended EKG
leads, placed inferior to the tip of the left scapula (V8)
and in the left paraspinal line at the same level (V9),
reveal small pathognomonic ST elevations. Posterior
wall MIs are the result of occlusion of the posterior
descending coronary artery or the posterior left ven-
tricular branch, either of which may be a branch from
the RCA (more commonly) or the left circumfl ex cor-
onary artery. Lateral wall MIs are characterized by an
ST elevation in some or all of leads I, aVL, V5 and V6
(Figure 3-3). They may occur in isolation, or they may
be associated with anterior MIs as described earlier or
with inferior or posterior MIs. This is because the lat-
eral wall of the heart is variably supplied with blood
by the LAD, the left circumfl ex, and the RCA. Isolated
lateral wall MIs are most frequently found with left
circumfl ex occlusion, and the EKG often shows recip-
rocal ST depressions in leads II, III, and aVF.
Laboratory studies are generally unhelpful in the
diagnosis of a STEMI. Although there are numerous
cardiac biomarkers that will rise during myocardial
infarction, none currently available are suffi ciently
sensitive or specifi c in a time frame that is useful for
the emergency physician. The most sensitive and spe-
cifi c of these at the current time are troponins, which
Figure 3.3 12-lead EKG shows ST elevation in leads I and avL consistent with acute lateral STEMI. Note also the reciprocal
ST depressions in leads III and avF. Reproduced with the permission of David F. M. Brown, M.D.
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
47
PCI capability. Rapid treatment is again important,
with a target goal “door-to-needle” time of less than
30 minutes. Fibrinolytic therapy is indicated for
patients who present with symptoms consistent with
a STEMI within 12–24 hours of symptom onset, meet
the EKG criteria (Table 3-1), and do not have an abso-
lute contraindication (Table 3-2). The presence of rel-
ative contraindications (Table 3-3) must be weighed
against the risk of treatment delay when primary PCI
is not readily available.
fi brinolytic therapy remains the most common strat-
egy worldwide, primary PCI is considered preferable
in terms of safety and effi cacy, and has become the
more common choice in the US. When a primary PCI
strategy is chosen, the IRA must be opened within
90 minutes of patient arrival to the hospital in order
to achieve maximum effi cacy.
2
This interval is referred
to as the door-to-balloon (DTB) time. Note that the
90-minute DTB time includes time spent at the initial
hospital if transfer to a PCI-capable facility is required.
If a 90-minute DTB time cannot be routinely achieved,
then revascularization with a fi brinolytic agent is pref-
erable; this is particularly the case for those patients
who present early (within 3 hours of symptom onset).
2
For patients in cardiogenic shock or in those with
absolute contraindications to fi brinolytic therapy, pri-
mary PCI should be performed as soon as possible. In
addition, those patients with a STEMI who fail to rep-
erfuse with fi brinolytic therapy, as evidenced by ongo-
ing anginal symptoms and persistent ST elevations an
hour or more after treatment, should be referred for
rescue PCI, which should be performed as soon as
possible.
Patients with a STEMI who are treated with pri-
mary PCI should also receive aspirin, clopidogrel, and
unfractionated heparin (UFH) as discussed below.
While it is reasonable to also treat these patients with
a GP 2b-3a inhibitor, which inhibits the fi nal common
pathway of platelet aggregation, there is no evidence
that administering this in the ED is more effi cacious
than at the time of PCI in the catheterization labora-
tory.
3
None of these adjunctive therapies should delay
transfer of the patient from the ED to the cardiac cath-
eterization laboratory, which is the highest priority. A
number of validated strategies should be utilized to
decrease DTB time. Those that specifi cally involve the
ED include (A) empowering the emergency physician
to activate the entire cardiac catheterization labora-
tory team with a single page, (B) increasing the capac-
ity to obtain prehospital EKG tracings on patients
with chest pain, and allowing subsequent activation
of the catheterization team for those patients with a
fi eld-identifi ed STEMI while still en route to the hospi-
tal, and (C) providing prompt feedback to all clinical
providers involved in the care of the patient.
4
Despite the focus on primary PCI in recent years,
fi brinolytic therapy remains a viable treatment option
for patients with a STEMI; this is especially true for
those who present to community hospitals that lack
Table 3-1. EKG criteria for fi brinolytic therapy.
1. ST segment elevation of ⬎0.1 mV in two or more
contiguous leads
2. Left bundle branch block not known to be old
3. ST-segment depressions and prominent R waves in
leads V1-V4
Table 3-2. Absolute contraindications to fi brinolytic
therapy.
1. Prior history of intracranial hemorrhage
2. Known cerebrovascular lesion (e.g., arteriovenous
malformation)
3. Known malignant intracranial neoplasm
4. Suspected aortic dissection
5. Active bleeding (excluding menses) or known bleeding
diasthesis
6. Signifi cant closed head or facial trauma within 3 months
7. Ischemic stroke within 3 months (except if within
3 hours)
Table 3-3. Relative contraindications to fi brinolytic
therapy.
1. Uncontrolled hypertension on presentation (SBP
greater than 180 mm\Hg or DBP greater than
110 mmHg)
2. History of chronic severe poorly controlled
hypertension
3. Prior ischemic stroke greater than 3 months
4. Traumatic or prolonged (⬎ 10 minutes) CPR
5. Recent major surgery (less than 3 weeks)
6. Recent (within 2 to 4 weeks) internal bleeding
7. Noncompressible vascular punctures
8. Pregnancy
9. Active peptic ulcer
10. Current use of anticoagulants
CHAPTER 3
48
normal. This will reduce any areas of the lung that
are poorly oxygenated, which in turn will reduce the
possibility of shunting and subsequent hypoxia.
Platelet inhibitors are indicated as well, with aspirin
remaining the most important of these agents. Aspirin is
inexpensive, well tolerated, and independently reduces
mortality by approximately 23%.
7
It should be admin-
istered orally (chewed and swallowed) or rectally in a
standard dose of 162–325 mg. Enteric-coated prepara-
tions should be avoided. The only contraindication is a
prior history of severe allergic reaction, in which case
clopidogrel should be administered in its stead.
Clopidogrel is also indicated in the treatment of a
STEMI. Clopidogrel is a thienopyridine, a class of drugs
that inhibits ADP-mediated platelet aggregation. As an
adjunct to fi brinolytic therapy, clopidogrel has been
shown to improve clinical outcomes when a 300-mg
oral loading dose is given with aspirin, as compared to
aspirin alone.
8
For those STEMI patients undergoing a
primary PCI, it is reasonable to administer clopidogrel
with or without a loading dose, though this may instead
be deferred until the time of catheterization.
Beta-blockers are an important therapy for patients
with STEMI, although their role has been dimin-
ished in the most recent ACC/AHA guidelines.
9
Beta-
blockers reduce the effects of catecholamines on the
heart, slowing the heart rate, and reducing myocardial
contractility, thereby reducing myocardial demand
for oxygen. They are also effective antidysrhythmic
agents, reducing the risk of ventricular fi brillation
associated with a STEMI. However, beta-blockers
also increase the risk of development of cardiogenic
shock in patients with a STEMI, particularly in those
patients over age 70, those with heart rate ⬍60 beats/
min, or blood pressure ⬍120 mmHg.
10
In these lat-
ter subsets of patients, beta-blockers should not be
given intravenously, though they may still be given
orally. Absent these conditions, beta-blockers may
still be given intravenously, though it may be more
prudent to administer them only orally in patients
with a STEMI. Several different agents are available,
including metoprolol, atenolol, propranolol, and the
ultra-short-acting esmolol. Beta-blockers in any form
are contraindicated in patients with AV nodal block,
bradycardia, hypotension, asthma, and acute severe
congestive heart failure.
Anticoagulant therapy is indicated for patients with
a STEMI who are being treated with fi brin-specifi c
fi brinolytic agents, or with a primary PCI. At present,
There are several fi brinolytic agents available.
Streptokinase, which is not fi brin specifi c and is admin-
istered as an intravenous infusion of 1.5 million units
over an hour, is used mostly outside the United States,
and has the advantage of being rather inexpensive. In
the United States, fi brin-specifi c agents are used almost
exclusively; the fi rst of these to be developed was tis-
sue plasminogen activator (t-PA), which is delivered
as a bolus followed by two separate weight-adjusted
infusions. This regimen is cumbersome, and it is easier
and safer to administer one of the bolus fi brin-specifi c
agents, retavase (r-PA) or tenecteplase (TNK), which
have equivalent clinical effi cacy and similar costs to
t-PA. Dosing of r-PA is a non-weight adjusted double
bolus of 10 units intravenously at time zero and again
at 30 minutes. TNK is administered in a weight-tiered
fashion as a single bolus of 30–50 mg. An additional
advantage of the bolus agents is that they are easy to
administer in the prehospital setting if that is a consid-
eration. All STEMI patients who are treated with fi brin-
olytic therapy should also receive aspirin, clopidogrel,
and beta-blockers in the absence of contraindications
(see above). If a fi brin-specifi c agent is administered,
UFH should also be given in a dose of 60 units/kg
(maximum of 5000 units) and an infusion of 12 units/
kg/hr (maximum 1000 units/hr). Enoxaparin can be
safely and effectively substituted for UFH in patients
with normal renal function who are less than 75 years
of age.
5
Heparin preparations should not be given to
patients treated with streptokinase.
There has been considerable interest in combina-
tion pharmacological therapy for a STEMI during
the past decade. The most promising combination
has been half-dose fi brinolytic therapy paired with
full dose GP 2b-3a inhibitor. This combination pro-
vides better angiographic outcomes in the IRA at
90 minutes; however, no mortality benefi t has been
shown in large clinical trials.
6
Combination therapy
does appear to confer a small reduction in the risk of
recurrent MI, and in the need for rescue angioplasty.
6
However, it is more expensive than standard fi brin-
olytic therapy, and more cumbersome to administer.
Hence, despite being an FDA-approved regimen for a
STEMI, it should be utilized only in remote locations
where transfer for rescue PCI is very diffi cult.
In addition to prompt revascularization treatment, a
number of adjunctive agents are indicated in the treat-
ment of a STEMI. Oxygen should be administered to
all patients, even if the initial oxygen saturation is
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
49
may cause hypotension or sedation. The latter may
compromise respiratory drive, and increase the risk
of aspiration.
Prognosis
All patients with a STEMI should be admitted to a
cardiac intensive care unit under the care of a cardi-
ologist. The short-term prognosis for those patients
with a STEMI who are treated with prompt revascu-
larization and state of the art adjunctive therapies is
quite good. Thirty-day mortality is between 5–6% in
most studies, and is generally related to complications
of a STEMI, which may be mechanical or electrical.
Complications of a STEMI
Bradyarrhythmias frequently complicate a STEMI,
occurring in 25–30% of cases. The most common
fi nding is sinus bradycardia, which is generally due
to a predominance of vagal tone seen in a signifi cant
subset of STEMI patients. Sinus node dysfunction
(sinus arrest or sinus exit block) may also compli-
cate a STEMI (Figure 3-1), again generally related to
increased vagal tone (rather than sinus node ischemia
or infarction, which is rare). Sinus node-related bra-
dyarrhythmias rarely need acute therapy, with pacing
reserved for those with evidence of impaired cardiac
output related to the slow heart rate. Generally, when
the acute phase of the MI is over, balance between the
sympathetic and parasympathetic nervous systems
is restored, and the sinus node function recovers.
Atrioventricular (AV) nodal block is a more ominous
fi nding when it complicates a STEMI, particularly
when associated with an acute anterior MI. While
an AV block may be due to increased vagal tone in a
subset of patients with acute inferior MI, it indicates
extensive myocardial necrosis when complicating
an acute anterior MI. High grade AV block (Mobitz
type II second degree or third degree block) in the
latter setting responds poorly to therapy, and carries
a markedly increased mortality. First line therapy in
the ED is directed at transcutaneous pacing. Atropine
should be avoided, as it is not likely to be effective,
and will increase the risk of a ventricular tachydys-
rhythmia by creating unopposed sympathetic stimula-
tion of ischemic myocardium. Figures 3-4 and 3-5 are
examples of 2:1 AV block and third degree AV block
complicating an acute STEMI.
available agents include unfractionated heparin (UFH),
low molecular weight heparin (LMWH), and direct
thrombin inhibitors. The principal LMWH utilized in
patients with ACS is enoxaparin. The heparins (UFH
and enoxaparin) activate antithrombin-3, which in
turn inhibits thrombin and factor Xa. Enoxaparin also
directly inhibits factor Xa. Direct thrombin inhibi-
tors, which include argatroban and bivalirudin, act
directly on thrombin. The end result of therapy with
any of these anticoagulant drugs, is the prevention of
the conversion of fi brinogen to fi brin, thereby limit-
ing thrombus propagation. These drugs are contrain-
dicated in patients with active bleeding. In addition,
the heparins are contraindicated in patients with a
history of heparin-induced thrombocytopenia (HIT).
For patients with a STEMI who are being treated with
a primary PCI, UFH is administered as an intrave-
nous bolus of 60 units/kg (maximum 5000 units) fol-
lowed by an infusion of 12–15 units/kg/hr (maximum
1000 units/hr). If fi brin-specifi c fi brinolytic therapy
is being utilized as the revascularization strategy, the
maximum bolus dose of UFH should be reduced to
4000 units, and the infusion rate limited to 12 units/
kg/hr (maximum 1000 units/hr).
1
Enoxaparin (1 mg/
kg
2
b.i.d. with a 30 mg IV loading dose for those
older than 75 years of age without increased bleed-
ing risks) may be substituted for UFH as an adjunct
to fi brin-specifi c fi brinolytic therapy.
5
Note that if
streptokinase is utilized as the fi brinolytic agent, no
adjunctive use of an anticoagulant is necessary. Use of
direct thrombin inhibitors, which are very expensive
and have not been shown to be superior to the hepa-
rins, should be limited to those patients with a known
history of HIT.
Nitrates, which are available in a number of forms,
may be used in patients with a STEMI. Most commonly,
sublingual tablets are administered fi rst, followed by
an intravenous infusion of nitroglycerin as tolerated
and needed. While nitrates may reduce symptoms of
chest pain, there is no evidence that they reduce mor-
tality. As such, since they may cause hypotension, they
should be used judiciously, and withheld from patients
with hypotension, RV infarction, and recent (within
24–48 hours) phosphodiesterase inhibitor use.
Morphine sulfate is an intravenous opioid analge-
sic agent that has a very limited role in the treatment
of patients with a STEMI. It may be administered
in small doses (2–5 mg increments) to patients with
refractory ischemic pain or anxiety, but morphine
CHAPTER 3
50
drug class of choice, or directed at treating the underly-
ing causative condition (e.g., congestive heart failure).
Rapid atrial fi brillation of presumed new onset, com-
plicating a STEMI is best treated with sedation and car-
dioversion. Ventricular tachydysrhythmias (ventricular
Tachydysrhythmias are frequent complications of
a STEMI. Most are supraventricular in origin, with
sinus tachycardia and atrial fi brillation the most com-
mon entities. Treatment for a sinus tachycardia may be
pharmacological, with intravenous beta-blockers the
Figure 3.4 12-lead EKG shows ST elevation in leads II, III, and aVF consistent with inferior STEMI complicated by 2:1 AV
block. Reproduced with the permission of David F. M. Brown, M.D.
Figure 3.5 12-lead EKG shows ST elevation in leads II, III, and aVF with ST depressions in leads V1-V3 consistent with acute
inferoposterior STEMI complicated by third-degree AV block. Reproduced with the permission of David F. M. Brown, M.D.
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
51
preload, which may require several liters of intravenous
crystalloid, and should not require the use of inotropic
agents. The presence of a RV infarction complicating
an acute inferior MI increases the mortality rate to that
of anterior MI.
Myocardial rupture may be a complication of an
AMI. While the majority of cases occur several days
after a STEMI, approximately one-third of cases will
develop in the fi rst 24 hours. Depending on the site of
rupture, the patient may present with sudden death
or with acute mitral valve regurgitation (due to papil-
lary muscle rupture), acute ventricular septal defect
(VSD) (due to septal infarction and rupture) or acute
cardiac tamponade (due to free wall rupture). Acute
mitral regurgitation (MR) and acute VSD will pres-
ent similarly with severe and abrupt hemodynamic
instability, coupled with acute pulmonary edema and
a new very loud systolic murmur. Clinically, inferior
and posterolateral MIs are associated with papillary
muscle rupture, while anteroseptal MIs are associated
with an acute VSD. Distinguishing between the mur-
murs of MR (a blowing systolic murmur loudest at
the apex) and a VSD (a harsh systolic murmur heard
best at the left sternal border) is diffi cult because of
the marked pulmonary rales that are invariably pres-
ent. Diagnosis is confi rmed by echocardiography with
doppler imaging, or by cardiac catheterization with
left ventriculography. Both conditions are acute car-
diac surgical emergencies, and require immediate sur-
gical intervention. Temporizing measures in the ED
include intubation and mechanical ventilation with
100% oxygen, and afterload reduction with an agent
such as nitroprusside, if tolerated. Fibrinolytic ther-
apy is not indicated. Acute mitral valve regurgitation
may also complicate an ACS due to ischemia and dys-
function of a papillary muscle rather than infarction
and rupture. In this situation, efforts should focus on
the treatment of the myocardial ischemia as well as
managing the acute pulmonary edema.
Free wall myocardial rupture may present as sudden
death, or with fi ndings of acute or subacute cardiac
tamponade. The absence of classic EKG fi ndings of a
pericardial effusion (electrical alternans or low QRS
voltage) does not exclude this diagnosis. Presenting
symptoms include agitation, recurrent chest pain, and
altered mental status. Signs include a precipitous fall
in blood pressure, tachycardia, and jugular venous
distention with signs of pulmonary edema. Mortality
in this situation is high, and immediate cardiac
tachycardia and ventricular fi brillation) occur less fre-
quently as complications of an acute myocardial infarc-
tion (AMI). Primary ventricular fi brillation (VF) is seen
in approximately 4% of patients, and more than half
of these episodes occur in the fi rst four hours after the
onset of symptoms. Treatment is immediate defi brilla-
tion for VF and pulseless ventricular tachycardia (VT).
For patients with a VT who are awake and maintaining
a normal blood pressure, time may be taken for intra-
venous sedation followed immediately by synchronized
cardioversion.
Pump failure or acute left ventricular dysfunction
is a common complication of a STEMI. It can present
across the spectrum of severity from mild congestive
heart failure to cardiogenic shock. Cardiogenic shock
is present if there is severe impairment of cardiac out-
put that is unresponsive to efforts to increase preload,
and causes impaired end-organ perfusion, as indicated
by such fi ndings as hypotension, pulmonary edema,
altered mental status, and reduced urinary output.
Generally, cardiogenic shock is associated with exten-
sive myocardial necrosis of over half of the left ven-
tricle, and carries a very poor prognosis. It must be
distinguished from other conditions that may cause
shock in the setting of a STEMI, including pericardial
tamponade, acute valvular incompetence, and acute
ventricular septal defect. Cardiogenic shock should be
treated by mechanical intervention as rapidly as pos-
sible, which generally involves placement of an intra-
aortic balloon pump and emergent revascularization
via either PCI or coronary artery bypass grafting.
Temporizing measures in the ED include intuba-
tion and mechanical ventilation with 100% oxygen,
intravenous crystalloid to increase preload, inotropic
agents (e.g., dobutamine) to improve cardiac contrac-
tility, and afterload reduction with an agent such as
nitroprusside, if tolerated. Fibrinolytic therapy may
be utilized as a last resort when mechanical interven-
tion is not available, but there is little evidence that
this improves mortality.
A RV infarction can complicate an acute inferior MI,
or, much more rarely, may occur in isolation. Right-
sided electrocardiographic chest leads, if obtained, may
show pathognomonic ST elevations in lead R-V4 or
R-V5, but the absence of this does not exclude the diag-
nosis. A RV infarction presents clinically with hypoten-
sion or a marked hypotensive response to agents that
reduce preload, such as nitrates. A RV infarction is
generally well treated with aggressive efforts to restore
CHAPTER 3
52
Section IV: Decision making
An immediate EKG should be performed in all •
patients with chest pain or other anginal equivalent
symptoms.
A revascularization strategy should be in place in •
all EDs that allows a DTB of less than 90 minutes
or a door-to-needle time of less than 30 minutes in
the vast majority of cases.
Aspirin should be given to all patients with a •
STEMI except those with a true allergy.
Clopidogrel, unfractionated heparin, and judicious •
use of beta-blockers are also indicated in appropriate
patients with a STEMI.
For patients treated with a primary PCI, no •
adjunctive treatment should be allowed to delay
transfer to the catheterization laboratory.
Anticipate and treat electrical and mechanical •
complications of a STEMI as they arise.
All patients with a STEMI require admission to a •
coronary care unit.
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diocentesis is indicated as a temporizing measure in
the ED for patients in extremis. Be aware that intuba-
tion and positive pressure ventilation in the setting of
tamponade (an extremely pre-load dependent state)
can cause critical hemodynamic collapse because of
the deleterious effect of positive pressure ventilation
on preload.
Pericarditis can complicate AMI, either in the
fi rst week (infarct pericarditis) or in a more delayed
fashion (a Dressler’s syndrome). Infarct pericarditis
presents with new chest pain that is often pleuritic
or positional in nature. Pathologically, the pericardial
infl ammation is limited to the area adjacent to the
transmural myocardial infarction. A Dressler’s syn-
drome presents weeks to months after an AMI, and
is characterized by fever and malaise as well as pleu-
ritic or positional chest pain. In either case, there may
be a pericardial friction rub, and the EKG may show
the new characteristic ST changes and PR depressions
seen in pericarditis. Non-steroidal anti-infl ammatory
drugs are fi rst line therapy. Echocardiography can be
performed to assess for the presence of pericardial
effusion if there is a clinical concern for impending
tamponade, and while not often necessary to deter-
mine in the ED, may enable the patient to be safely
discharged home if there is no sign of an effusion.
An acute cerebrovascular accident (CVA) can com-
plicate an AMI, with ischemic thromboembolic stroke
being the most common kind of stroke seen. Sources
of thromboembolism in AMI include the left ventricle,
which may have mural thrombus in areas of hypoki-
nesis; the left atrium, particularly if atrial fi brillation is
present; and the carotid artery if there is concomitant
carotid artery disease. A hemorrhagic CVA is a par-
ticular risk in patients with a STEMI who are treated
with fi brinolytic therapy, occurring in approximately
0.9% of such cases, with the incidence sharply higher
in the elderly. This accounts for the lower overall risk
of stroke in patients with a STEMI treated with pri-
mary PCI (0.7%) compared with those treated with
fi brinolytic therapy (1.6%).
The long-term prognosis after a STEMI is related to
the size of the infarct, and the severity of the under-
lying coronary artery disease. Patients who develop
congestive heart failure or ventricular dysrhythmias
have higher mortality rates. Improved survival may be
seen after aggressive risk factor modifi cation.
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
53
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focused update of the ACC/AHA 2004 Guidelines
54
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.
Unusual causes of
myocardial ischemia
Robin Naples
1
& Richard Harrigan
2
1
Assistant Professor of Emergency Medicine, Temple University School of Medicine,
Philadelphia, Pennsylvania, USA
2
Professor of Emergency Medicine, Temple University School of Medicine, Philadelphia,
PA, USA
4
Section I: Case presentation
A 31-year-old woman with a history of hyperten-
sion and a possible transient ischemic event presented
with complaints of “not feeling well for four days.”
Specifi cally, she complained of intermittent mid-ster-
nal to left precordial chest pain that was nonpleuritic,
which had lasted for minutes before resolving spon-
taneously. Associated symptoms included dyspnea,
diaphoresis, lightheadedness, and a near syncopal
episode occurring shortly prior to presentation. She
also complained of an increasing global weakness
over that period of time. Enroute to the emergency
department (ED), the blood pressure was noted to be
70/40 mmHg by the paramedic team.
The past medical history was signifi cant for a chole-
cystectomy, hypertension, and a transient ischemic
attack (TIA). An echocardiogram 2 months prior
showed an ejection fraction of 60%, and trivial
mitral regurgitation. Current medications included
aspirin, clopidogrel, and irbesartan/hydrochlorothi-
azide. The social and family histories were noted for
prior tobacco use, no illicit drug use, and no known
coronary artery disease or coagulation disorders.
On physical examination, the vital signs were: tem-
perature 36.8⬚C (98.2⬚ F), pulse 84 beats/min, respi-
rations 22 breaths/min, blood pressure 88/52 mmHg
and O
2
saturation 100%. The skin was nondiapho-
retic, the eyes had no conjunctival pallor, and the neck
was without jugular venous distention. The lungs
were clear. The cardiovascular examination showed a
regular rate and rhythm without murmurs, gallops, or
rubs. The abdomen was soft, nontender, and without
masses or bruits. The extremities showed equal pulses
and no peripheral edema. The neurologic examina-
tion showed a questionable ptosis, mild symmetric
motor weakness, and normal deep tendon refl exes.
Laboratory studies were notable for a potassium of
2.5 mmol/L. A complete blood count, urinanalysis,
BNP, troponin, and CPK were within normal limits.
A chest X-ray study was normal, and CT angiography
showed no pulmonary embolism. The electrocardio-
gram (EKG) is noted in Figure 4-1.
Section II: Case discussion
Dr David Brown: What would be your initial approach
to a patient like this who presents with these com-
plaints and the EKG fi ndings as outlined?
Dr Shamai Grossman: This EKG is worrisome for car-
diac ischemia and injury, and the story could be consis-
tent with cardiac ischemia. Even 31-year-old women
do have cardiac ischemia, although they don’t rep-
resent the most common population for this disease.
Particularly concerning in this case is that this patient
is hypotensive with a blood pressure of 70 mmHg
while with the paramedics, and still fairly hypotensive