ECG PPT

1. Identification Of Myocardial
Ischemia, Myocardial
Infarction and Angina in ECG

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

4. Myocardial ischemia and injury
• Mismatch between perfusion and demand
• Ischemic myocardium goes for anaerobic
metabolism to sustain itself
• Can survive but cannot function
• Remains in resting state and does not
participate in contraction
• Reversible if blood supply is restored or
demand is lowered

5. • If blood flow is restored before glycogen gets
depleted, cells resume contraction promptly
(ischemia)
• If severe depletion of glycogen has occurred, it
becomes stunned and recovery is delayed
(injury)
• If complete depletion of glycogen occurs,
necrosis of the cells results, leading to
infarction

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

7. ECG CHANGES IN ISCHEMIA

8. ECG effects of myocardial ischemia
• Manifest by changes in T waves

9. • T waves may become
– Flattened
– Inverted
– Tall or
– Biphasic
ECG effects of myocardial ischemia

10. • T waves that are deep and symmetrically
inverted (arrowhead) strongly suggest
myocardial ischaemia.
• At least 1 mm deep
• Present in ≥ 2 continuous leads that have
dominant R waves (R/S ratio > 1)
• Dynamic — not present on old ECG or
changing over time
T wave inversion

11. Widespread T wave inversion due to myocardial ischaemia

12. Point to note
• Inverted T waves are normal in leads III, aVR,
and V1
• Associated with a predominantly negative QRS
complex.

13. A – T wave in coronary insufficiency
B – T wave in LVH with strain
C – T wave in digitalis effect
Other causes of T inversion

14. ECG CHANGES IN MYOCARDIAL
INJURY

15. 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
– St elevation

17. Forms of ST depression
• Horizontality
• Upward sloping ST depression
• Downward sloping ST depression

18. ST depression
• Horizontal or downsloping ST depression ≥ 0.5
mm at the J-point in ≥ 2 contiguous
leads indicates myocardial ischaemia.
• ST depression ≥ 1 mm is more specific and
conveys a worse prognosis.
• ST depression ≥ 2 mm in ≥ 3 leads is associated
with a high probability of NSTEMI and predicts
significant mortality (35% mortality at 30 days).
• Upsloping ST depression is non-specific for
myocardial ischaemia.

19. Normal ST segment
Horizontality of ST segment
Plane ST segment Upwards sloping ST Downsloping ST segment

20. Horizontal ST segment depression

21. Upwards sloping ST depression in V2 – V5

22. Downsloping ST depression with T inversion in I, aVL, V5, V6

23. Other causes for ST depression
DEPRESSED ST --->
• D - Drooping valve (MV Prolapse)
• E - Enlargement of the left ventricle
• P - Potassium low
• R - Reciprocal ST Depression (eg. Inferior MI)
• E - Encephalon (Intracerebral) Haemorrhage
• S - Subendocardial Infarct
• S - Subendocardial Ischaemia
• E - Embolism (Pulmonary)
• D - Dilated Cardiomyopathy
• S - Shock
• T - Toxicity (Digitalis/Quinidine

24. ST

25. ST elevation
• Epicardial injury – ST deviated towards
epicardial surface
• Leads oriented towards the epicardial surface
eg Lead V6 will have a raised ST segment
• Leads oriented away will have a depressed ST
segment eg aVR

26. ECG Changes in Acute and Chronic
Myocardial Infarction

27. Characteristic Changes in Acute
Myocardial Infarction
ST segment elevation over area of damage
ST depression in leads opposite infarction
Inverted T waves
Pathological Q waves

28. Hyperacute MI
• Q waves and prominent doming ST
segment elevation in II, III, and aVF,
findings which are characteristic of an
acute inferior myocardial infarction. ST
elevation in the right precordial leads -
V4R, V5R, and V6R - indicates right
ventricular involvement

29. Acute MI
• Evolving Q-wave anterior MI:
loss of R waves in leads V1 to
V3, ST segment elevations in
V2 to V4, and T wave
inversions in leads I, aVL, and
V2 to V5. Sinus bradycardia (55
beats/min) is present due to
concurrent therapy with a beta
blocker

30. Evolved MI
• Later stage in the
evolution of an acute
anterior myocardial
infarction. There is a QS
pattern in leads V1 to
V3 and T wave
inversion in leads V2 to
V4. The ST segment
elevations in these
leads have almost
disappeared

31. ST Elevation MI

32. According to the ACC/AHA guidelines for STEMI, there
must be “ New ST elevation at the J point in at least 2
contiguous leads of >= 2 mm (0.2 mV) in men or 1.5 mm
(0.15 mV) in women in leads V2- V3
and/ or
Of >=1 mm (0.1mV) in other contiguous chest leads or the
limb leads
Thus, 1 mm in any 2 contiguous leads EXCEPT leads V2 or
V3 where the elevation must be 2 mm in men or 1.5 mm
in women.

33. ECG evaluation in Non-Perfused MI

34. Location of Infarct Combinations

35. Anterior Wall ST Elevation MI
ECG Findings:
1. ST segment elevation in the anterior leads at J point and sometimes in
septal or lateral leads depending on the extent of the myocardial
infarction
2. Reciprocal ST segment depression in the inferior leads (II, III and aVF)

36. Inferior Wall ST Elevation MI
ECG Findings:
1. ST segment elevation in the inferior leads (II, III, aVF)
2. Reciprocal ST segment depression in the lateral and/or high lateral
leads (I, aVL, V5, and V6)

37. Posterior Wall MI
ECG Findings :
1. ST segment depression in the septal and anterior precordial leads (V1 to V4)
2. The ratio of the R wave to S wave in leads V1 or V2 is > 1
3. ST elevation in the posterior leads of a posterior ECG (leads V7 to V9)
4. ST elevation in the inferior leads (II, III, and aVF) may be seen if an inferior MI is
also present[

40. Reciprocal Changes in MI
 Commonly observed on ventricular wall opposite to the transmural
injury
Increases the specificity of STEMI
In AWMI- Reciprocal changes in inferior leads are seen in 40-70% of
the cases
In IWMI- Reciprocal depression in I and aVL and lateral leads

42. NON ST Elevation MI
ECG feature can be any of the following:
1. ST depression (70-80% sensitivity)
2. T wave inversion (10-20% sensitivity)
3. Both ST depression and T wave insertion
4. Normal ECG

43. STEMI vs Acute Pericarditis

44. Wellen’s Syndrome
 Wellens’s syndrome (or sign) is a pattern of deeply inverted or biphasic T waves in
V2-3, which is highly specific for a critical stenosis of the left anterior descending
artery (LAD)
 Subacute LAD Occlusion (within the next week)

46. De Winter ST/T Waves

47. Brugada Syndrome
 A hereditary syndrome, marked by right bundle branch block and ST segment
elevation in the right precordial leads, and a high risk of sudden death from
ventricular arrhythmias

48. Benign Early Repolarization
 Widepread concave ST elevation
 Notching or slurring at the J-point
 Prominent, slightly asymmetrical T-waves that are concordant with the QRS complexes
 No reciprocal ST depression to suggest STEMI (except in aVR)
 ST changes are relatively stable over time (no progression on serial ECG tracings)

49. Hypothermia
 Osborne waves (= J waves)
 Prolonged PR, QRS and QT intervals
 Shivering artefact
 Ventricular ectopy
 Cardiac arrest due to VT, VF, or asystole

50. Sgarbossa’s Criteria
 ST elevation >=1 mm in a lead with a positive QRS complex (ie :
concordance)- 5 points
 ST depression >= 1 mm in lead V1, V2, or V3- 3 points
 ST elevation >= 5 mm in a lead with a negative (discordant) QRS complex- 2
points
 >= 3 points = 90% specificity and 20% sensitivity

52. ECG in Chronic MI

54. LV Aneurysm
 ST elevation seen > 2 weeks following an acute myocardial infarction
 Most commonly seen in precordial leads
 May exhibit concave or convex morphology
 Usually associated with well- formed Q or QS waves
 T- waves have a relatively small amplitude in comparison to the QRS complex

55.  Factors Favouring Left Ventricular aneurysms
 ECG identical to previous ECGs
 Absence of dynamic ST segment changes
 Absence of reciprocal ST depression
 Factors Favouring Acute STEMI
 New ST changes compared with previous ECGs
 Dynamic/progressive ECG changes- the degree of ST elevation increases
on serial ECGs
 Reciprocal ST depression
 High clinical suspicion of STEMI- ongoing ischemic chest pain, sick
looking patient (eg. Pale, sweaty ), hemodynamic instabilty

56. ECG changes during Angina
ECG at rest
ECG during angina

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