MI ECG LOCALISATION ST ELEVATION DIFFERENTIAL DIAGNOSIS

1. MI LOCALISATION

2. • NON CORONARY CAUSES OF ST- ELEVATION

3. • ventricular aneurysm
• Acute pericarditis
• Normal variants (including the classic early
repolarization pattern;
• LVH, LBBB (V1-V2 orV3 only)

4. • Hypothermia (J wave, Osborn wave)
• DC cardioversion (just following)
• IVH
• Hyperkalemia
• Brugada pattern (RBBB-like pattern and ST-
segment elevations in right precordial leads)
• Type 1C antiarrhythmic drugs
• Hypercalcemia

5. • Other (rarer)
– PTE(right midchest leads
– Hypothermia (J wave, Osborn wave;
– Myocardial injury
– Myocarditis (may resemble myocardial infarction or
pericarditis)
– Tumor invading LV

6. • LeftVentricular Aneursym
•
• Persistent ST elevation >2WKS
• some degree of ST elevation remains in 60% of anterior STEMI and
5% of inferior STEMI.
• incomplete reperfusion and transmural scar formation following an
acute MI.

8. Factors favouring left ventricular aneurysm
The ratio of T-wave to QRS complex amplitude

9. • Early Repolarization
• ST segment elevation without
underlying disease
– An upward concave elevation of
the RS-T segment with distinct or
"embryonic" J waves
– slurred downstroke of R waves or
distinct J points or both
– RS-T segment elevation commonly
encountered in the precordial leads
and more distinct in these leads
– rapid QRS transition in the
precordial leads with
counterclockwise rotation
– persistence of these characteristics
for many years
– absence of reciprocal ST depression
– large symmetrical T waves

10. • Acute Pericarditis
Degree of ST elevation is typically modest (0.5 – 1mm).
Less than 50% of patients progress through all four classical stages

12. • most sensitive -ST-segment elevation,which reflects the abnormal
repolarization that develops secondary to pericardial inflammation.
• ST-segment depression in leads aVR andV1.
• no changes during depolarization, -P wave and QRS complexes are
normal.
• Depression of the PR segment -very specific = subepicardial atrial
injury and occurs in all leads except aVR andV1.
• These leads may exhibit PR-segment elevation.

13. • The ST-segment elevation
1. “concave,” compared with the “convex” during MI.
2. widespread ST-segment elevation not corresponding with any specific
arterial territory, unlike MI.
3. reciprocal changes are absent
4. return to baseline in a few days and are followed by diffuseT-wave
inversion, in conjunction with the ST segment at baseline
5. Absence of Q waves and the absence ofT-wave inversion at the time of
ST-segment elevation,
6. Loss of R-wave progression is not present .
7. Low voltage (i.e., decreased amplitude of the QRS complex) may also
be present.
8. Arrhythmias are uncommon

15. ST/T ratio in lead V6. This is calculated by dividing the millimeters of ST-segment
elevation by the millimeters to the tallest point of the T wave. Each value is measured
from the isoelectric point.
An ST/T ratio of greater than 0.25 in lead V6 suggests acute pericarditis
PericarditisBenign Early Repolarisation

16. • advances Hyperkalemia > 8-8.5meq/dl
• nonhomogeneous depolarization in different portions of the
myocardium.
Electrolyte disturbances
Hyperkalemia – ST changes
1. Typical coving pattern(convexity) not seen
2. Associated T wave changes( tall , narrow base , pointed T )
3. Reversibility

17. Electrolyte disturbances
Hyperkalemia – ST changes

18. Electrolyte disturbances
Hyperkalemia
ECG K levels Changes
T waves changes > 5.5 Tall pointed narrow based
QRS > 6.5 Prolonged QRS
P & PR > 7.0 Inc.PR , absent P
ST > 8-8.5 Elevation
Rhythm changes >10.0
> 12.0
Irregular wide QRS complex
Ventricular asystole

19. An increased extracellular calcium concentration shortens the ventricular action
potential duration by shortening phase 2 of the action potential.
Hypercalcemia sometimes produces a high takeoff of the ST segment in leads V1 and
V2 and can thus simulate acute ischemia
HYPERCALCEMIA

20. The ST elevation in V1-3 is simply in proportion to the very deep S
waves (“appropriate discordance”).
LVH

21. • Raised ICP
• Widespread giant T-wave inversions (“cerebralT waves”).
• QT prolongation.
• Bradycardia (the Cushing reflex - indicates imminent brainstem herniation).
• ST segment elevation / depression – this may mimic myocardial
ischaemia or pericarditis.
• Increased U wave amplitude.
• Other rhythm disturbances: sinus tachycardia, junctional rhythms,
premature ventricular contractions, atrial fibrillation.

22. There is widespread ST elevation with a pericarditis-like
morphology and no reciprocal change (except in aVR and V1).

23. • Osborn waves (
• camel-hump sign, late delta wave, hathook junction, hypothermic
wave, prominent J wave , K wave,H wave or current of injury) .
• positive deflections occurring at the junction between the QRS
complex and the ST segment, where the S point, also known as the J
point, has a myocardial infarction-like elevation.
– hypothermia with a temperature of less than 32 C (90 F),
– hypercalcemia,
– brain injury,
– vasospastic angina, or
– ventricular fibrillation

24. BRUGADA SYNDROME

25. In type 1, the ST segment gradually descends to an
inverted T wave.
In type 2, the T wave is positive or biphasic, and the
terminal portion of the ST segment is elevated ≥1
mm.
In type 3, the T wave is positive, and the terminal
portion of the ST segment is elevated <1 mm

26. • Moving the right precordial chest leads up to the second or third intercostal space
or using bipolar chest leads may increase the sensitivity of detecting these
abnormalities .
• e widened S wave in left lateral leads that is characteristic of RBBB is absent
• a high takeoff of the ST segment in the right precordium, ie, a "J" wave rather than
a true RBBB .
• QT interval prolongation =right precordial leads .
• degree of prolongation =modest but some patients have genetic abnormalities that
cause both BS and long QT syndrome .

27. Tako-Tsubo Cardiomyopathy
Typically occurs in the context of severe emotional distress (“broken heart syndrome”).

28. The ECG In Pulmonary Embolism

29. MASSIVE PE

30. • Arrhythmogenic right ventricular dysplasia (ARVD).
• Definition
• EpsilonWave-The epsilon wave is a small positive deflection (‘blip’)
buried in the end of the QRS complex.

32. ECG in ACS with ST-Segment Elevation
(STE-ACS)
Localisation of infarct related artery

33. Threshold Values for ST-Segment Changes

34. • Typical ECG pattern:
• The new occurrence of an ST-segment elevation >2 mm at 60 ms
after the J point inV2 toV3 and >1 mm in other leads, present in at
least two consecutive leads, is considered abnormal and evidence of
acute ischemia in the clinical setting of ACS (presence of precordial
pain or equivalents).
• Whenever possible, it is important to compare this pattern with
previous ECGs.

35. • The ST elevation prevails in the leads facing the affected
zone as a direct ECG pattern.
• In general, in some opposed leads, the ST-segment
depression is seen as an indirect ECG pattern .
• These same features also occur in the chronic phase, with a
Q wave as the direct pattern and an R wave as the indirect
pattern .

36. LOCALISATION OF INFARCT RELATED
ARTERY

37. • Anterior Myocardial Infarction
• LAD
• worst prognosis -larger infarct size.
The magnitude of the reciprocal change in the inferior leads is determined by the
magnitude of the ST elevation in I and aVL (as these leads are electrically opposite to III
and aVF), hence may be minimal or absent in anterior STEMIs that do not involve the
high lateral leads.

38. precordial leads can be classified
different infarct patterns -according to maximal ST elevation

39. • LMCA
• Widespread horizontal ST depression, most prominent in leads I, II
andV4-6
• ST elevation in aVR ≥ 1mm
• ST elevation in aVR ≥V1

40. • ST elevation in aVR is not entirely specific to LMCA occlusion.
• It may also be seen with:
– pLAD occlusion
– SevereTVD
• ST elevation is aVR -
• Diffuse subendocardial ischaemia (producing reciprocal change in
aVR)
• Transmural ischaemia / infarction of the basal interventricular
septum (e.g. due to a proximal occlusion within the left coronary
system)

41. • PredictiveValue Of STE In AVR
• In the context of widespread ST depression + symptoms of
myocardial ischaemia:
• STE in aVR ≥ 1mm = proximal LAD / LMCA occlusion or severe
3VD
• STE in aVR ≥ 1mm - CABG
• STE in aVR ≥V1 differentiates LMCA from proximal LAD occlusion
• Absence of ST elevation in aVR -excludes a significant LMCA lesion
Patients with ≥ 1 mm STE in aVR may potentially require early CABG;
therefore these patients should ideally be discussed with the interventional
cardiologist (± cardiac surgeon) before thienopyridines are given.

42. • Wellens' syndrome
• classicT-waves =V2-V3 during pain-free periods
• high-grade stenosis of pLAD
• 75% =develop MIs within one week .

43. • Diagnostic criteria-
1. Progressive symmetrical
deep T wave inversion in
leads V2 and V3
2. Slope of inverted T waves
at 60°-90°
3. Little or no cardiac
marker elevation
4. Discrete or no ST
segment elevation
5. No loss of precordial R
waves.
6. Pattern abnormal during
chest-pain free periods

44. • Wellen's syndrome T-wave.
• Type A =more common
• 75%
• deeply inverted T-waves in V2 and
V3.
• Type B
• 25%
• biphasic T-waves in V2 and V3
• diagnostic leads =V2 and V3= lesion
between the first and second septal
branches of the LAD
• if the lesion is more proximal in the
LAD=T-wave changes will be more
widely spread along the precordial
leads.
Type A
Type B

45. EKG in someone with Wellens' syndrome when they were having chest pain
EKG of the same person when pain free, note the biphasic T waves in leads V2 and V3

46. • S1 =basal part of the
interventricular septum,
including the bundle
branches (corresponding to
leads aVR and V1)
• D1 =high lateral region of
the heart (leads I and aVL).
LEFT CORONARY ARTERY

47. • Occlusion proximal to S1
• Signs of basal septal involvement:
• ST elevation in aVR
• ST elevation in V1 > 2.5 mm
• Complete RBBB
• ST depression inV5,II,III,aVF.

49. • ST elevation in aVR of any magnitude is 43% sensitive
and 95% specific for LAD occlusion proximal to S1.
• RBBB in anterior MI -poor prognosis=the extensive
myocardial damage involved rather than the conduction
disorder itself.

50. OCCLUSION BETWEEN FIRST SEPTAL AND FIRST DIAGNOL

51. OCCLUSION BELOW FIRST SEPTAL AND FIRST DIAGNOL

53. Algorithm to precisely locate the left anterior descending (LAD) occlusion in the case of an
evolving myocardial infarction with ST elevation in precordial leads

55. • LAD is larger and longer to the point
of extending beyond the cadiac apex and“wrapping around” to
supply the undersurface of the heart.
• At times it may even serve the function of the PDA.
• simultaneous ST segment elevation
in inferior and anterior lead areas.
• such infarctions are often quite large
“wraparound” LAD

56. “wraparound” LAD

57. • Suspect acute apical infarction when there is
ST elevation in both anterior as well as inferior lead
areas.
• Probable Culprit Vessel —
A “wraparound" LAD

58. Extensive anterior MI (“tombstoning” pattern

59. • Inferior STEMI--
• 40-50% of all MI.
• more favourable prognosis
• in-hospital mortality only 2-9%
• Up to 40% = concomitant RVMI in (worse prognosis).
• Up to 20% =significant bradycardia due to second- or third-degree AV block.
increased in-hospital mortality (>20%).
• posterior infarction=worse prognosis

60. occlusion of all three coronary arteries:
• ~80% -occlusion of the dominant (RCA).
• Less commonly ( 18% of the time), =dominant (LCx).
• Occasionally= occlusion of a “type III” or “wraparound” left anterior
descending artery (LAD).This produces the unusual pattern of
concomitant inferior and anterior ST elevation.

61. • RCA territory
• covers the medial part of the inferior wall, including the inferior
septum.
• directed inferiorly and rightward
• ST elevation in lead III > lead II (as lead III is more rightward facing).
• LCx territory
• covers the lateral part of the inferior wall and the left posterobasal
area.
• directed inferiorly and leftward
• ST elevation in the lateral leads I andV5-6.

62. • RCA occlusion
• STE in lead III > lead II
• reciprocal ST depression in lead
I,aVL
• Signs of right ventricular
infarction: STE in V1 and V4R
• Circumflex occlusion
• STE in lead II =/> lead III
• Absence of reciprocal ST
depression in lead I,aVL
• Signs of lateral infarction: ST
elevation in the lateral leads I and
aVL or V5-6
Relative Q-wave depth in leads II and III is not useful in determining the culprit
artery.

63. RCA
LCX

64. • Bradycardia And AV Block In Inferior STEMI
• Up to 20% of inferior STEMI
• Ischaemia of the AV node
– due to impaired blood flow via the AV nodal artery.
– arises from the RCA 80%
– involvement in inferior STEMI due to RCA occlusion.
• Bezold-Jarisch reflex =
– increased vagal tone secondary to ischaemia.

65. • RightVentricular Infarction-subtle and easily
missed
– ST elevation inV1 -
– ST elevation in lead III > lead II -
– lead III is more “rightward facing” than lead II a
– more sensitive to the injury current produced by the
right ventricle.

66. • If the magnitude of ST elevation inV1 exceeds the magnitude of ST
elevation inV2.
• If the ST segment inV1 is isoelectric and the ST segment inV2 is
markedly depressed.
• The combination of ST elevation inV1 and ST depression inV2 is
highly specific for RVMI.

67. • ST elevation in V3R-V6R
• ST elevation in V4R =sensitivity of
88%, specificity of 78% and
diagnostic accuracy of 83%
• transient phenomenon
• lasting less than 10 hours in 50%
Right-Sided Leads

69. IWMI+RVMI

72. Posterior Myocardial Infarction
•15-20% of STEMIs
•context of an inferior or lateral infarction.
•Isolated =less common (3-11% of infarcts).
•Posterior extension of an inferior or lateral infarct =much larger area of
myocardial damage
•increased risk of left ventricular dysfunction and death
Term posterior be abandoned and that the term inferior be applied to the
entire LV wall that lies on the diaphragm.
CIRCULATION,2006

73. • V1-3:
– Horizontal ST depression
– Tall, broad R waves (>30ms)
– UprightT waves
– Dominant R wave (R/S ratio > 1) inV2
– The progressive development of pathological R waves in posterior infarction
(the“Q wave equivalent”) mirrors the development of Q waves in
anteroseptal STEMI.
• presence of ST elevation and Q waves in the posterior leads
(V7-9).

74. MIRROR IMAGE

75. • Posterior Leads
• Leads V7-9 are placed on the
posterior chest wall in the
following positions.
• V7 – Left posterior axillary
line, in the same horizontal
plane as V6.
• V8 – Tip of the left scapula, in
the same horizontal plane as
V6.
• V9 – Left paraspinal region, in
the same horizontal plane as
V6.
The degree of ST elevation seen in V7-9 is typically modest – note that
only 0.5 mm of ST elevation is required to make the diagnosis of
posterior MI

76. Posterior Myocardial Infarction

77. • Lateral STEMI
• branches of LAD and LCx
• occurs as part of a larger territory infarction, e.g. anterolateral
STEMI.
• Isolated lateral STEMIs = less common, but may be produced by
occlusion of smaller branch arteries that supply the lateral wall, e.g.
D1/OM or the ramus intermedius.

78. • ST elevation primarily localised to leads I and aVL =a high lateral
STEMI.
• Reciprocal change in the inferior leads is only seen when there is ST elevation
in leads I and Avl
• reciprocal change may be obliterated when there is concomitant inferior ST
elevation (i.e an inferolateral STEMI)

79. This pattern is consistent with an acute infarction localised to the superior
portion of the lateral wall of the left ventricle (high lateral STEMI).
The culprit vessel in this case was an occluded first diagonal branch of the
LAD

80. Different ECG morphologies of lead V1 that can be found in lateral myocardial
infarction (MI) (the necrosed areas are seen as grey-white with gadolinium
enhancement). Note that the cardiovascular magnetic resonance imaging shows
that the inferobasal segment (segment 4) is not affected. D. On the contrary, the
inferobasal segment is completely affected in inferior MI, and the morphology in V1
is normal rS pattern.

81. Algorithm to predict the culprit artery (right coronary
artery [RCA] vs left circumflex artery [LCX]) in case of
evolving myocardial infarction with ST elevation in inferior
leads

82. Algorithm to predict the culprit artery (right coronary
artery [RCA] vs left circumflex artery [LCX]) in case of
evolving myocardial infarction with ST elevation in inferior
leads

84. LV walls divided into 17 segments according to AHA consensus.

85. Segments of anteroseptal and inferolateral zones and areas of shared perfusion. B to
D. Perfusion of these segments by the corresponding coronary arteries can be seen
in a bull's eye perspective. E. The correlation with ECG leads. DP, descending
posterior; LAD, left anterior descending; LCX, left circumflex artery; OM, marginal;
PB, posterobasal; PL, posterolateral; RCA, right coronary artery

86. ANTEROSEPTAL ZONE

87. INFEROLATERAL ZONE
Therefore, the terms posterior and high lateral MI are incorrect when applied
to these patterns and should be changed to lateral wall MI andmid-anterior
wall MI, respectively.

88. Atrioventricular (AV) dissociation

89. • Atrioventricular (AV) dissociation

90. • not an arrhythmia
• symptom of an arrhythmia—
– (1) slowing of the primary pacemaker,
– (2) acceleration of a subsidiary pacemaker,
– (3) block, and
– (4) interference.

91. • Slowing of the Primary Pacemaker
– Junctional pacemaker cells -40 to 60 /minute, and
– Ventricular pacemaker cells - 20 to 40 /minute
– If the sinus node (primary pacemaker) slows enough, a junctional
or ventricular pacemaker can emerge to take control of the
ventricles, resulting in AV dissociation.

92. From the fourth beat in the top strip to the seventh beat in the
bottom strip, there is AV dissociation between a sinus rhythm controlling the
atria and a junctional rhythm controlling the ventricles, caused by slowing of
the primary pacemaker.

93. • Acceleration of a Subsidiary Pacemaker
• If a junctional or ventricular pacemaker increases its rate of
firing above that of,the sinus node, the subsidiary pacemaker
can take over control of the ventricles while the sinus node
still controls the atria, resulting inAV dissociation.

94. • Beats 1, 2, 9, 12, and 13 are capture beats that occur when the sinus
impulse happens to arrive in theAV node at a time when conduction
to the ventricle is possible.
• TheAV dissociation in this strip is due to acceleration of a subsidiary
pacemaker (ie, the junctional focus) above the rate of the sinus node.

95. • Nonparoxysmal junctional tachycardia
– Junctional rhythm/tachycardia occur at a rate faster than the sinus
rate, without retrograde atrial capture.
– This is observed in clinical situations such as digoxin toxicity;
sinus bradycardia with escape junctional rhythm; and after cardiac
surgery, particularly valve surgery or replacement.
• Accelerated idioventricular rhythm

96. • Ventricular tachycardia
• AV dissociation in the presence of a wide QRS
tachycardia is virtually diagnostic ofVT, although the
absence ofAV dissociation does not disproveVT.

97. • Block
• The term AV dissociation is often used incorrectly as a synonym
for third-degree block.
• ThirddegreeAV block results inAV dissociation because the
atria remain under the control of a sinus or atrial rhythm
while the ventricles are controlled by a junctional or
ventricular escape rhythm.

98. • shows atrial fibrillation with third-degree block.There is
dissociation between the fibrillating atria and a junctional
escape pacemaker at a regular rate of 40 beats per minute.
The ventricular rhythm in atrial fibrillation is never
regular unless there is AV dissociation.

99. • Interference (or Pause Producers)
• Anything that interferes with the ability of an atrial impulse to
conduct to the ventricles can result in AV dissociation.AV
dissociation can result from pauses produced by premature
beats; the pause presents an opportunity for a subsidiary
pacemaker to emerge and take charge of the ventricles.
• Contradirectional interference results when 2 stimuli arising in
different foci in any part of the heart spread in opposite
directions toward each other.
• Interference dissociation is defined as that type of dissociation
which is due to repetitive contradirectional interference.

100. • dissociation due to interference between the
following pairs of rhythms:
– Normal sinus rhythm andA-V nodal rhythm,
– normal sinus rhythm and multifocal idioventricular
rhythms,
– sinus tachycardia and paroxysmal ventricular
tachycardia,
– paroxysmal atrial tachycardia with block and
idioventricular rhythm,

101. Sinus rhythm is present at rate of about 65 beats per minute. The third beat is a
premature junctional complex that conducts with right bundle branch block
aberration, creating refractoriness in the AV node (gray area in the AV level of the
ladder diagram) that prevents the next sinus impulse from conducting to the
ventricle. The failure of the sinus impulse to conduct creates a pause

102. The perturbations of the QRS complexes are due to their occurring
simultaneously with sinus P waves. Thus, there is isorhythmic dissociation of an
accelerated junctional rhythm from sinus rhythm

103. • benign phenomenon =complete or incomplete.
• Incomplete= some of the P waves conduct and
capture the ventricles (ie, interferenceAV
dissociation), but if they do not, it is completeAV
dissociation.
• Complete = mimic AV block, but the fact that none
of the P waves conduct has more to do with timing
of the P waves in relation to the QRS complex
rather than the presence ofAV block.

104. • AV dissociation by default (an independent
ventricular pacemaker responds to slowing of the
dominant atrial pacemaker)
• AV dissociation by usurpation (acceleration of a
latent pacemaker takes control of cardiac
conduction by exceeding the intrinsic atrial rate).

105. AR>VR