ECG Discussion

• STEMI equivalent/OMI
• STEMI mimics
 Traditional definition of STEMI
Per the 2018 AHA “Fourth Universal Definition of Myocardial
Infarction,” ECG manifestations suggestive of MI
New ST elevation at the J point in 2 contiguous leads with the cut points:
≥ 2.5 mm STE in V2-V3 for males < 40 years*
≥ 2 mm STE in V2- V3 for males ≥ 40 years*
≥ 1.5 mm STE in V2-V3 for females regardless of age*
≥ 1 mm STE all other leads
*New J-point elevation ≥ 1 mm from prior ECG should be considered ischemic

The J-point is defined as the junction between the QRS termination and the ST-segment
onset, and the ST-segment should be measured against the isoelectric TP segment
(assuming a stable baseline).
 STEMI equivalent :
ECG changes which represent
coronary occlusion but does not
fulfils the traditional definition of
STEMI

• New onset or presumed new

LBBB which fulfill the modified
Sgarbossa Criteria
• RBBB with ST elevation
• Isolated Posterior MI
• De Winter T Waves
• T wave inversion in aVL with
any ST elevation in inferior
leads
• ST elevation in aVR with
diffused ST depression
• Wellen’s Syndrome
A previously healthy patient presented in acute
pulmonary edema, and had this ECG recorded:
 Approach:
• Compare with
previous ECG if
available. If it is a
new LBBB treat as
STEMI.
• Use Modified
Sgarbossa Criteria
to guide your
decision
 Lets go back to our patient

Concordant ST elevation in
leads with positive QRS
 What about this ECG

Concordant ST depression at
lead V2 and V3 which is > 1mm
 What about this ECG

ST/S ratio at lead v3 = 3/5 = 0.6

Concordance ST elevation at lead I, aVL, V5, V6
An elderly woman presented with 30 minutes of
chest pain after working out
• There is sinus rhythm with RBBB
• ST Elevation in V1.
• In RBBB, the ST segment that comes after a
large R'-wave in V1-V3 should have slight ST
depression (in other words, the ST segment
should be discordant to the R'-wave, similar
to discordance in LBBB).
ST elevation at
lead V1

Typical RBBB
• Further supported by her previous ECG that
does not have RBBB

Management (CPG STEMI 2019)

54 yo female with h/o smoking, DM, HTN, c/o chest pain for 3 hours,
substernal radiating to both shoulders

Sinus tachycrdia
ST depression at V2, V3 with Tall R wave and upright T wave
No ST elevation over inferior/lateral leads
Next step is to do a posterior ECG and look for ST elevation > 0.05mm av V7,8,9
Without posterior ECG, patient might only be treated as NSTEMI
 Posterior ECG

Lead V7,8,9 shows ST elevation > 0. 5mm( half small box)

This case is suggestive of isolated Posterior MI
Usually, posterior MI is associated with Inferior or Lateral MI
Isolated posterior MI is rare (3-11%)
Often missed and treated as NSTEMI
 A male in his 30's complained of sudden severe substernal chest
pain. He was rushed to the critical care area where they
recorded this ECG:

Tall prominent, symmetrical T wave at the precordial leads

De Winter T wave Upslopping ST segment depression >1mm

It may preceded or followed by STEMI on serial ECG
Suggestive of LAD occlusion and warrant immediate revascularization
 45yo male, ischemic chest pain

It can be:
ST depression and T wave inversion at aVL with ST
-Significant mid-LAD lesion
elevation at lead III and hyperacute T waves in other
- Evolving inferior MI and
inferior lead
possible RV involvement
 60-year-old man calls MECC after experiencing sudden onset chest pain, palpitations,
and shortness of breath. Here are his vital signs:

HR: 130-160, BP: 140/75, RR:22, Temp: 37.2, SaO2: 98%

ST elevation at aVR ≥1mm

Diffuse ST depression
Can be present in LMCA stenosis/LAD stenosis or severe triple
vessel disease
- Indicates subendocardial infarction and aVR ST elevation
is actually a reciprocal changes to ST depression of the
lateral leads
- Not a typical transmural infarction in STEMI
STE-aVR with multilead ST depression was associated with acutely thrombotic
coronary occlusion in only 10% of patients and none of those lesions were left
main or left anterior descending occlusion. Routine STEMI activation in STE-
aVR for emergent revascularisation is not warranted, although urgent, rather
than emergent, catheterization appears to be important.
 A 40 y.o male presented to triage. He had suffered a couple bouts of typical
chest pain in the last 24 hours. This ECG was recorded immediately after the
last episode of pain spontaneously resolved. The pain had lasted about one
hour.

Classic Wellens' waves in V2-V5

It is a Wellens’s Type A: biphasic T wave
Wellen’s Type B (in 75% cases) :deep and symmetrically inverted T wave
Critical LAD stenosis
 Why Wellen’s Syndrome is called a
syndrome
• Patients with Wellen’s syndrome typically
presented to ED are pain-free after a period of
chest pain. The cardiac enzymes is usually normal.
• This is due to the temporary occlusion of LAD
(spontaneously clot lysis).
• However due to the unstable nature of coronary
perfusion, these patients are at high risk for
extensive anterior wall MI and Death.
• Basically it is a continuum or a pre-infarction state
Example: A 45yo male, typical ischemic chest pain, call
EMRS. This is the PHC team ECG during the chest pain.
Upon arrival to ED, he is pain free.
Repeated ECG
10 minutes after the first ECG in ED, he had a
recurrent chest pain. ECG stat done

The biphasic T waves has gone and became an upright

(PSEUDONORMALIZATION)
In a busy, overcrowded ED, this may be missed.
Patient still have persistent chest pain,
repeated ECG shows:

Evolution of ST elevation
STEMI mimics: ST elevation but without evidence
of occlusive coronary artery on angiography or ruled
out on clinical/biochemical grounds
STEMI mimics: ST elevation but without evidence
of occlusive coronary artery on angiography or ruled
out on clinical/biochemical grounds
E lectrolytes (Hyperkalemia)
L BBB
E arly Repolarisation (BER)
Ventricular hypertrophy
Aneurysm (LV aneurysm)
T akotsubo, Traumatic Head Injury/ICH
I nflammation (Pericarditis), Injury (Cardiac contusion)
Osborn J Wave (Hypothermia)
Non-atherosclerotic vasospasm (Prinzmetal Angina)
 60yo female, underlying ESRF, missed HD.
complaining of generalised lethargy

Sinus rhythm, wide QRS complex, ST elevation at V1-3 with tall tented T wave
(narrow and pointed T wave) in almost all leads except 1, aVL
This ECG suggestive of mild hyperkalemia correlates to K+ level 5.5 – 6.5

*Hyperacute T wave in STEMI has a broad base and localised to an

anatomic area of infarct
 25yo, healthy male, atypical chest pain.

Widespread concave ST elevation, most prominent in the mid-to-left precordial leads

(V2-5)
Notching or slurring at the J point seen at lead II, III, aVF and V5
Good R wave progression, no reciprocal changes
No reciprocal ST depression or Q wave to suggest Occlusion MI
This ECG is suggestive of BER.
 70 yo with h/o MI, recent anteroseptal MI,
thrombolysed, has acute onset of chest pain.

ST elevation at V1-3
Well formed Q waves V1-4. It depends on previous region of infarct, if previously
patient sufffer from inferior MI, the LV Aneurysm ECG changes is seen in inferior
leads
T wave/QRS ratio < 0.36 (5/18) in all precordial leads
History and ECG suggestive for LV Aneurysm
28yo, healthy male, pleuritic chest pain, relieves
with leaning forward.

Sinus tachycardia
Widespread concave STE and PR depression (II, III, aVF, V4-6)
PR elevation in aVR
Spodick’s sign best visualised in lead II
History and ECG finding is suggestive of Pericarditis
 40yo woman, headache, seizure and less responsive,
absent gag reflex, CT Brain shows SAH. Your staff nurse
shows her ECG:

Widespread, giant T-wave inversions/roller coaster T wave (“cerebral T waves”)

The QT interval is also grossly prolonged
The narrow and pointy QRS with the giant T-wave produce a spike helmet sign
Patophysiology: Increase ICP -> reduced CBF-> stimulate sympathetic response to increase
MAP -> Carotid Baroreceptor detect increase in systemic BP -> stimulate parasympathetic
response -> reduce AV conduction -> Bradycardia and repolarisation disturbance -> prolonged
QT and ST depression/T inversion in ECG
28yo, healthy male, missing during hiking and was found 3 days
later, weak, shivering. brought by ambulance. Rectal
temperature 30.

Uncertain rhythm, but appears to be sinus rhythm, or possibly junctional, with

PVCs.
Osborn waves (positive deflection, dome shape at the J point) in all leads
Osborn J waves can also be found in Hypercalcemia, Brugada Syndrome, BER,
Takotsubo Cardiomyopathy
THANK YOU !!