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

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.

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

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.

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.

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.

-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.

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.

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

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

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

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.

QT interval may be prolonged due to increase

in durationof depolarization and repolarization

and appearance of new conduction defects.

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

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

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

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 PRIORLBBB IS SGARBOSSA CRITERIA1.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 oneleads with prominant negative QRS[2] A total of >= 3 points suggests

An acute IWMI in presence of LBBB can be

diagnosed as there is no masking effect of

LBBB in inferior leads.

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.

New horizontal or down sloping ST segment of

>0.05mv in two contiguous leads suggests

ongoing myocardial ischaemia

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

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)

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.

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