ECG DIAGNOSIS OF ACUTE CORONARY SYNDROME

1. ECG DIAGNOSIS OF ACS
DR SHIVANI RAO
ASSISTANT PROFESSOR
DEPARTMENT OF
CARDIOLOGY
IGMC SHIMLA

2. TOPICS TO BE COVERED
• IMPORTANCE OF ECG
• ACS SPECTRUM
• Basics about ECG
• how to define STEMI/NSTEMI on ecg
• EVOLUTION OF STEMI ON ECG
• LOCALISATION OF OCCLUDED ARTERY ON ECG
• FEW STEMI /NSTEMI MIMICS
• CASE DISCUSSION

3. • ECG remains a key test for diagnosis and management of ACS
• But it is the not the only tool alone to diagnose it
ECG
CLINICAL
CORELATION
OLD ECG
/SERIAL ECGS
EXPERT
CONSULTATION
HISTORY AND
RISK

4. ACUTE CORONARY
SYNDROME
ECG
<10 MINUTES
NO ST ELEVATION
STEMI
CARDIAC BIOMARKERS
-VE +VE
UNSTABLE ANGINA NSTEMI

5. WHY IMPORTANT TO DISTINGUISH BETWEEN
BETWEEN STEMI AND NSTEMI?
MANAGEMENT IS
DIFFERENT !!
STEMI
IMMEDIATE REPERFUSION
THERAPY
NSTEMI

6. WHAT TO LOOK IN THE ECG
AXIS

8. Need reference point
Compare to TP segment
DO NOT use PR segment as reference

9. Waveform Components: Practice
• Find J-points and ST segments

10. MORPHOLOGY OF STE
 Concave shape STE – non AMI causes
 AMI causes – usually demonstrate
convex/straight STE
J point
Apex of T wave
Concave STE
Convex STE

11. MORPHOLOGY OF T WAVE

13. STEMI is defined as new ST elevation at the J point in at least two
contiguous leads
[in the absence of left ventricular (LV) hypertrophy or left bundle branch block
LBBB)]
V2-V3

14. NSTEMI ON ECG
• ST Depression
• T wave inversion
• Or both
• Normal ECG
NEW horizontal or downsloping ST depression of >0.5mm in atleast two anatomically contiguous
leads

15. 38/YEAR /FEMALE /DM /CHEST PAIN SINCE 7 HOURS
STEMI OR NSTEMI/UA???

16. RECIPROCAL AND INDICATIVE CHANGES
RECIPROCAL
CHANGES
depressed ST
segments
associated with
acute MI
INDICATIVE
CHANGES
Coved ST and
elevated ST
SEGMENTS acute MI

17. 78YR/M/SMOKER/HTN/DM/DYSLIPIDEMIA/CHEST
PAIN 1 HOUR

18. The injury vector is always oriented toward the injured area. The lead
facing the injury vector head shows ST-segment elevation and the lead

19. ECG EVOLUTION OF MI
PHASE
1:HYPERACUTE
PHASE
PHASE 2:FULLY
EVOLVED PHASE
PHASE 3:CHRONIC
STABALISED PHASE
PHASE 1:HYPERACUTE PHASE
• Tall,symmetrical ,peaked
&widened T wave
• Slope elevation of ST segment
• Increased amplitude of R wave
• Increased ventricular activation
time

29. WHICH AREA OF THE HEART IS EFFECTED ???
WHICH VESSEL IS EFFECTED?????

30. LOCALISATION
Inferior: II, III, AVF
Septal: V1, V2
Anterior: V3, V4
Lateral: I, AVL, V5, V6
I
II
III aVF V3
aVR V1
aVL V2
V4
V5
V6

31. 69 year old/ male/smoker chest pain since 1 hour
TNK

32. 56 yrs/male/DM/chest pain since 4 hours/
ALTEPLASE

33. Thrombolysed with alteplase

34. 45 year old male /dyslipidemic/HTN/h/o chest
pain since 1 day

35. 65 YEAR/FEMALE/SMOKER CHEST PAIN SINCE
1 HOUR

36. Localization - Extensive Anterior MI
33

37. 62 year/male/chest pain 3.5 HRS
bp=100/80mmHg pulse 80/min

38. Localization Criteria: Occluded
artery to the ECG

39. precordial leads can be classified
different infarct patterns -according to maximal ST elevation
ANTERIOR WALL MI

40. Amount of LV myocardium at risk of infarction in
case of AWMI depends largely on the site of
occlusion
Proximal
MID
DISTAL
EARLY IDENTIFICATION
OF PROXIMAL LAD
OCCLUSION IS
IMPORTANT

41. Proximal LAD occlusion
(Dominance of Basal area)
Injury vector is directed anteriorly and upward, and somewhat to the right or left

42. Distal LAD occlusion
(Dominance of inferoapical area)

43. • The 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.Awareness of the possibility of a
“wraparound” LAD lesion explains the ECG pattern of simultaneous ST segment
elevation in inferior and anterior lead areas.
• Not surprisingly, such infarctions are often quite large
“wraparound” LAD

45. • PROXIMAL LAD LESION
ST elevation in I, aVL and V1-V6 WITH ST depression in II, III, aVF
• qRBBB and ST elevaton in aVR may also be associated

46. ECG CHANGES THAT CAN BE
MISSED IN A PATIENT WITH
AWMI
PROXIMAL LAD
LMCA
WELLENS
And DE WINTERS
SIGN

47. classical pattern of left main coronary artery (LMCA)
occlusion:
Widespread horizontal ST depression, most prominent in leads I, II and V4-6
ST elevation in aVR ≥ 1mm
ST elevation in aVR ≥ V1

48. Extensive anterior MI
(“tombstoning” pattern)

49. WELLEN’S SYNDROME
• deeply inverted or biphasic T waves in V2-3, which is highly specific
for a critical stenosis of the left anterior descending artery (LAD).
• Patients may be pain free by the time the ECG is taken and have
normally or minimally elevated cardiac enzymes; however, they are at
extremely high risk for extensive anterior wall MI within the next few
days to weeks.
• these patients usually require invasive therapy;

51. De-winters sign
anterior STEMI equivalent that presents without obvious ST segment
elevation
•Tall, prominent, symmetric T waves in the precordial leads
•Upsloping ST segment depression >1mm at the J-point in the precordial
leads
•Absence of ST elevation in the precordial leads

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

53. •more favourable prognosis than AMI
40%-50% of patients will have a concomitant right ventricular infarction(severe
hypotension in response to nitrates and generally have a worse prognosis).
Up to 20% will develop significant bradycardia due to second- or third-degree AV
block. These patients have an increased in-hospital mortality (>20%).
may also be associated with posterior infarction, which confers a worse prognosis
due to increased area of myocardium at risk.
INFERIOR STEMI--CLINICAL SIGNIFICANCE

55. STEIWMI
80%
RCA
AROUND 18%
LCX
OCCLUSION OF
TYPEIII/WRAP
AROUND LAD

56. 40-50% IWMI MAY HAVE ASSOCIATED RVMI
• Right ventricular infarction
is confirmed by the presence
of ST elevation in the right-
sided leads (V3R-V6R).

57. RCA LCX
SUPPLY covers the medial part of the inferior
wall,including the inferior septum
covers the lateral part of the
inferior wall and the left
posterobasal area
INJURY CURRENT is directed inferiorly and rightward,
producing ST elevation in lead III > lead
II (as lead III is more rightward facing)
directed inferiorly and
leftward, producing ST
elevation in the lateral leads I
and V5- 6.
LEADS I,AVL ST Depression No ST depression but if lateral
WMI elevation will be present

59. RCA OR LCX?
STEMI or NSTEMI

60. 70 YEAR /FEMALE/DM/RESTROSTERNAL CHEST PAIN X
YEARS
BP=150/80 PULSE 80/MIN
RIGHT SIDED
LEADS

61. THROMBOLYSED WITH TNK

62. LCX
STE II>III
In lead I and
aVL STE OR
ISOELECTRIC
STD in lead
v1-v3

63. LCx Occlusion

64. POSTERIOR MYOCARDIAL
INFARCTION
• Posterior infarction accompanies 15-20% of STEMIs, usually
occurring in the context of an inferior or lateral infarction.
• 12 lead ECG is a relatively INSENSITIVE TOOL FOR
DETECTING PWMI.This is due to the absence of standard
leads facing the posterior wall of LV
• Posterior infarction is confirmed by the presence of ST
elevation and Q waves in the posterior leads (V7-9).
• PWMI is suggested in V1-3:
– Horizontal ST depression
– Tall, broad R waves
– Upright T waves
– Dominant R wave (R/S ratio > 1) in V2

65. MIRROR IMAGE
– The progressive development of
pathological R waves in posterior
infarction (the “Q wave
equivalent”) mirrors the
development of Q waves in
anteroseptal STEMI.

67. STEMI or NSTEMI RCA OR LCX?

68. 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

69. ST-SEGMENT ELEVATION IN III>II
And
ST –SEGMENT DEPRESSION IN LEAD I and aVL or both
RCA
YES
NO
IN ADDITION ST- SEGMENT ELEVATION IN V1 and V4R or
both
Proximal RCA with RVMI
ST- SEGMENT ELEVATION IN I,aVL,V5,V6
And depression in V1-V3
LCX

70. ACUTE MI IN PRESENCE OF LBBB

71. • QRS duration of > 120 ms
• Dominant S wave in V1
• Broad monophasic R
wave in lateral leads (I,
aVL, V5-V6)
• Absence of Q waves
in lateral leads (I, V5-V6;
small Q waves are still
allowed in aVL)
• Prolonged R wave peak
time > 60ms
in left precordial leads
(V5-6)

73. 5 POINTS

74. 3 POINTS

75. 2 POINTS

78. STEMI/NSTEMI MIMICS
• BENIGN EARLY REPOLARISATION
• HYPERKALEMIA
• PERICARDITIS
• LVH/LBBB
• WPW
• ICH

79. BENIGN EARLY REPOLARISATION
• WIDESPREAD CONCAVE ST ELEVATION
• NOTCHING OR SLURING OF J POINY
• NO RECIPORCAL STD TO SUGGEST STEMI
• CHANGES ARE STABLE OVER TIME
• NO TERRITORIAL DISTRIBUTION

80. HYPERKALEMIA

81. PERICARDITIS
• Widespread concave ST elevation and PR depression throughout most
of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).
• Reciprocal ST depression and PR elevation in lead aVR (± V1).

83. LVH

84. ECG Diagnostic Criteria for LVH
R in aVL> 11mm 11 100
Other Criteria include Romhilt and Estes Point Score System
Chan TC, Brady WJ, Harrigan RA et al. ECG in Emergency Medicine and
Acute Care. 1st ed. Pennsylvania: Elsevier Mosby; 2005.
100
11
R1 + SIII>25 mm
96
42
Cornell Voltage Criteria
SV3+RaVL>28 mm (men), 20mm(women)
100
22
Sokolow-Lyon Index
SV1 + (RV5 or RV6)>35mm
Specificity
Sensitivity

85. WPW

87. 68 male/chest pain since 1.5 hours bp 98/60 pulse
88/min

88. Thrombolysis with tnk

89. 58 year f/DM/chest pain retrosternal since 4
hours

90. 80 year female/pain epigastrium/bp 220/130
PR 86

92. TREAT THE PATIENT NOT THE ECG
THANK YOU