Managing STEMI Mimics

in the Prehospital Environment

The Problem: Most STE is not
MI

… and most providers can’t

tell the difference
“Unfortunately, STE is a not an
uncommon finding on the ECG of
the chest pain patient; its cause
infrequently involves AMI.”

Brady et al., Electrocardiographic ST-

segment elevation: correct identification
of acute myocardial infarction (AMI) and
non-AMI syndromes by emergency
physicians (Acad Emerg Med 2001;
8(4):349-360)
How common?

Brady et al., Cause of ST segment abnormality in

ED chest pain patients (Am J Emerg Med 2001
Jan;19(1):25-8)

• Retrospective review of ED charts over

3-month period
• Looked at 902 adults with cc “chest
pain”
• Looked for STE in contiguous leads,
>1mm limb leads, >2mm precordials
• Compared final diagnoses, MI vs. other
Results

Only 15% of STE patients had MI!

85% had non-MI diagnosis

What were they?
• Left Ventricular Hypertrophy — 25%
• Left Bundle Branch Block — 15%
• AMI — 15%
• Benign Early Repolarization — 12%
• Right Bundle Branch Block — 5%
• Nonspecific BBB — 5%
• Ventricular aneurysm — 3%
• Pericarditis — 1%
• Undefined/unknown — 17%

STEMI-mimic was 6 times as likely as STEMI!

MI was not even single most likely cause!
In other words:

Any monkey can recognize ST elevation

STEMI recognition and diagnosis

requires distinguishing MI from non-
ischemic causes
How do we do at this?

Bad!

51% false-positive rate

Sejersten et al. Comparison of the Ability of
Paramedics With That of Cardiologists in
Diagnosing ST-Segment Elevation Acute
Myocardial Infarction in Patients With Acute
Chest Pain (Am J Cardiol 2002 Nov 1;90(9):995-8)

Half of our diagnoses were wrong

Why does it matter?

Maybe it doesn’t!

Overtriage is better than undertriage…

Maybe it’s better to play it safe…

But there are downsides

Downsides of false positive STEMI
diagnoses

• Compromises systems. Cath labs that

can’t rely on you eventually won’t activate
for you. Increased D2B times.
• Weakens true positives. If you lack
confidence in recognizing mimics, you’ll lack
confidence in making the call for true
STEMI.
• Degrades professional respect. Field
providers that do their job right encourage
further development of progressive EMS-
hospital interfaces.
More downsides of false positive STEMI
diagnoses

• Missed alternate diagnoses. Some non-

MI diagnoses are also critical – think aortic
dissection, hyperkalemia, etc. “Call it
STEMI” is not always “playing it safe.”

• Wrong treatment. Nitro? Aspirin?

Fibrinolytics? Getting it right affects field
and hospital treatment.

• Wrong transport destination.

Unnecessarily bypassing non-PCI hospitals
damages continuity of care, burdens
families, antagonizes facilities.
More downsides of false positive STEMI
diagnoses

• Stretches limited resources and causes

iatrogenic harm.

o Inappropriate activation from the field will not

always be reversed by ED/cardiology upon arrival
due to liability

o Unnecessary activations tax staff and facilities,

divert resources from other patients

o Unnecessary angiography (or worse,

thrombolysis) can cause renal/vascular damage

o Wrongly rushing the patient to the cath lab means

they aren’t getting treated for their real problems
More downsides of false positive STEMI
diagnoses

“… the issue of false-positive catheterization

laboratory activation remains a significant
concern because unnecessary emergency
coronary angiography is not without risk to
the patient and may impose a burden on
limited human and physical catheterization
laboratory resources.”

Larson et al, "False-Positive" Cardiac Catheterization Laboratory

Activation Among Patients With Suspected ST-Segment
Elevation Myocardial Infarction. JAMA. 2007;298(23):2754-2760.
What are our tools for addressing this?

• Clinical correlation. Any suspicious ECG

findings should be matched against patient
presentation and physical exam.

• History and risk factors. Does hx

supports MI – smoker, diabetic,
hypertensive, aspirin use, etc?

• Old ECGs. Extremely valuable tool when

available for establishing baseline.

• Serial ECGs. Repeat 12-leads may reveal

dynamic changes with time/treatment.
More tools for addressing this

• Supportive ECG findings. Subtler red

flags (pink flags?) that further support or
undermine diagnosis of STEMI.

• Expert consultation. Upload or interface

with medical control, where available.

• Computer interpretation. Automatic

algorithms provide a “virtual consult,” an
always-available second opinion.
More tools for addressing this

But wait!

• No clinical sign/symptoms are completely

reliable
• No ECG findings are completely reliable
• Hx regularly fools us

The answer?

You must look at the whole picture

Diagnosis is based on a
constellation of datapoints –
not any one finding!
Computer interpretations

Useless? Infallible?

Neither! Just another tool.

Understanding its strengths and

weaknesses is essential to effective use
GE Marquette 12SL

Developed in 1980, continuously updated since

Used in most cardiac monitors including Zoll,

Lifepack, most in-hospital monitors – but not
the Philips MRx

*** ACUTE MI SUSPECTED ***

~100% specific!
~61% sensitive
Massel D et al., Strict reliance on a computer algorithm or
measurable ST segment criteria may lead to errors in
thrombolytic therapy eligibility. Am Heart J 2000 Aug; 140(2) 2216
GE Marquette 12SL

Bottom line:

*** ACUTE MI SUSPECTED ***

Not very sensitive

But very specific
Exactly what we need!

Great tool for screening out false positives

GE Marquette 12SL

Caveats:

• Very dependent on data quality!

• Stable baseline
• No artifact
• Proper electrode placement
• Zoll may warn you: “Poor data quality,
interpretation may be adversely affected”

• Fooled by SVT – distrust interpretations

with HR > 100

• Can be fooled by PR depression

GE Marquette 12SL

More on data quality:

• Proper precordial placement

• Limb electrodes go on the limbs
• Manage shivering
• Park the truck if necessary
• Prevent patient movement
• May need to prepare skin – shave, dry,
tincture?
• Undress fully from waist up when
appropriate
• Stay organized
Signs that point to MI

Your basic model for STEMI should be:

Significant ST elevation in contiguous

leads, with reciprocal changes, in the
setting of clinical correlation

• Significant means significant relative to the

QRS amplitude; microvoltages = small STE!

• Contiguous means: know your coronary

arteries to understand which occlusions
make anatomical sense (“go together”)
Signs that point to MI

Your basic model for STEMI should be:

Significant ST elevation in contiguous

leads, with reciprocal changes, in the
setting of clinical correlation

• Reciprocal changes are the most valuable

addition to your basic criteria for increased
specificity (90+%). Look closely; changes
may be subtle.

Akhras, et al. Reciprocal change in ST segment in acute myocardial infarction: correlation with findings on exercise
electrocardiography and coronary angiography. Br Med J (Clin Res Ed). 1985 June 29; 290(6486): 1931–1934.

Otto, et al. Evaluation of ST segment elevation criteria for the prehospital electrocardiographic diagnosis for acute
myocardial infarction. Ann Emerg Med. 1994 Jan;23(1):17-24.
Signs that point to MI

Your basic model for STEMI should be:

Significant ST elevation in contiguous

leads, with reciprocal changes, in the
setting of clinical correlation

• Reciprocal changes may also be your only

indication of posterior-wall MI. Have a high
index of suspicion and consider V7–V9.

A riddle: why does every patient seem to breathe 16 times a minute?

Signs that point to MI

Your basic model for STEMI should be:

Significant ST elevation in contiguous

leads, with reciprocal changes, in the
setting of clinical correlation

• Clinical correlation means the classics (CP,

dyspnea, N/V, etc.) but also everything
from dandruff to microdeckia. Be open!
• 1/4 – 1/3 may present with unusual or no
complaints. Elderly, diabetics, females,
cardiac hx more likely to present atypically,
and have worse prognosis.
Pope et al. Missed Diagnoses of Acute Cardiac Ischemia in the Emergency Department. N Engl J Med 2000; 342:1163-1170
Kannel. Silent myocardial ischemia and infarction: insights from the Framingham Study. Cardiol Clin. 1986 Nov;4(4):583-91.
More signs that point to MI

• ST morphology. Most benign elevation presents

with concave (scooped) ST segments; convex
(rounded) elevation is a fairly specific indicator of
MI.
• For ST depression, flip it over, same thing
• 97% specific; 77% sensitive

Brady et al. Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic
analysis of the ST segment. Acad Emerg Med. 2001 Oct;8(10):961-7.
More signs that point to MI

• Changes on serial ECGs. ACS is a

dynamic process of supply/demand
imbalance; consecutive 12-leads should
reveal ongoing changes. Mimics are
typically electrically stable.
• When possible, obtain an initial ECG prior to
treatment; oxygen/nitro may erase ischemic
changes.
• Perform serial recordings and watch for evolution
over time; subtle becomes obvious, NSTEMI
becomes STEMI, etc. Any changes are suspicious.
• One of the best tools for distinguishing STEMI
vs. mimics!

Early and continuous prehospital ECGs can play

a crucial role in eventual care!
More signs that point to MI

• Changes from old ECGs. When available

(from facility or patient), previous 12-leads
can establish a baseline -- but this only
proves changes since the time of that
tracing.
Sgarbossa’s Criteria

Aka

The rule of appropriate discordance

Aka

The gift that keeps on giving

Originally developed in 1996 as system for

ruling in MI in setting of LBBB

Sgarbossa et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left
Bundle-Branch Block. N Engl J Med 1996; 334:481-487February 22, 1996
Sgarbossa’s Criteria

The rule of appropriate discordance:

 A QRS with a positive terminal

deflection should be followed by a
negatively shifted ST/T (ST depression,
T wave inversion)

 A QRS with a negative terminal

deflection should be followed by a
positively deflected ST/T (ST elevation,
upright T wave)

 ST elevation/depression should be
proportional to the size of the QRS
Sgarbossa’s Criteria

Deviations from this suggest MI!

Sgarbossa’s Criteria

This principle applies to:

 LBBB
 RBBB
 LVH (“strain pattern”)
 Paced ventricular rhythms
 Non-paced ventricular rhythms
(including PVCs)
 WPW and other preexcitation

How useful!
Sgarbossa’s Criteria

The actual criteria

In the setting of chest pain and LBBB:
 Concordant STE ≥1mm in any lead with a
positive QRS (5 points)
 Concordant ST depression ≥1mm in V1, V2,
or V3 (3 points)
 Discordant ST elevation ≥5mm in any lead
with negative QRS

Sum up the points:

≥3 is 98% specific for MI, 20% sensitive
≥2 is 61–100% specific, 20–79% sensitive
Tabas et al. Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle
branch block: a meta-analysis. Ann Emerg Med. 2008 Oct;52(4):329-336.e1. Epub 2008 Mar 17.
Sgarbossa’s Criteria

“Discordant ST elevation ≥5mm in any lead

with negative QRS”

 The most controversial rule due to the

lowest specificity

 The majority of problems arise with large

amplitudes (LVH), when 5mm may be
normal discordance
Sgarbossa’s Criteria

Smith’s Modification

Make it proportional!

“Discordant ST elevation ≥.2 (1/5) of terminal

S wave”

 Reduces false positives from large QRS

 May reduce false negatives from small QRS
(microvoltages)

Smith et al. (2012) Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-
Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012 Aug 31 Epub
Sgarbossa’s Criteria

Modified or not, has the sensitivity/specificity of

Sgarbossa been studied for any rhythm except
LBBB?

Paced ventricular rhythms (similar results)

… and nothing else!

Does it work for LVH, etc?

Yes!

Use the principles – don’t sweat the numbers

Now, bring in the mimics!
Left Ventricular Hypertrophy

 Single most common STEMI mimic

 May or may not exhibit ST changes
 Sgarbossa works well when it does
 Can be difficult to determine true size of
QRS (overprinting or clipping)
 Tip: True anterior STEMI almost never
present in setting of profound LVH
 Tip: ST segment may be benignly convex
 Voltage criteria generally irrelevant to
question of MI

Dr. Smith, unpublished

Left Bundle Branch Block

A big can of worms.

 Second most common STEMI mimic

 Traditionally either considered
“nondiagnostic,” or de facto evidence of MI.

AHA still recommends fibrinolysis/TPA:

“… in patients with [signs/symptoms of ACS and] …
new or presumably new left bundle branch block …”

Why?
“… because they have the highest mortality rate
when LBBB is due to extensive AMI”
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 10: Acute Coronary
Syndromes
Left Bundle Branch Block

(The pathophysiology here probably stems from

the fact that a LAD occlusion proximal enough
to involve the bundle branches is endangering a
great deal of myocardium.)

Another, implicit reason is because MI is

difficult to definitively diagnose in the setting of
LBBB.

Prehospitally, the result is that new LBBB

is often assumed to be AMI.
Left Bundle Branch Block

Problem #1: How do you know it’s “new”?

Answer: Patient history

Answer: Old ECGs

Answer: You can’t

Left Bundle Branch Block

Problem #2: Even “new” LBBB is not an

indicator of MI!

2008 observational study looked at three

groups of ED patients with complaints of ACS:
 Those with new LBBB
 Those with old LBBB
 Those with no LBBB

Result: All groups had equal probability of AMI

Chang et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. American
Journal of Emergency Medicine (2009) 27, 916–921
Left Bundle Branch Block

In short: new LBBB in the setting of AMI may

be an indicator of high risk

But it is not an indicator of AMI!

Diagnosis must still occur.

Left Bundle Branch Block

How?

You already know it:

 Sgarbossa! That’s what it’s for and we

know it works.
 Serial ECGs. Uncomplicated LBBB is
electrically stable.
 Old ECGs. Old LBBB vs. new does not
change the probability of MI, but if there is
an old LBBB, you can compare old vs. new
to find acute changes
Right Bundle Branch Block

 Fifth most common STEMI mimic

 Nevertheless, usually easier to manage, as
it often does not elevate the ST segment (T
wave inversion and ST depression more
common)
 Like LBBB, morbidity + mortality may be
very high when AMI is associated with
RBBB
 Principles are the same! Use your
Sgarbossa, etc.; remember to base
discordance on terminal QRS deflection
 Watch out for posterior reciprocal changes
deepening your normal ST depression
Right Ventricular Hypertrophy

 Second verse, same as the first. Use

your Sgarbossa!
 Only notable differences from LVH:
– Generally most evident in V1–V3
– Generally has right-axis deviation
 Presents similarly to posterior-wall MI with
reciprocal changes, so keep an eye out
Benign Early Repolarization

Aka Normal variant aka J-point elevation

 Fourth most common STEMI mimic

 Some degree of benign variance very
common in healthy population
 Most prevalent in young; decreases in
frequency with age
 May be especially noticeable in athletes

The bad news: very common, non-specific

ECG characteristics
The good news: changes are generally limited
to a few specific features
Benign Early Repolarization

Typical ECG findings:

 ST elevation focused in anterior precordials
(V2–V5)
 that is not too profound (<5mm)
 and is concave
 and may have a notched J-point.

Permissible ECG findings:

 Large, slightly asymmetrical T waves
 Some movement of ST segment or T wave
on serial recordings

Brady, et al. The Diagnosis: Benign Early Repolarization. Emergency Medicine News 23(12):30,36 (2001)
Benign Early Repolarization

Should not be present (suggest MI):

 Should be no reciprocal changes!
 Should be no convex ST segments!
 Should be no pathological Q waves!
 Should be no acute evolution!
 Should be no clinical signs/symptoms!

In short, except for ST elevation and big T

waves, it shouldn’t look like MI!
Benign Early Repolarization

Two more pearls to distinguish BER from

anterior MI:
 BER is almost always associated with well-
developed R waves
 BER is almost always associated with short QTc

So, if any two of the following are true, it is MI

with sensitivity/specificity of 90%:
 R wave in V4 <13mm
 QTc >392
 ST elevation (measured 1.5 boxes after J point)
more than 2mm

Smith et al. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment Elevation Myocardial Infarction.
Ann Emerg Med. 2012 Jul;60(1):45-56.e2. Epub 2012 Apr 19
Ventricular Rhythms

 Paced ventricular rhythms the only rhythm

other than LBBB with empirical support for
Sgarbossa’s criteria
 Do people with pacemakers have heart
attacks? . . .
 Nothing new here – use the rules – follow
serial ECGs – use your head
 Atypical pacer lead placement (not in apex
of right ventricle – or biventricular) may not
fit this model

Sgarbossa et al. Early Electrocardiographic Diagnosis of Acute Myocardial Infarction in the Presence of Ventricular Paced Rhythm. Am J
Cardiol, 1996; 77: 423–424.
Left Ventricular Aneurysm

 Refers to persistent aftereffects of a

previous MI, which often includes
chronically-elevated ST segment
 May or may not actually entail aneurysm
(bulging of a weakened section of
myocardium)
 Can present essentially identical to MI
since that’s what it was!
 Somewhat more common in anterior leads
 Look into the past: PMH includes prior MI?
Old ECG available?
Left Ventricular Aneurysm

Biggest clues:

 Q waves! This is an old infarct, and should

therefore exhibit pathological Q waves.
Look for substantial negative “QS” waves
with no notable R wave.

 No exaggeration of T waves. As there is

no acute ischemia, T waves should not be
hyperacute
Left Ventricular Aneurysm

In other words: compare QS depth to T

height. The first should be relatively large,
the second relatively small. Otherwise
suspect AMI.

If you want numbers: amplitude of T wave

should be no more than .36 (~1/3) of QS
depth in each lead V1–V4. If ratio is
greater, suspect AMI.

Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J Emerg
Med. 2005 May;23(3):279-87.
Pericarditis

 Inflammation of the pericardial sac, often

infectious
 Clinical signs are suggestive although not
specific:
– Chest pain that may be sharp and pleuritic
– Pain is alleviated by sitting up or leaning forward
– May be accompanied signs/symptoms of infection
(fever, etc.)
– Friction rub appreciated on auscultation
– No relief with nitro
Pericarditis

Initial ECG findings:

 Diffuse, nonlocalized ST elevation, often in
all leads except V1 and aVR (which will be
depressed instead)
 No reciprocal changes!
 Widespread PR depression
 Morphology resembles BER – generally
modest STE that is concave, often notched,
with substantial T waves

Generally, approach it similarly to BER!

Your main clues are global ST elevation
and PR depression, with no supportive
signs of ACS like reciprocal changes.
Pericarditis

The disease process produces four distinct

stages on the ECG over hours/days:

 Stage 1: ST elevation
 Stage 2: Normalization
 Stage 3: T wave inversion
 Stage 4: Normalization

Depending on when you show up, you may

see any of these.
Pericarditis

WARNING! WARNING!

A much more sinister cause can closely

resemble pericarditis: occlusion of the LCA
(left main) or acute three-vessel disease,
causing injury to nearly the entire left
ventricle
Pericarditis

If you see widespread ST elevation (or

depression) and start to think pericarditis,
consider two things:
Pericarditis

 Clinical context. These patients will usually

look terrible and so will their rhythms.

 aVR. Pericarditis should show ST depression

in aVR; LCA patients typically exhibit ST
elevation instead.

Elevation in aVR greater than in V1 may

be 80%+ predictive for LCA occlusion

Yamaji, et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. J Am Coll
Cardiol, 2001; 38:1348-1354
Pericarditis

Despite their acuity, LCA patients need a

facility with PCI and CABG – thrombolysis
is not beneficial

Mortality can be over 70%

Do your best!
That does it for the common mimics!

How about some of the lesser players?

Brugada Syndrome

 Distinct combination of ECG findings found

to be a risk factor for sudden polymorphic
VT or VF
 Initially described in 1992, well-studied
since and found to have a genetic factor
 Only confirmed cause of Sudden
Unexpected Death Syndrome among young
males in Southeast Asia
 Risk of sudden arrhythmia and possible
death is variable (worse if there is hx of
syncope), but may be upward of 8% per
year; treatment is EP study + ICD
Brugada et al. Long-Term Follow-Up of Individuals With the Electrocardiographic Pattern of Right Bundle-Branch
Block and ST-Segment Elevation in Precordial Leads V1 to V3. Circulation. 2002;105:73.
Brugada Syndrome

ECG findings:
 ST elevation in V1–V2, sometimes V3, with
particular morphology
 RBBB or similar appearance
 Appearance may fluctuate over time
 ECG changes may be inducible with certain
antiarrhythmics

Hallmark morphology is most visible in V1

and V2
Brugada Syndrome

Bottom line:
 Learn the basic morphology
 Screen for it on all ECGs
 Make it part of your differential for syncope
in young, healthy patients
 If suspected, monitor continuously and
transport to cardiac care

Brugada is the “evil twin” of BER. . .

your 12-lead may be the only chance to
catch a young, asymptomatic Brugada
patient early
Brain injury and intracranial hemorrhage

 Head injury (traumatic and non-traumatic)

can induce cardiac dysfunction in 50%–
100% of cases
 Some degree of heart failure is the most
common result
 Thought to involve myocardial “stunning,”
possibly resulting from neurogenically-
mediated vasospasm
 Effects are typically transient, but not
necessarily benign
 ECG signs are variable, can include ST
changes and giant inverted “neurogenic” T
waves; Osborne wave elevation is possible.
Jain, et al. Management of Patients with Stunned Myocardium Associated with Subarachnoid Hemorrhage. American
Journal of Neuroradiology 25:126-129, January 2004
Brain injury and intracranial hemorrhage

Bottom line:
 Primary point is not to be confused if you
see ECG abnormalities when assessing the
brain injury patient. Consider the
circumstances, but the likelihood of
concomitant ACS is very low.

 Monitor for cardiogenic shock; patient may

need cardiovascular support in immediate
injury period.
Thoracic Aortic Dissection

 Diagnosing TAD is critical due to its high

mortality and potential for rapid
deterioration
 Complicated by its similarity in presentation
to AMI, which can include ECG findings
 Distinguishing the two is critical due to
radically different treatment paths
(different destination facilities, surgery vs.
thrombolysis, etc.)
 Mechanism for ECG changes is physical
impingement on coronary arteries from
retrograde dissection (i.e. it is true
ischemia but not ACS)
Thoracic Aortic Dissection

Clinically:
 No signs/symptoms are highly diagnostic
for TAD vs. AMI
 The best is patient description of pain:
>80% will describe it as abrupt, maximal at
onset, and “worst ever.”
 40–60% describe it as sharp or
tearing/ripping
 Vast majority localize the pain to the chest
area (anterior or posterior)
 Hypertension is present in >70% of
patients
 Pulse or BP differential not sensitive or
specific
Thoracic Aortic Dissection

ECG findings:
 May present with LVH baseline due to
prevalence of background hypertension in TAD
patients
 8% will show ST elevation
 42% will show some form of ischemic
changes, including ST depression or T wave
inversion
– 75% of the time in inferior leads
– 25% of the time in lateral leads

Mattu, A et al. Avoiding Common Errors in the Emergency Department. 2010.

Schubert. Thoracic aortic dissection: Distinguishing it from acute myocardial infarction. Canadian Family Physician.
Available from http://www.cfpc.ca/cfp/2003/May/vol49-may-clinical-3.asp
Thoracic Aortic Dissection

Bottom line:
 A very difficult and high-stakes diagnosis
that still has no good solutions
 Have a high index of suspicion; TAD should
be on your differential for all chest pain
patients
 If history and clinical picture leans toward
TAD over MI, weigh the risks/benefits and
get to a hospital fast
Prinzmetal (Vasospastic) Angina

 A still-largely-idiopathic disorder involving

spontaneous vasoconstriction of the
coronary vessels
 Distinguished from typical angina by its
arbitrary onset, unrelated to exercise
 Often occurs in setting of CAD, but
produces symptoms disproportionate to
degree of stenosis
 Typically benign unless very severe, but in
combination with CAD can contribute to
poor outcomes
Prinzmetal (Vasospastic) Angina

ECG findings:
 ST elevation, typically slight (1mm or less)
but occasionally severe; sometimes with T
wave inversion
 Inverted U waves may be present
 Transient duration, generally relenting
within several minutes
 ECG changes normalize with termination of
episode, although some T wave inversion
may persist

Miwa et al. Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of
variant anginal attacks. Jpn Circ J. 1983 Dec;47(12):1415-22.
Prinzmetal (Vasospastic) Angina

Bottom line:
 Atypical or not, it’s angina! It will look and
smell like angina!
 Nitro will likely be very effective
 It’ll pass – one more reason for serial ECGs.
Signs/symptoms 10+ minutes start to point
to AMI.
 May not be distinguishable from aborted or
“stuttering” MI (“winking and blinking”),
and those patients do need cardiac care, so
play it safe
Wolf-Parkinson-White Syndrome

 Accessory pathway allows preexcitation of

ventricles outside of standard conduction
pathways
 Due to transverse conduction, morphology
resembles BBB, and produces STE for same
reason
 Risk factor for sudden death in the setting
of arrhythmia (reentry or conduction of A-
fib)
 Diagnosis is important for two reasons:
– Distinguishing it from STEMI
– Providing appropriate anti-arrhythmic treatment
Wolf-Parkinson-White Syndrome

ECG findings:
 Slurred initial entrance to QRS (“delta
wave”)
 Short PR (<120ms)
 Wide or borderline wide QRS
 Often resembles LVH and is confused with it
 ST elevation generally discordant with QRS
Wolf-Parkinson-White Syndrome

Bottom line:
 Start by recognizing the preexcitation
 Sgarbossa actually works in most cases,
but not reliably – each accessory pathway
is different and conduction is unique.
Approach it like LVH but keep an open
mind.
 If diagnosis of WPW is clear, be skeptical
about STEMI; symptoms are much more
likely related to arrhythmia than to MI.
Hyperkalemia

 Manifests with ECG findings that can

resemble ACS
 ECG presentation may correlate unreliably
with level of serum potassium
 May require immediate field treatment and
management for arrhythmias
 History should be highly suggestive! Renal
insufficiency is a major risk factor. Also
consider meds and major soft tissue trauma
(crush syndrome, burns) as potential
causes.
Hyperkalemia

ECG findings:
 Early sign is hyperacute T waves, which
classically appear:
– Fairly symmetric
– Narrow at the base and slim
– With a “sharp” point
– With a concave ST segment

 As it progresses, the QRS and T start to

widen and merge, which both can cause
apparent ST elevation (or depression if QRS
is positive) and can start to hide the
narrowness of the T waves
Potassium 7.1
Potassium 8.5
Potassium 9+
AMI
Hyperkalemia

Bottom line:
 Hyperkalemia should be in your differential
for every known dialysis patient with
general complaints or altered mental status
 Most diagnostic early ECG change is T wave
morphology: peaked and narrow
 More advanced stages may be less clear,
but by then (as QRS begins to resemble
BBB or ventricular rhythm) it should be
obvious there is something other than AMI
going on
 Guard against arrhythmias and manage
acutely (calcium, bicarb, fluids, etc.)
Tako-Tsubo Cardiomyopathy
Aka Stress Cardiomyopathy
Transient Apical Ballooning
“Ampulla” Cardiomyopathy
or Broken Heart Syndrome

 An interesting acute cardiac disorder, with

growing recent awareness; first described
in Japan
 90% of cases occur in post-menopausal
women, often without substantial cardiac
risk factors
Tako-Tsubo Cardiomyopathy

 Involves a transient myocardial stunning of

the LV apex, causing the heart at systole to
resemble an “octopus pot” (tako-tsubo)

 Its hallmark feature is an onset provoked

(in >2/3 of cases) by stress: emotional
(bad news, near-drowning), physical
(trauma), chemical (drugs)
Tako-Tsubo Cardiomyopathy

 Can resemble AMI in nearly every respect:

clinically, ECG, biomarkers. Primary
diagnosis occurs when no acute occlusions
are found on angio.

 ECG changes may resemble Prinzmetal’s,

with modest ST elevation and bizarre T
wave inversion

 Mechanism not understood; theories

include vasospasm, aborted MI, and various
neurogenic pathways

 Provoking stressor can be acute or chronic

Tako-Tsubo Cardiomyopathy

 Primary harm is from acute heart failure

(LVEF often ~40%)

 Like cardiac stunning secondary to brain

injury, prognosis is generally excellent if
the acute period is survived; no true
myocardial damage has been incurred

 Patients may require cardiovascular support

if cardiogenic shock exhibits
Tako-Tsubo Cardiomyopathy

Bottom line:
 Sudden onset of ACS-like symptoms after
some form of stress should make you
suspicious
 Nevertheless there is no way to rule out
true MI; most patients will be going to the
cath lab regardless

Tomich, et al. Cardiomyopathy, Takotsubo. eMedicine. http://emedicine.medscape.com/article/1513631-overview

And that’s that!
Bringing it all together

So how do you make sense of 1,000,000

different mimics?

 Start with the patient history and

background. Is this patient young or
old? History of CAD, risk factors, past
procedures? Is there a provoking
event? How likely is a congenital
pathology? Is there an old ECG
available?

 Consider the complaint. Is it typical for

MI or more consistent with another
etiology?
Bringing it all together

 Obtain an early 12-lead, before

treatment if possible. Are there ST or
T-wave changes? How profound? What
is their morphology?

 Are there reciprocal changes?

 What does the computer think?

 Does the ECG support an alternate

diagnosis? Would it explain the chief
complaint? Is it more or less likely
than MI? If likely, what is the
probability of a comorbid MI?
Bringing it all together

 Is there any chance of an alternate

diagnosis that is as or more pressing
than STEMI? (Aortic dissection,
advanced hyperkalemia, etc.)

 Obtain serial ECGs to guide or confirm

diagnosis.

 Weigh risk/benefit of transport

destinations. Consult medical control
as appropriate.

 Provide your findings to the receiving

staff.
That’s all, folks! Go home!
Thanks to:

 Tom Bouthillet, FF/EMT-P, of

ems12lead.com, for much of the
information, many of the example
ECGs, and the spiritual inspiration for
this material

 Dr. Stephen Smith for numerous ECGs

and many of the unpublished evidence-
based rules provided

 Dr. Brady, Dr. Sgarbossa, and the other

researchers whose work is heavily
featured