Stemi, Stemi Equivalents and STEMI Mimics: Kyaw Soe Win

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STEMI , STEMI

equivalents and STEMI


mimics
Kyaw Soe Win
Department of Cardiovascular Medicine
Mandalay General Hospital
Anatomy of a 12-Lead ECG

I Lateral aVR V1 Septal V4 Anterior

II Inferior aVL Lateral V2 Septal V5 Lateral

III Inferior aVF Inferior V3 Anterior V6 Lateral


Anatomy of a 12-Lead EKG - ST Segment
•The ST segment is normally iso-electric (baseline)
neither elevated or depressed.

• May slope upward toward a relatively tall T wave

•The ST segment is probably the single most


important element to identify on the ECG when
looking for evidence of AMI.
The Three I’s in Myocardial Infarct
• Ischemia
• lack of oxygenation
• ST depression or T inversion
• Injury
• prolonged ischemia
• ST elevation
• Infarct
• death of tissue
• may or may not show in Q wave
ST T changes in Acute Coronary Syndrome
Criteria
for diagnosing

STEMI
on ECG
Conventional STEMI

 standard teaching for STEMI typically has the


following criteria
≥1 mm (0.1 mV) of ST segment elevation in the limb leads
≥ 2 mm elevation in the precordial leads and present in
anatomically contiguous leads

There are several variations from the classic


STEMI ECG changes that do not fit this definition
New Criteria for STEMI
• ST segment elevation at the J point in two contiguous ECG leads

• In V2-3
• ≥ 0.2mV in men ≥ 40 years
• ≥ 0.25mV in men <40 years
• ≥ 0.15mV in women
examples of ST-elevation in MI

• In other leads
• ≥ 0.1mV for both sexes
General pitfalls
Beware of baseline ECG abnormalities ( Artefacts) that may obscure interpretation

Sinus tachycardia
STEMI location
• septal
• V1, V2
• inferior
• II, III, aVF
• reciprocal changes: I, aVL
• lateral
• I, aVL, V5, V6
• reciprocal changes: II, III, aVF
• anterior
• V3, V4
• anteroseptal
• V1, V2, V3, V4
• anterolateral
• I, aVL, V3, V4, V5, V6
• reciprocal changes: II, III, aVF
• posterior
• V7, V8, V9
ECG 1

Anterolateral STEMI
ECG 2

Inferior STEMI
ECG 3

Inferolateral STEMI
+ Horizontal ST depression V1-3
+ Tall R waves, upright T-waves V2-3
ECG 3 + posterior leads

Inferior-lateral-posterior STEMI
ECG 3 + RV leads

RV leads

Inferior-lateral-posterior-RV STEMI
Overview of Infarcts
Location of Infarct Arterial Supply Indicative Reciprocal
Changes Changes
Anterior LAD V1-V4 II, III, aVF
Inferior RCA II, III, aVF I, aVL
Lateral Circumflex I, aVL, V5, V6 V1
Posterior Posterior Descending None V1, V2
(RCA)
Septal Septal Perforating Loss of R wave in V1, None
(LAD) V2, or V3
Posterior Descending
(RCA
The ECG in ST Elevation MI
The Hyper-acute Phase
Less than 12 hours
• “ST segment elevation is the hallmark ECG abnormality of acute myocardial
infarction” (Quinn, 1996)
• The ECG changes are evidence that the ischaemic myocardium cannot completely
depolarize or repolarize as normal
• Usually occurs within a few hours of infarction
• May vary in severity from 1mm to ‘tombstone’ elevation
The Fully Evolved Phase
24 - 48 hours from the onset of a myocardial infarction
• ST segment elevation is less (coming back to baseline).
• T waves are inverting.
• Pathological Q waves are developing (>2mm)
The Chronic Stabilised Phase
• Isoelectric ST segments
• T waves upright.
• Pathological Q waves.
• May take months or weeks.
Reciprocal Changes
• Changes occurring on the opposite side of the myocardium that is
infarcting
Reciprocal Changes ie S-T
depression in some leads in MI
STEMI equivalents
STEMI equivalents
B B
• Hyperacute T waves L B
• De Winter ST T complex ew
= N
• Wellens T waves t s
l en
• Posterior MI
i va
• Shark T q u
I E
• Diffuse ST depression with aVR ST elevation EM
ST
• Persistent Pain e r
ng
• Sgarbossa Criteria
Lo
• Left Ventricular Hypertrophy No

• Hyperacute T waves
• Tall , often asymmetrical, broad- based anterior T waves often associated
with reciprocal ST depression

• De Winter ST-T complex


• ST segment depression at the J point with ascending ST segment and tall,
asymmetrical T waves in the reciprocal leads, often combined with a 1-2mm
elevation of ST segment in aVR

• Wellens T waves
• These ECG patterns are not always yet accompanied by chest pain and usually
precede overt ST elevation myocardial infarction. They can be interpreted as
an early sign of impending coronary occlusion ( with 24 hr)
• Type A: deeply- inverted anterior T waves
• Type B: biphasic anterior T waves
• Posterior MI
• 0.05 mV ST depression in V1-3 especially associated with positive T waves (0.05 mV elevation in
V7-9)

• Shark T
• J point depression transitioning in a convex ST segment

• Diffuse ST depression
• aVR /V1= 0.1mV + 8 leads with ST depression = 0.1mV is moderately suggestive of left main
coronary artery occlusion.

• Persistent Pain
• Persistent pain despite medical treatment, especially in the presence of RBBB or pace maker
rhyhthm should be regarded as a possible coronary occlusion in the absence of a clear alternative
explanation
Criteria for STEMI in the presence of LBBB and LVH

• Sgarbossa Criteria
• LBBB or pace maker rhythm with concordant or = 5mm ST elevation

• Left Ventricular Hypertrophy


• ST elevation in the presence of LVH can be tricky to interpret. ST elevation
> 25% of QRS amplitude AND ( presence of STE in 3 contiguous leads OR
presence of T wave inversions in the anterior leads) is strongly suggestive of
acute myocardial infarction
STEMI Equivalents
Hyperacute T waves
Tall , often asymmetrical, broad- based anterior T waves often
associated with reciprocal ST depression
STEMI Equivalents
De Winter’s T wave
• Suggestive of proximal LAD lesion
• 12-Lead ECG findings
• Precordial ST-segment depression at the J-point
• Tall, peaked, symmetric T waves in the precordial leads
• Lead aVR shows slight ST-segment elevation in most cases
De Winter’s T wave
De Winter’s T wave
De Winter’s T wave
STEMI Equivalents
Wellen’s syndrome ( Widow maker syndrome)
• ECG findings in absence of chest pain, but with recent cardiac chest pain symptoms
• Represents critical stenosis of the LAD
• Not necessarily STEMI equivalent but will require PCI in the next 24-48hr
• 12-Lead ECG findings
• Deeply-inverted or biphasic T waves in V2-3
• Isoelectric or minimally-elevated ST segment (<1 mm)
• Absent precordial Q waves with preserved R waves
• Two T wave characteristics:
• Type A: Inversion pattern - 75% - Deeply inverted and symmetric T-waves
• Type B: Biphasic pattern - 25% - Biphasic T-waves (initial + deflection and terminal -
deflection)
Wellen’s syndrome
Wellen’s syndrome
Wellen’s syndrome
STEMI Equivalents
Isolated Posterior MI
• RCA (90%), LCA (10%)
• 12-Lead ECG findings
• ST-segment depression (horizontal >> downsloping/upsloping
• Prominent and broad R wave (>30ms)
• R/S wave ratio >1.0 in lead V2
• Prominent, upright T wave
• Combination of horizontal ST-segment depression with upright T wave
• Posterior ECG or 15-lead ECG may be helpful
• V7: Left posterior axillary line along the 5th ICS
• V8: Tip of the left scapula line along the 5th ICS
• V9: Left paraspinal area line along the 5th ICS
• Posterior ECG findings
• ≥1 mm ST-segment elevation
Isolated Posterior MI
STEMI Equivalents

LMCA Occlusion
• Seen with occlusion or near-occlusion of the left main artery
• Has been reported in occlusion of the proximal left anterior
descending artery and severe multivessel coronary artery disease
• 12-Lead ECG findings
• ST elevation in aVR ≥ 1mm
• ST elevation in aVR ≥ V1
• ST depression typically seen in lateral leads ( V4-6)
LMCA Occlusion
Criteria for STEMI in the
presence of LBBB and LVH
STEMI in LBBB
Sgarbossa’s Criteria
• Used to identify STEMI in the setting of LBBB or pacemaker
• Original Criteria
≥3 points = 98% probability of STEMI
≥2 is 61–100% specific, 20–79% sensitive

• ST elevation ≥1 mm in a lead with upward (concordant) QRS complex - 5 points


• ST depression ≥1 mm in lead V1, V2, or V3 - 3 points
• ST elevation ≥5 mm in a lead with downward (discordant) QRS complex - 2 points
• Smith's modification
• Changes the 3rd rule of original Sgarbossa's Criteria to be ST depression OR elevation
discordant w/ the QRS complex and w/ a magnitude of at least 25% of the QRS
increases Sn from 52% to 91% at the expense of reducing Sp from 98% to 90%
Sgarbossa’s Criteria Sgarbossa’s Criteria
Also known as This principle applies to:

The rule of appropriate discordance


• LBBB
• RBBB
Also known as
• LVH (“strain pattern”)
The gift that keeps on giving • Paced ventricular rhythms
• Non-paced ventricular rhythms
Originally developed in 1996 as system for (including PVCs)
ruling in MI in setting of LBBB • WPW and other preexcitation

Sgarbossa et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Lef
Bundle-Branch Block. N Engl J Med 1996; 334:481-487February 22, 1996
How useful!
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

STEMI
Deviations from this suggest MI!
Sgarbossa’s Criteria
Smith’s Modification “Discordant ST elevation ≥.2 (1/5) of terminal S wave”
• Reduces false positives from large QRS
• May reduce false negatives from small QRS (microvoltages)
Make it proportional!

Smith et al. (2012) Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Lef Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule . Ann Emerg
Med. 2012 Aug 31 Epub
Not STEMI STEMI
STEMI
STEMI in LVH
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
No Longer STEMI Equivalents
New LBBB
• New LBBB alone is no longer a reason to activate the cath lab
• However, careful work up for ACS should be taken for symptomatic
patients with LBBB
• 12-Lead ECG findings
• QRS > 0.12 in limb leads
• Leads
• Large and wide R waves — leads I, aVL, V5, and V6
• Small R wave followed by deep S wave —leads II, III, aVF, V1–V3
New LBBB
The Problem: Most STE is not MI

“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)

Results
Only 15% of STE patients had MI!

85% had non-MI diagnosis

Brady et al., Cause of ST segment abnormality in ED chest pain patients (Am J Emerg Med 2001 Jan;19(1):25-8)
In other words:

Any monkey can recognize ST elevation

STEMI recognition and diagnosis requires distinguishing MI from non-ischemic


causes
STEMI mimics
What were they? STEMI mimics
• Left Ventricular Hypertrophy — 25%
• Left Bundle Branch Block — 15%
• AMI — 15%
• Benign Early Repolarization — 12% I !
E M
• Right Bundle Branch Block — 5% ST
as se!
ely au
• Nonspecific BBB — 5% li k ly c
as ike
• Ventricular aneurysm — 3% e s tl
tim os
• Pericarditis — 1% s 6 le m
wa ing
• Undefined/unknown — 17% ic ns
i m ve
• Early repolarization I-m ot e
E M sn
• Takotsubo ST wa
• Intracranial pathology M I
Overtriage is better than undertriage…

Maybe it’s better to play it safe…

But there are downsides of false positive STEMI diagnoses

• Weakens true positives.


• If you lack confidence in recognizing mimics, you’ll lack
confidence in making the call for true STEMI.
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.
Left Bundle Branch Block
• 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

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
Also known as 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)
• is concave
• 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

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
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!
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.

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.
L V aneurysm
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

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
Pericarditis
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.

The disease process produces four distinct stages on the ECG over hrs/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.
pericardit
is

Infarct

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.
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

Despite their acuity, LCA patients need a facility with PCI and CABG –
thrombolysis is not beneficial

Mortality can be over 70%

Yamaji, et al. Prediction of acute lef main coronary artery obstruction by 12-lead electrocardiography. J Am Coll Cardiol, 2001; 38:1348-1354
less common STEMI mimics
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 ofNeuroradiology 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
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

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
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
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.
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

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.
Hypertrophic cardiomyopathy
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.

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
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
• 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.
• 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.
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.
What are our tools for addressing for MI?

• Clinical correlation.
• Any suspicious ECG findings should be matched against patient presentation
and physical exam.

• History and risk factors.


• Does h/o 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.
Computer interpretations
Useless?
Infallible?

Neither! Just another tool.

Understanding its strengths and weaknesses is essential to


effective use
Computer interpretations
*** ACUTE MI SUSPECTED ***
fi c !
ec i e
Not very sensitive p
s siti v
0 0% e n
But very specific ~1 1% s
Exactly what we need! ~6

Great tool for screening out false positives

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
Computer interpretations
• Fooled by SVT – distrust interpretations with HR > 100

• Can be fooled by PR depression

More on data quality:


• Proper precordial placement
• Limb electrodes go on the limbs
• Manage shivering
• Prevent patient movement
• May need to prepare skin – shave, dry, tincture?
• Undress fully from waist up when appropriate
More tools for addressing this

But wait!
• No clinical sign/symptoms are completely reliable
• No ECG findings are completely reliable
• H/O regularly fools us

The answer?

You must look at the whole picture


Diagnosis is based on a constellation of datapoints – not any one finding!
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”)
• Reciprocal changes are the most valuable addition to your basic criteria for increased
specificity (90+%). Look closely; changes may be subtle.
• Clinical correlation means the classics (CP, dyspnea, N/V, etc.) but also everything from
dandruff to microdeckia. Be open!
• ***Silent MI -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.
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!
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.
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 do you think and 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?
• 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.
Bringing it all together
So how do you make sense of 1,000,00 different mimics?

• Start with the patient history and background.


• Is this patient young or old?
• 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?
Thank c k
a
You M is s i on :
Hea rt Att

u r ro m
O i e f l e!
ld D u s c
ho u is M !
e S m e L if e
O n T i is
No im e
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