ECG On ACS

ECG ON ACUTE CORONARY SYNDROME
MUCHTAR NORA ISMAIL SIREGAR, MD FIHA

• 35 yo M, smoker
• Typical chest pain 30 min before
admission
• No PMH
CASE-1
• BP 110/70 mmHg HR 60 bpm RR
20 tpm SpO2 98%
• Unremakable Physical exam finding
CASE-2
• 30 yo M, smoker
• Syncope
• No PMH
• BP 110/70 mmHg HR 60
bpm RR 20 tpm SpO2 98%
• Unremakable Physical
exam finding
ACUTE CORONARY SYNDROME
Spectrum of conditions compatible with acute myocardial
ischemia and/or infarction that are usually due to an
abrupt reduction in coronary blood flow.
ECG should be performed and interpreted by an

experienced physician within 10 minutes of Emergency
Department arrival
SPECTRUM ACUTE CORONARY SYNDROME
STE -ACS
ST-ELEVATION ACS
1. ST Elevation (Hypercute T
wave) with/without resiprocal
2. Location (leads involved)
and possibility culprit artery
3. Other abnormality (block,
extrasystole, and other
arrythmias)
4. Evolution
1. ST ELEVATION (HYPERACUTE T WAVE)
• ST Elevation ?
• Characteristic of ischaemic ST Elevation
• Fulfiled Criteria? Example of ST Elevation caused
by ISCHEMIA
ISCHEMIA
NON-ISCHEMIA
1. ST ELEVATION (HYPERACUTE T WAVE)
New ST Segment elevation in at least two anatomically contiguous leads
• Man age ≥ 40 years: ≥ 2 mm in V2-V3 and ≥ 1mm in all other leads

• Man age < 40 years: ≥ 2.5 mm in V2-V3 and ≥ 1mm in all other leads
• Woman (any age): ≥ 1.5 mm in V2-V3 and ≥ 1mm in all other leads
• Man and Woman V4R and V3R: ≥ 0.5 mm
• Man and Woman V7-V9: ≥ 0.5 mm
2. LOCATION (LEADS INVOLVED) AND POSSIBILITY
CULPRIT ARTERY
Schematic overview of coronary arteries and

their relation to the ECG leads
3. OTHER ABNORMALITY (BLOCK, EXTRASYSTOLE, AND
OTHER ARRYTHMIAS)
• Ventricular Arrhythmia: PVC, run VT

• Supraventricular arrhythmia: AF, PAC
• Conduction disturbances: AV block
(Inferior STEMI >>), new bundle
brunch block (RBBB in anterior
STEMI)
4. EVOLUTION
• Confirmation MI
• Prediction of onset
• Clinical correlation
MIMICKING STEMI
CAUSE OF ST SEGMENT ELEVATION
1. Pericarditis
2. Benign Early Repolarization
3. Brugada Pattern
4. LBBB
5. LV aneurysm
6. LVH
7. Takotsubo Cardiomyopathy
8. Ventricular Paced Rhythm
9. Raised Intracranial Pressure
NON STE -ACS
NON ST ELEVATION ACS
Transient ST Persistent or
Elevation transient ST T wave Inversion
depression
Flat T wave Pseudonormalization May be normal

of T wave
ST DEPRESSION
• Upsloping, downsloping, and horizontal
• Horizontal or downsloping ST
depression ≥ 0.5 mm at the J-point in ≥
2 contiguous leads
• Upsloping STD is commonly seen in

person at tachycardia, usually not
indicative for myocardial ischemia
• STD ≥ 1 mm is more specific and

conveys a worse prognosis
• STD ≥ 2 mm in ≥ 3 leads is associated

with a high probability of NSTEMI and
predicts significant mortality (35%
mortality at 30 days)
ST DEPRESSION
• Widespread ST depression (≥ 6 leads) typically present in
inferior and anterolateral leads, often associated with inverted T
waves and STE in lead aVR  manifestation of diffuse
subendocardial ischemia caused by left main, or severe three
vessel disease
• ST depression localised to a particular territory (esp. inferior or

high lateral leads only) is more likely to represent reciprocal
change due to STEMI.
DIFFERENTIAL DIAGNOSIS IN ST SEGMENT DEPRESSION
Delayed Conduction: LBBB, RBBB
Enlarged Ventricle: LVH, RVH
Pre-excitation: WPW
Resiprocal to ST Elevation
Early Occlusion: the Winter
SVT
Subendocardial ischemia
Electrolyte: Hipokalemia
Digoxin
NORMAL T WAVE
• I,II, -aVR, V5-V6 positive T wave in

adults
• aVR  negative T wave in adults
• III and aVL --> isolated T wave
inversion
• aVF--> positive T wave or flat
• V1inverted or flat
• V7-V9--> positive
ISCHAEMIC T WAVE
T wave inversion Indicative for

myocardial ischemia:
• At least 1 mm deep
• Present in ≥ 2 continuous leads
that have upright QRS complex ;
dominant R waves (R>S ratio >1)
• Dynamic – not present on old ECG
or changing over time
WELLEN SYNDROME
• Highly specific for critical stenosis of the
Left Anterior Descending
• High risk for extensive anterior wall MI

within the next 2-3 weeks
• Symmetric and deeply inverted T waves

or biphasic T waves in leads V2 and V3
in a pain-free state, plus isoelectric or
minimally elevated (<1 mm) ST segment
• Absence of precordial Q waves, the

presence of history of angina, and
normal or slightly elevated cardiac serum
markers
• Tall, prominent, symmetric T waves in the
precordial leads
DE WINTER • Upsloping ST segment depression >1mm at

• Pattern of upsloping ST depression with the J-point in the precordial leads
symmetrically peaked T waves in
precordial leads • Absence of ST elevation in the precordial leads
• Highly specific for an acute occlusion of
Left Anterior Descending, considered • ST segment elevation (0.5mm-1mm) in aVR
STEMI equivalent
• “Normal” STEMI morphology may precede or

follow the de Winter pattern

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ECG ON ACUTE CORONARY SYNDROME

MUCHTAR NORA ISMAIL SIREGAR, MD FIHA

ECG should be performed and interpreted by an

New ST Segment elevation in at least two anatomically contiguous leads

• Man age ≥ 40 years: ≥ 2 mm in V2-V3 and ≥ 1mm in all other leads

Schematic overview of coronary arteries and

• Ventricular Arrhythmia: PVC, run VT

Flat T wave Pseudonormalization May be normal

• Upsloping STD is commonly seen in

• STD ≥ 1 mm is more specific and

• STD ≥ 2 mm in ≥ 3 leads is associated

• ST depression localised to a particular territory (esp. inferior or

• I,II, -aVR, V5-V6 positive T wave in

T wave inversion Indicative for

• High risk for extensive anterior wall MI

• Symmetric and deeply inverted T waves

• Absence of precordial Q waves, the

DE WINTER • Upsloping ST segment depression >1mm at

• “Normal” STEMI morphology may precede or

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