This document summarizes electrocardiogram (ECG) findings related to myocardial infarction (MI). It describes the ECG changes that occur in the hyperacute, evolved, and chronic phases of MI. These include ST segment elevation, T wave changes, Q wave development, and other abnormalities. It also discusses ECG patterns related to injury of specific coronary artery territories and criteria for diagnosing MI when a left bundle branch block is present.

2. M.I denotes cellular damage due to prolonged
ischaemia .Sudden cardiac death is a frequent
presenting feature of MI with most of deaths
occuring within one hour due to ventricular
arrythymias.
In presence of ischaemic symptoms the diagnosisof MI
is based upon one of the following
1.Development of new pathological Q waves.
2.Presence of ST segment elevation or depression
3.Development of new LBBB

3.  The changes in ECG should be present in two
contiguous leads.
 Confirmation by diagnosis can be done by
demonstration by elevation in cardiac
enzymes,ECHO,or by coronary angiography.

4. Based on ECG, MI is further differentiated as
STEMI and NSTEMI.
Evolution of NSTEMI into STEMI is possible and
therefore both subsets should be treated as
aggresively as possible

5. The ECG changes evolve over a period of time
and are described as
1.HYPERACUTE PHASE(over minutes-hours)
2.EVOLVED PHASE(over hours)
3.CHRONIC STABILISED PHASE(over days-weeks)
The changes in ECG of chronic stabilised phase
persists throughout life and generally represent
changes of changes of old MI in absence of further
progession of disease.

6. The ECG changes in this phase are
1.Tall,symmetrical,peaked and widened T waves
2.Slope elevation of ST segment
3.Increased amplitude of R wave/changes in
Terminal QRS complex
4.Increased ventricular activation time
This phase is critical because complication of
Ventricular fibrillation is most likely to occur and
Coronary reperfusion during this phase totally
reverses changes without any residual myocardial
damage.

7. The Twaves are tall and wide sometimes itmay
exceed amplitude of associated R wave.
Although for individual leads,different
thresholds of calling tall T waves exist,roughly
>0.5mv in limb leads and >1mv in precordial
leads can be considerded tall.

8. -One of most noticeable and characteristic
feature is slope elevation of ST segment,which
loses its upwards concavity and becomes
straightened with upward slope
-New onset J point and ST elevation of >0.1m in
leads ll,III,aVF,V4,V5,V6,I and aVL
and in leads V2,V3 of >0.2mv in males >40yr
and>0.25mv in Males <40yrs
and >0.15mm in females
-in absence of ventricular hypertrophy or LBBB
represent best variables for diagnosis of MI.

9. The R wave becomes taller than normal.
Tall R wave,slope elevated ST segment and tall
widened T wave at times merge with each other
so that it is difficult to separate 3 deflections
and the resulting wide complex is result of
QRS-ST-T fusion.

10.  There is increase in ventricular activationtime,
the time from beginning of QRS complex to
apexof the R wave
 The ventricular activation time is delayed
beyond 40ms

11. This phase is characterised by
1.Appearance of new q waves and decrease in
R wave height
2.J point and ST segment elevation
3.T wave inversion
4.Increase in ventricular activation time and
appearance of new conduction defects,blocks
5.QT prolongation

12.  Appearance of new q waves is considered
pathognomic of myocardical necrosis and
indicates irreversible myocardial damage.
 Q waves >20ms in V1 to V4 and >30ms in
other leads except III and aVR is considered
pathological.
 J point and ST elevation decreases in this
phase

13.  Tall peaked wave of hyperacute phase start to
decrease in amplitude and becomes inverted in
the infarcted area which occurs simultaneously
along with new q waves and decrease in ST
segment
 The QRS complex becomes wider due to
increase in ventricular activation time due to
slow conduction and delayed depolarization
in affected area.

14. QT interval may be prolonged due to increase
in durationof depolarization and repolarization
and appearance of new conduction defects.

15. This phase is characterised by
1.Changes in QRS complex: the q waves evolve
maximally in QS, QR or Qr pattern and sometimes
disappear.
2.Changes in J point and ST segment: elevated
J point and ST segment returns to baseline and
isoelectric
3.Changes in T wave :the inverted T waves
regains its positivity
4.Normalization of QT interval :occurs once
ischaemia is relieved

18. LEFT MAIN CORONARY ARTERY :
1.Left anterior descending:upper 2/3 septum,
anterior wall, lateral wall and apex of
L.ventricle
2.Left circumflex:lateral wall and posterior/
inferior wall
RIGHT CORONARY ARTERY:
right ventricle, inferior/posterior wall and
lower 1/3 septum

23. 1.ST elevation in lead
III>aVF>II
2.ST depression in lead
I and aVL.
3.Sum of ST depression in
lead I –III /sum of ST
elevation in lead
inferior leads <1
4.S/R ratio in lead avl >3
1.ST elevation in lead
II>aVF>III and leads V5
V6
2.No ST depression or
sometimes ST elevation
in lead I and aVL
3. 3.Sum of ST depression
in lead I –III /sum of ST
elevation in lead inferior
leads >1
4.S/R ratio in lead avl <3

26. New onset of LBBB suggests acute MI.
In patients with documented LBBB earlier,it is
difficult to diagnose AWMI due to masking
effect of LBBB on QRST changes.
CRITERIA USED FOR ACUTE AWMI WITH PRIOR
LBBB IS SGARBOSSA CRITERIA
1.ST elevation in atleast one lead of >1mm
concordant to positive QRS complex[5]
2.ST depression of >1mm in V1 to V3[3]
3.Discordant ST elevation >5mm in atleast one
leads with prominant negative QRS[2]
A total of >= 3 points suggests

27. An acute IWMI in presence of LBBB can be
diagnosed as there is no masking effect of
LBBB in inferior leads.

28. Characterised by ST segment depression dueto
Myocardial ischaemia of subendocardial region.
Following are ECG changes in NSTEMI:
1.ST segment depression
2.T wave inversion
There is little or no alternation of QRS
complex.

29. New horizontal or down sloping ST segment of
>0.05mv in two contiguous leads suggests
ongoing myocardial ischaemia

30. T wave inversion of >0.1mv in two contiguous
leads with prominent R wave suggests
myocardial ischaemia.
T wave inversion accompanies changes of ST
segment depression in NSTEMI

31. RISK OF ASSESSMENT IN NSTEMI BASED ON
ECG
1.LBBB
2.ST segment deviation of >0.05mv(1/2 small
sq)
3.T wave inversion of >0.3mv(3 small sq)

32. Descibed in a patient who presents with
history of chestpain.
ECG during during episode appears to be
normal, with ST segment in V2 and V3 being
either concave or straight and which is
Isoelectric or minimally elevated.
Following chest pain symmetric and deep T
Wave invwesion may develop in pain free
periods with no pathological Q waves and there
is no significant biochemical alternation.
This is due to tight proximal LAD stenosis.

33. The ECG dignosis reinfarction following initial
infarction may be confounded by the initial
evolutionary ECG changes.
Reinarction should be considered when ST
elevation of 0.1mv reoccurs in a patient having
lesser degree of ST elevation or new
pathognomic Q waves appear in atleast two
contiguous leads when associated with
Ischaemic symptoms for >= 20 min