Ec gs in ami

ECGs in AMI
Kyaw Soe Win
Department of Cardiovascular Medicine
Mandalay General Hospital

Important to remember!
•ECG is not sufficiently specific or
sensitive to be used without a patient's
clinical history

“Other cardiac” includes, among other, myocarditis, Tako-Tsubo cardiomyopathy, or tachyarrhythmias.
“Non-cardiac” refers to thoracic diseases such as pneumonia or pneumothorax. . If the initial evaluation suggests
aortic dissection or pulmonary embolism, D-dimers and MDCT angiography are recommended
2015 ESC Guideline for management ofACS

ECG changes in AMI
ST Elevation MI
non-ST Elevation MI

Acute Myocardial Infarction
The leading symptom in patients with suspected AMI is chest pain.
• Non-STEMI
• No ST-elevation
• Partially blocked artery
• STEMI (STEMI)
• ST-elevation myocardial infarction
• Completely blocked artery
• Critical need for quick reperfusion

• When blood supply is abruptly reduced or cut off to a region
of the heart, a sequence of injurious events occur with
• Ischemia
• injury
• necrosis (infarction)
• fibrosis (scarring) if the blood supply isn't restored in an
appropriate period of time.
• The ECG changes over time with each of these events…
ST Elevation and
non-ST Elevation MIs

ST depression
ST elevation
Q wave

Ways the ECG can change include:
Appearance
of pathologic
Q-waves
T-waves
peaked flattened inverted
ST elevation &
depression
ECG Changes in the MI

Ischaemic ECG changes
Q wave
Infarct
Myocardial salvage possible No Myocardial salvage

ECG effects of myocardial injury
▪Deviation of the ST segment
▪ST segment deviated towards
the surface of the injured tissue
▪Patterns of deviation
▪ST depression- transmural &
epicardial
▪ST elevation- endocardial
The position of the ST segment is
commonly judged as normal or
abnormal using the baseline of the
PR or TP interval as a reference

TRANSMURAL Injury
ST Elevation
ECG Changes in the MI
There are two distinct
patterns of ECG
change depending if
the infarction is:
Non-ST Elevation
(Subendocardial or
non-Q-wave)
ST Elevation
(Transmural or
Q-wave),

ECG changes in myocardial ischemia
• Manifest by changes in
Ventricle repolarization
(ST segment and T waves)
▪ST- isoelectric
▪T - same polarity with QRS
Normal

ECG changes in myocardial ischemia
• Manifest by changes in
Ventricle repolarization
(ST segment and T waves)
▪ST- isoelectric
▪T - same polarity with QRS
• Imbalance between myocardial
oxygen demand and supply
• ST depression and/or T inversion
Normal
Ischaemia

Types & causes of
ST depression • A – upward ➔ may be normal
• B – down sloping ➔ strain / digoxin effect
• C – planar ➔ ischaemia***▪Angina
▪NSTEMI
▪LVH
▪Digoxin effect
Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in
≥ 2 contiguous leads indicates myocardial ischaemia.

T Wave
• Deep and symmetrically inverted
T waves may suggest cardiac
ischemia
• A T wave elevated more than half
the height of the QRS complex
(peaked T wave) may indicate a
new onset of myocardial
ischemia or hyperkalemia
▪At least 1 mm deep
▪Present in ≥ 2 continuous leads
▪Dynamic — not present on old
ECG or changing over time

Widespread T wave inversion
due to myocardial ischaemia
Types of T wave changes in ischaemia

Point to note
• Inverted T waves are normal in leads III, aVR, and V1
• Associated with a predominantly negative QRS complex.
Other causes of T inversion
A – T wave in coronary insufficiency
B – T wave in LVH with strain
C – T wave in digitalis effect

ST depression & T-wave inversion
The ECG changes seen with a non-ST elevation infarction are:
Before injury Normal ECG
ST depression & T-wave inversion
ST returns to baseline, but T-wave
inversion persists
Ischemia
Infarction
Fibrosis
Non ST Elevation MI

ECG manifestations suggestive of acute NSTEMI
( in the absence of LVH and BBB)
Fourth universaldefinition of myocardial infarction , EHJ (2018)00,1-33
ST depression
T wave inversion
Use Sgarbossa!

NSTEMI “subendocardialinfarct”
▪ Clinical spectrum of acute coronary syndrome
▪ sub-total occlusion of coronary vessel
▪ Current guideline emphasize risk stratification of UA/NSTEMI
patients with respect to selecting a conservative versus an
early invasive approach
Ragavendra R. Baliga , MD , MaGraw-Hill Specialty Board Review , ISBN978-0-07-161410-8

Why ECG is clinically important in NSTEMI?
▪When ECG changes occur in association with chest
pain but without frank infarction, they confer
prognostic significance.
▪About 20% of patients with ST depression and 15%
with T inversion will experience severe angina,
myocardial infarction, or death within 12 months of
their initial presentation.

Why ECG is clinically important in NSTEMI?
• ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of
NSTEMI and predicts significant mortality (35% mortality at 30 days).

Management
Early diagnosis
Early treatment
Time = myocardium
STEMI
.Life–threatening condition
.Plaque rupture
.Acute obstruction of infarct
artery (s)
Mortality is higher if a
greater number of ECG
leads show ST elevation

ST depression, peaked T-waves, then
T-wave inversion
The ECG changes seen with a ST elevation infarction are:
Before injury Normal ECG
ST elevation & appearance of Q-waves
ST segments and T-waves return to
normal, but Q-waves persist
Ischemia
Infarction
Fibrosis
ST elevation MI

ST elevation MI
A. Normal ECG prior to MI
C. Infarction from ongoing ischemia
results in marked ST elevation
B. Ischemia from coronary artery
occlusion results in ST depression (not
shown) and peaked T-waves
D/E.Ongoing infarction with appearance of
pathologic Q-waves and T-wave inversion
F. Fibrosis (months later) with persistent Q-
waves, but normal ST segment and T- waves

STEMI is a clinical syndrome defined by
characteristic symptoms of myocardial ischemia in
association with persistent (ECG) ST elevation and
subsequent release of biomarkers of myocardial
necrosis.
STEMI Diagnosis

Criteria
for diagnosing
STEMI
on ECG
It is always impossible to
identify STEMI without
the 12 leads

• 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
Conventional STEMI

2013 STEMI criteria
Diagnostic ST elevation in the absence of left ventricular (LV)
hypertrophy or left bundle-branch block (LBBB) is defined as new
ST elevation at the J point in at least 2 contiguous leads of:
In V2-3
≥ 0.2mV in men ≥40 years
≥ 0.25mV in men <40 years
≥ 0.15mV in women
In other leads
≥ 0.1mV for both sexes
examples of ST-elevation in MI

1.New or presumed new “Left Bundle Branch Block” in isolation is
no longer an indication for a STEMI
2. Providers should use Sgarbossa’s Criteria to diagnose STEMI in
the presence of LBBB
3. Isolated S-T depression in V1-4 is an indication of a posterior MI
4. Widespread S-T depression with S-T elevation in aVR is an
indication of proximal LAD or LMCA occlusion.
5. Hyperacute T-waves without S-T elevation may be an early
indicator of a STEMI
2013 changes in STEMI criteria

• The ECG is considered an essential part of the diagnosis and
initial evaluation of patients with acute chest pain.
• The information that can be obtained from the admission ECG
in patients with STEMI
• Various ECG patterns and the localisation of the infarct and
the underlying coronary anatomy.
• Reperfusion vs conservative & types of reperfusion
• prediction of infarct size
• estimation of prognosis
Why ECG is important in STEMI

In transmural MI, ischemia in the subendocardium spreads to
the epicardium and involves full thickness of the myocardium.
In the acute phase, the ECG signs are ST segment elevation.
ECG changes in infarction
NSTEMI/ischaemia Transmural infarct: STEMI

STEMI??
Phase??
Site??
High Risk patient??
ST elevation
!!!

Identify the J Point
Junction Point or J Point

Don’t compare J Point to the PRI
segment, there are medical conditions
that my cause PRI depression
Identify the J Point elevation

Identify the J Point elevation
The TP segment
provides the best
baseline to evaluate ST
elevation
▪ Locate the J-Point
▪ Compare it to the TP Segment
▪ Determine if the J point is elevated by
1mm or more above the TP Segment

ST segment morphology in other conditions
Convexity upward
infarction
STEMI Mimic
Concavity
upward

Hours to days later during
the evolving phase,
pathological Q waves
appear, the elevated ST
segments return towards
baseline, and the T waves
become inverted.
ECG changes in infarction
Hyperacute T waves may
precede ST segment
elevation (A) or seen at
the same time with ST
elevation (B) during this
acute phase.
ST elevation
The elevated ST
segment may slope
upward or be
horizontal or
dome-shaped.

Hyperacute T-waves
Tall, narrow, symmetrically
peaked T-waves are
characteristically seen in
hyperkalaemia.
asymmetrically peaked or
‘hyperacute’ T-waves are seen in the
early stages of ST-elevation MI (STEMI)

Q wave
• Normal
✓Lateral leads (I,aVL,V5,V6)
✓III alone may be present
Pathologic Q-waves
▪ ¼ of following R wave
▪ >0.04sec width(>1 mm)
▪ > One leadsNotice the small Normal Q
Notice the deep & wide
Infarction Q

Evolutionary changes( Phases) in STEMI
• Tall T waves
• ST elevation
• Decrease of ST elevation with the beginning of Q wave & T waves inversion
• Q wave, Isoelectric ST with symmetrical T wave inversion
• Q wave, Isoelectric ST with upright T wave
Hyper-acute Evolving Fully evolved Old
Bayes de Luna ,The 12-lead ECG in ST elevation myocardial infraction , ISBN-13: 978-1-4051-5786-5
Minutes Hour(s) days Weeks/month

Anterior STEMI: evolving
ST No Q/ no T inversion Benefit for reperfusion therapy

Anterior STEMI: evolving
Benefit for reperfusion therapyST Q/ T inversion

Anterior STEMI: fully evolved
QS ST T inversion No Benefit for reperfusion therapy

Old Anterior MI
QS & upright T waves

Maximizing information from the ECG in acute MI
•Which artery is blocked?
•Where is the artery blocked? (extent of infarct)
•Can one identify the high risk patient?
•Large/ extensive infarct?
•AV block?
•VT/VF?
•AF?

In order to recognize STEMI you have to know 2 things
• What to look for (ST elevation)
• Where you are looking (which Lead)
STEMI-Location
• Look in all leads for ST elevation except aVR
• Is ST elevation present in 2 contagious leads?
• Localize the STEMI based upon the leads showing the ST elevation
• Area of infarction is reflected by the area of ST-Elevation
• Reciprocal changes are NOT necessary to diagnose a STEMI. It needs to
estimate time of STEMI (Phase)

Right
Ventricle Left
VentricleS
Posterior Wall
Lateral Wall
Anterior WallV1
V2 V3 V4
V5
V6
Septum
Anatomic Contiguous Leads

Arrangement of Leads on the ECG
Limb leads chest leads

Anatomic Groups (Anterior Wall)

Anatomic Groups (Inferior Wall)

Anatomic Groups (Lateral Wall)

Anatomic Groups (Contiguous Leads)

Contiguous Leads
extensive anterior V1 V2 V3 V4 V5 V6 I aVL II III aVF

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left Ant Descending artery
Anterior infarction Culprit vessel: LAD
ST elevation V1 -4 I aVL,reciprocal ST depression in II III aVF

Anterior MI : anteroseptal
ST-Elevation in leads V1 V2 V3 and V4
Culprit vessel: LAD

ST elevation V1 V2 V3 V4, reciprocal ST depression in II III aVF
Anterior MI : anteroseptal Culprit vessel: LAD

LADA
ST elevation V1 V2 V3 I aVL, reciprocal ST depression in II III aVF
Culprit vessel: LADAnterior MI : anterolateral

ST elevation V2 V3 V4 V5 V6 I aVL, reciprocal ST depression in II III aVF aVR
Anterior MI : anterolateral Culprit vessel: LAD

Left circumflex artery
Lateral infarction Culprit vessel: LCX
ST elevation V5 V6 I aVL, reciprocal ST depression in II III aVF

• Low Lateral AMI
Lateral MI
ST elevation V4 V5 V6 I aVL, reciprocal ST depression in III
Culprit vessel: LCx

Inferior Infarction
Right coronary artery
Culprit vessel: RCA
ST elevation II III aVF

Inferior MI
• ST-Elevation in leads II,III, and AVF
• Reciprocal changes in leads I and AVL
Culprit vessel: RCA

RCA vs LCx in Acute Inferior MI

Inferior Infarction
Right coronary artery
• ST elevation Lead III > Lead II
• AV nodal block
• ST-segment vector is directed
toward the right (lead III).
• ST-segment elevation in lead V1
-proximal occlusion of RCA with
associated RVMI
Left circumflex artery
▪ ST elevation Lead II > lead III
▪ ST-segment vector directed
toward the left (lead II).
▪ There is an isoelectric or ST
segment elevation in lead aVL
Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med 2003;348:933-940

ST elevation withQ waves in the inferior leads with reciprocal changes in I and aVL
ST elevation III > II
Inferior MI
Culprit vessel: RCA

Inferior MI
Culprit vessel: LCX
ST elevation in the inferior leads, I and aVL
ST elevation II > III

Association of inferior wallMI
✓Heart block ( any degree )
✓sinus node disease
✓Posterior wall MI
✓RV infarction
✓Mechanical complication ; acute mitral regurgitation

Posterior wall MI
▪Difficult to diagnose by Surface ECG
▪Posterior leads(V789) show ST elevation
▪Manifested by ST depression and
upright T waves in V1 and V2( Just
opposite to MI)
Posterior MI accompanies 15-20% of
STEMIs, usually occurring in the context
of an inferior or lateral infarction.

V7-V9 = Posterior leads
2
52017 ESC Guidelines for the management of acute myocardial infarctionin patients presentingwith ST-segmentelevation
Posterior wallSTEMI
( may or may not be associated
with inferior wall MI)

Typical appearance of posterior infarction in V2
V2
V2
Mirror image of posterior
infarction in V2

Posterior wall STEMI
( concomitant with inferior wall MI)

Posterior wall STEMI: isolated
( no concomitant with inferior wall MI)

Inferior MI with
ST depression in
anterior leads
(ant ischaemia)
vs
inferior MI
combined with
posterior MI
Anterior ischaemia

Posterior wallMI
2017 ESC Guidelines for the management of acute myocardial infarctionin patients presenting with ST-segmentelevation
• Horizontal ST depression ≥0.5mm in posterior leads V7-9
• Horizontal ST depression ≥0.5mm
• Tall R waves :R/S ratio > 1 in V2 V3
• Upright T waves
Posterior MI: Tall R and Tall T with ST↓ in V1-V3

Right ventricularinfarction
▪ Usually associated with inf MI
▪ hypotension
▪ nitrates or diuretics may
compound the hypotension
▪ may respond to fluid
challenge
FrancisMorris, ABC of clinicalelectrophysiology , BMJ book , ISBN 0 7279 15363
2017 ESC Guidelines for the management of acute myocardial infarctionin
patients presenting with ST-segmentelevation
V3R V4R lead

2017 ESC Guidelines for the management of acute myocardial infarctionin patients presentingwithST-segmentelevation
V3R V4R lead

The three ST-Segment and T-Wave configurations
that an be identified by Lead V4R in patients with
Acute Inferoposterior Myocardial Infarction.
Wellens HJ. N Engl J Med 1999;340:381-383.
RVMI
▪Right leads show ST segment
elevation(V3R and V4R)
▪ST elevation in V1 in presence
of IWMI, suspect RVMI
▪In presence of IWMI, ST
elevation in lead III>II suspect
RVMI

Right ventricular infarction
( concomitant with inferior wall MI)
ST elevation in II , III and aVF andV1
ST elevation in V1 with
inferior infarct indicates RVMI

Combination STEMI • Inferolateral+post AMI
ST elevation II III aVF V5 V6, ST depression in v1–v4 aVR (post MI)Right coronary artery

The high risk patient
• Age > 75 years
• DM
• Previous MI
• Killip Class ¾ HF
• Shock
•Large MI: many leads
•Sustained monomorphic VT
•Late atrial fibrillation
•AV blocks
•VF
Clinical ECG
High mortality

ST elevation withQ waves in the inferior leads with reciprocal changes in I and aVL
▪ Diagnosis ; Acute inferior infarction with 2:1 AVblock

3:2 AV block & 4:3 AV Block
Anterior MI with AF

Ventricular fibrillation– complication ofSTEMI

Ventriculartachycardia
▪ Wide QRS complextachycardia
Abnormal impulse from
ventricular tissue
No P wave beforeQRS
complex
Life – threatening
condition
▪ Initial treatment
➢ Hemodynamic evaluation
✓ Stable hemodynamic ; antiarrhythmic
drugs:amiodarone IV or lidocaine IV
✓ Unstable hemodynamic ; electrical
cardioversion
✓ PulselessVT ; CPR withACLS and
defibrillation

J A C C : Case Reports , V OL . 1 , NO . 4 , 2 0 1 9 Asatryan et al. December 2 0 1 9 : 6 6 6 – 8 ECG Equivalents of STEMI
STEMI Equivalents

STEMI equivalents
• Hyperacute T waves
• De Winter ST T complex
• Wellens T waves
• Diffuse ST depression
• Shark T
• Sgarbossa Criteria
• Posterior MI
• New LBBB = No Longer STEMI Equivalents
Use Sgarbossa!

• 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

• Diffuse ST depression with ST elevation in aVR or V1
• aVR /V1= 0.1mV + 8 leads with ST depression = 0.1mV is moderately
suggestive of left main coronary artery occlusion.
• Shark T
• J point depression transitioning in a convex ST segment
• Sgarbossa Criteria
• LBBB or pace maker rhythm with concordant or = 5mm ST elevation
• Isolated Posterior MI
• 0.05 mV ST depression in V1-3 especially associated with positive T
waves (0.05 mV elevation in V7-9)

• The de Winter ECG pattern is an anterior STEMI equivalent
that presents without obvious ST segment elevation.
• Suggestive of proximal LAD lesion
• Precordial ST-segment depression at the J-point
• Tall, peaked, symmetric T waves in the precordial leads
• aVR may shows slight ST elevation in most cases
De Winter’s T wave
N Engl J Med 2018;378:e22

N Engl J Med 2015;372:66
Wellens’ syndrome
Critical stenosis of LAD
Type A: Biphasic T-waves
(initial positive deflection
and terminal negative
deflection)
Type B: Deeply inverted and
symmetric T-waves
• ECG findings in absence of chest
pain, but with recent cardiac chest
pain symptoms
• will require PCI in the next 24-48hr
( Widow maker syndrome)

Lawner et al. Cardiol Clin 2012; 30:591-99
Proximal LAD near-occlusion: Wellens syndrome
One manifestation is the presence of biphasic
T waves in the anterior precordial leads
The commoner pattern is deep T-wave
inversions in the anterior precordial leads

Isolated Posterior wallMI
2017 ESC Guidelines for the management of acute myocardial infarctionin patients presenting with ST-segmentelevation
• Horizontal ST depression ≥0.5mm in posterior leads V7-9
• Horizontal ST depression ≥0.5mm
• Tall R waves :R/S ratio > 1 in V2 V3
• Upright T waves
RCA (90%), LCA (10%)
Posterior MI: Tall R and Tall T with ST↓ in V1-V3

• Seen with occlusion or near-occlusion of the left main artery or
• Has been reported in occlusion of the proximal left anterior
descending artery and severe multivessel coronary artery
disease
• 12-Lead ECG findings
• ST depression is widespread and typically seen in lateral leads ( V4-6)
• ST elevation in aVR ≥ 1mm
• ST elevation in V1 ≥ 1mm
Diffused ST depression

Diffused ST depression with ST elevation in aVR
Left Main occlusion

Complete occlusion of the left main! After PTCA

ST elevation in aVR vs V1
•ST elevation aVR>V1: + ST depression in V4-6
• Left main
80% sensitivity and specificity
•ST elevation V1>aVR :+ ST depression in V4-6
• Ostial/ proximal LAD
Yamaji et al. JACC 2001; 38:1348-54

Proximal LAD occlusion
Diffused ST depression with ST elevation in V1

54y Male, Anterior MI on 11.6.2020 at MGH
Primary PCI
Ostial LAD

“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)
The Problem: Most STE is not MI

STEMI Mimic
Beware of baseline ECG abnormalities (Artefacts) that may obscure interpretation
❖ Benign early repolarization
❖ Peri/myocarditis
❖ Brugada
❖ WPW syndrome
❖ Hyperkalemia
❖ LBBB
❖ LVH
❖ RBBB
❖ Cardiac pacing
Sinus tachycardia

How common?
• Retrospective review of ED charts over 3-month period
• Looked at 902 adults with chief compliant of “chest pain”
• Looked for STE in contiguous leads, >1mm limb leads, >2mm precordials
• Compared final diagnoses, MI vs. other
Brady et al., Cause of ST segment abnormality in ED chest pain patients (Am J Emerg Med 2001 Jan;19(1):25-8)
Results
Only 15% of STE patients had MI!
85% had non-MI diagnosis
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)
51% false-positive rate
Half of our diagnoses were wrong

▪ 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 ECG may reveal dynamic changes with time/treatment.
What are our 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.
Depend on machine
Bottom line:
*** ACUTE MI SUSPECTED ***
Not very sensitive
But very specific
Exactly what we need!
Great tool for screening out false positives

Benign Early Repolarization
Normal variant / J-point elevation
most common STEMI mimic
▪ ST elevation focused in anterior (V2–V5)
▪ no reciprocal changes!
▪ no convex ST segments!
▪ no pathological Q waves!
▪ no acute evolution!
▪ no clinical signs/symptoms!
▪ almost always asso with well-developed
R waves
▪ almost always asso with short QTc
▪ may have a notched J-point
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

Pericarditis
•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

ECG inpericarditis
▪ Diffuse widespread ST/T elevation
▪ PR depression ( especially in lead II )
▪ 4 stages of ECG finding
Juan GuidoChiabrando, MD , Management of acute and recurrent pericarditis, JACC ,Vol 75, No 1 , 2020
Concavity upward ST elevation

Grasshopper -leg
Brugada’s Syndrome

• 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
If diagnosis of WPW is clear, be
skeptical about STEMI;
symptoms are much more likely
related to arrhythmia than to MI.
Wolf-Parkinson-
White
Syndrome

Hyperkalemia
• ECG findings that can resemble ACS
• ECG presentation may correlate unreliably with level of serum K
• History :Renal insufficiency is a major risk factor. medications and
major soft tissue trauma (crush syndrome, burns)
ECG findings:
• Early sign is hyperacute T waves, which classically appear:
• Symmetric, Narrow at the base and slim, With a “sharp” point
• With a concave ST segment
• Late sign: the QRS and T start to widen and merge, which both can
cause apparent ST elevation (or depression if QRS is positive)

Serum K-7mmol/L
Serum K-8mmol/L

Right Bundle Branch Block • In RBBB, the left
bundle branch
performs normally,
activating the left side
of the heart before the
right
• ECG characteristics
– Initial negative
deflection (S wave)
– RSR-prime pattern
– QRS (or in this case,
RSR) duration at
least 0.12 sec

Right Ventricular
Hypertrophy
▪ 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
Use Sgarbossa!

Left Bundle Branch Block
• In LBBB, the fibers that
usually fire the
interventricular
septum are blocked
• ECG characteristics:
– Initial Q wave in V1
– R wave in V1
– Deep, wide S wave (QS
pattern)
– QRS duration at least
0.12 sec

Left ventricular hypertrophy
There is left axis
deviation (positive in
I, negative in II) and
there are tall R waves
in V5, V6 and deep S
waves in V1, V2.

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

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
Even “new” LBBB is not an indicator of MI!
new LBBB in the setting of AMI may be an indicator of high risk

Sgarbossa’s Criteria
In the setting of chest pain and LBBB:
• Concordant STE ≥1mm in any lead with a positive QRS (5p)
• Concordant ST depression ≥1mm in V1, V2, or V3 (3p)
• Discordant ST elevation ≥5mm in any lead with negative QRS (2p)
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.
5 points 3 points2 points

LBBB , no MI LBBB with anterior MI
Sgarbossa score = 5 + 2

Left ventricular hypertrophy AMI with LVH
ST elevation > 25% of QRS amplitude AND STE in 3 contiguous leads OR of T
inversions in the anterior leads) is strongly suggestive of AMI

▪not ↑ ST segment
(T ↓ and ST↓ more
common)
▪Like LBBB, morbidity
+ mortality may be
very high when AMI
is associated with
RBBB
▪Use Sgarbossa
2017 ESC Guidelines for the management of acute myocardial infarctionin patients presentingwith ST-segmentelevation
Right Bundle Branch Block with MI

Marked ST segment elevation and absent R waves in lead V1-V6
Notching of the upstroke of the QRS complex ( Cabrera ‘ s sign ) is noted in V4
Acute MI in pacerhythm
Chou’s Electrocardiographyin clinical practice , ISBN : 978-1-4160-3774-3
Use Sgarbossa!
Pacing spikes

• Identify J point
• Identify J point elevation
• Myocardial injury ST elevation ?
• Localize the leads ( two or more contagious leads)?
• What does the computer think ?
• localize the site of occlusion
• Identify Phase of STEMI ? Are there reciprocal changes ?
• High risk patients ? Arrhythmias ?
• Does the ECG support an alternate diagnosis ? diagnosis other than STEMI?
• Repeat History & Exam
• Obtain serial ECGs to guide or confirm diagnosis
• an old ECG available ?
Bringing it all together

• Are there reciprocal changes ?
• Identify Phase of STEMI ? High risk patients ? Arrhythmias ?
infarction

• Are there reciprocal changes ?
• Identify Phase of STEMI ? High risk patients ? Arrhythmias ?

thank you
▪ ECG is not sufficiently specific or sensitive to be used
without a patient's clinical history
▪ You must look at the whole picture
▪ Diagnosis is based on a constellation of all data – not
any one finding!

Ec gs in ami

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