ECG IN ISCHEMIC DISEASE

MYOCARDIAL ISCHEMIA
 Definition = an imbalance between myocardial oxygen
supply (from arterial blood) and demand.
 Causes:
 A reduction in blood flow that may appear secondary to an
obstruction of the coronary artery (thrombus, embolus), a
stenosis (atheromatous plaque), or an increased coronary
vascular tone.
 An increase in the demand: in exercise, tachycardia.
 Typically there is an association, in different proportions, of
decreased supply and increased demand, that determines
myocardial ischemia.
 Another possibility is a reduced oxygen supply despite of a
normal blood flow: hypoxia
 The myocardium depends almost entirely on aerobic
metabolism.
 The subendocardium is more vulnerable than the midzone of
myocardium and subepicardium to the ischemic damage;
that is because of the anatomic distribution of arterial supply
(the subendocardium is most distal); also, in cases of
reduced arterial supply the subendocardium/subepicardium
flow ratio is reduced.
ECG TERMS
 ischemia= typical T wave modifications;
 injury = typical ST modification;

 necrosis = pathological Q wave.

 They are ECG terms and must not be taken as the

anatomopathological description!

 These modifications appear typically in more than one of a

group of localized leads: left leads, inferior leads, anterior
(antero-septal) leads, etc. depending on the territory that is
affected and the artery that is feeding that territory (these will
be described under the topography of myocardial infarction).
T WAVE MODIFICATIONS

 Subendocardial ischemia = positive, symmetric and

more pointed T wave.

 Subepicardial ischemia = negative, symmetrical and

more pointed T wave.

 Non-specific T wave modifications: flat T waves, either

positive or negative; biphasic T waves.
 SUBENDOCARDIAL ISCHEMIA
 The affected area remains longer electronegative during
repolarization. The leads that have positive electrode (for bipolar
leads)/exploring electrode (for unipolar leads) closer to the area will
register this modification.
 Vectors are oriented from negative towards positive.

 If the affected area is subendocardium, the local electrodes will

register a positive potential variation, and a positive T wave is
recorded in the respective leads.
SUBEPICARDIAL ISCHEMIA
 If the affected area is subepicardium, the local leads will
register a negative projection, and a negative T wave is
recorded in the respective leads.
ST MODIFICATIONS

 Subendocardial injury = depressed ST segment; usually j

point is also depressed; ST segment can be horizontally
depressed, descending/ ascending.

 Subepicardial injury = elevated ST segment; elevated j

point; ST segment can be horizontal, ascending, curved
with its convexity upwards.
SUBENDOCARDIAL INJURY
 The affected areas is later depolarized; remains longer
electro(+). The leads closer will register directly this
modification, as a projection. The vector is oriented
towards electro(+)
 If the affected areas is subendocardial, the local leads
will register a depression of the ST segment
SUBEPICARDIAL INJURY
 If the affected area is situated subepicardial, in the leads
that have positive electrode ( for bipolar leads) and
exploring electrode (for unipolar leads) nearby will
record a ST segment elevation
NECROSIS = PATHOLOGICAL Q WAVE

 A Q wave that doesn’t have the normal q wave criteria

should always be regarded as pathological.

 Sometimes we can consider as pathological a q wave that

hasn’t gone over the normal criteria if it is a new
acquisition and especially if it is associated with
suggestive ST and T changes, or in a suggestive clinical
context.
 The apparition of a pathological Q wave is associated
with a transmural MI – a acute obstruction of a coronary
artery that affects its territory from subendocard to
subepicard. The affected territory has no electrical
activity even if the cells aren’t dead yet.
 The rest of the tissue, that has electrical activity,
determines a resultant vector that has a sense in the
opposite way. The regional leads will register that vector
with a negative projection = Q wave.
MIRROR-IMAGE (RECIPROCAL CHANGES).

 If the regional leads will „see” a ST elevation, the leads

that are distanced from the affected area can register the
opposite image = a ST depression. We never consider a
ST elevation as a mirror image of a ST depression,
except maybe in aVR.
 If the regional leads will „see” a Q wave, the leads that
are distanced from the affected area can register the
opposite image = a taller R wave.
An ST elevation can determine a A Q wave can determine a mirror image
reflection image as a ST depression as a taller R wave. This can be useful in
posterior MI as we don’t use posterior
leads as a standard.
MYOCARDIAL INFARCTION

 ‚Natural’ evolution of a transmural MI = Q wave MI – the

evolution without treatment.
 There are four phases:
1. superacute phase ( or acute-initial);
2. acute phase;
3. subacute phase;
4. chronic phase.

 We must take note that, depending on the affected territory, the

described modification will appear only in certain leads (e.g. in
inferior MI the direct or typical modification will appear in
inferior leads: DIII, aVF, DII).
1. SUPERACUTE PHASE

The first 6 hours since the obstruction of the artery:

In the first moment appears a tall, positive, peaked T wave.

The ST segment starts to elevate and it is convex towards up.

ST elevates gradually until it includes T wave and forms a

Pardee wave.
2. ACUTE PHASE
 from the first 6 hours till 2 weeks from the onset.
 The ST segment is elevated, then gradually comes closer to
the isoelectric line (at the end of this phase ST is isoelectric).
 T wave starts to descend, and at the end of this phase is
negative.
 Q wave appears usually during this time. ( there are
exceptions – cases with precocious apparition of Q wave, in
the first 6 hours).
3. SUBACUTE PHASE
 from 2 weeks to 2 months.
In this state there are:
 Q wave

 isoelectric ST segment

 negative T wave

 ST segment can remain elevated (in case of a ventricular

aneurysm)
4. CHRONIC PHASE
 from 2 months onwards.
 The T wave becomes positive.

 Q wave can persist or in some cases (20%) it can

disappear.
 T wave can remain negative in the chronic phase.
STEMI = ST ELEVATION MI

 A more recent term; shows the importance of ST elevation.

 A majority of patients with STEMI develop Q waves and
follow the typical ECG evolution previously described.
 Some patients with STEMI don’t develop Q waves; some
modifications of QRS complex can appear in these cases, such
as diminution in R wave height or notching of the QRS
complex.
NSTEMI = NON-ST ELEVATION MI
 There are cases of myocardial infarction without ST
elevation on ECG: ST depression; negative T waves.
 The difference between NSTEMI and unstable angina is
made using biological markers for necrosis (e.g. cardiac
troponins).

 It is important to remember that the diagnostic in acute

coronary syndromes should be made by using a
corroboration between clinical signs, ECG, biological
markers.
 ARTERIAL DISTRIBUTION IN
MYOCARDIUM
 Left main coronary artery:
 LAD (left anterior descendant artery) =
anterior interventricular artery: anterior
wall of LV, anterior part of the septum, a part
of anterior wall of RV, right bundle brunch,
the 2 left fascicles.
 circumflex artery: lateral part of anterior
wall –LV, lateral wall LV, posterior wall of
LV.
 Right coronary artery (in 90% cases it
branches in posterior interventricular
artery = posterior descendant artery):
posterodiafragmatic wall of LV; most of RV,
posterior part of the septum, AV node, His
bundle, left posterior fascicle,
posterodiafragmatic wall of LV.
TOPOGRAPHY OF MI (I)
 Septum MI:
 Typical ECG modifications in V1, V2
 Anterior infarction:
 Typical (=direct) ECG modifications in V1, V2, V3, V4.
 The affected coronary artery: LAD (left anterior descending artery) = anterior interventricular
artery;
 Antero-lateral MI (or anterior-extended):
 Typical ECG modifications in V1, V2, V3, V4, V5, V6, DI, aVL.
 The affected artery: LAD in its proximal segment.
 Antero-inferior MI:
 Typical ECG modifications in precordial leads and in inferior leads.
 This happens in situations in which LAD is supplying the distal portion of the inferior wall.
 Inferior infarction:
 Typical ECG modifications in inferior leads.
 In most cases the affected artery is the right coronary or posterior descending artery (=
posterior interventricular artery). Usually posterior descending artery is a branch of right
coronary artery; in a minority (~10%) of cases, the posterior interventricular artery is a branch
of the circumflex coronary artery.
 In DI and aVL we can find reciprocal changes.
TOPOGRAPHY OF MI (II)
 Lateral MI:
 Direct image of MI in DI, aVL, V5, V6.
 The affected artery: circumflex artery.
 Infero-lateral MI:
 Direct image of MI in inferior leads, V5, V6.
 an occlusion of the circumflex artery (= a left dominance)/ an occlusion of right artery if
the affected right artery has extensive posterolateral branches that supply a part of the
lateral wall (=a right dominance).
 Posterior MI:
 Reciprocal changes in V1: taller R, depressed ST segment, positive T wave.
 Direct image of MI: in posterior leads.
 Usually this region is supplied by posterolateral branches of right coronary artery, from
its distal segment.
 RV infarction:
 Typical image: in V1, V2, V3R, V4R, V5R.
 The affected artery: right coronary artery, proximal. A distal obstruction of right
coronary artery is usually associated with inferior MI.
DIFFERENTIAL DIAGNOSIS OF MI

 QS waves in V1, V2 +/- ST elevation.

 Anterior MI
 LBBB
 LVH
 WPW syndrome B

 Tall R and ST depressed in V1

 Posterior MI.
 RVH
 RBBB
 WPW syndrome A