COMPLICATIONS OF

MYOCARDIAL INFARCTION
IN ECG
EDITED BY – MALIK
HAPPY
(3rd course)
 ECG/EKG
(electrocardiography)

- Transthoracic interpretation of electrical activity of heart

 OVERVIEW OF
• ECG
Record electrical activity of heart.
• Used to treat irregularities of the heart functions.
• Conducted by placing skin electrodes on different parts of the body.
MAIN POINTS TO REMEMBER IN
GRAPH
 WHAT ARE ECG
LEADS ???
• ECG LEADS : lead refer to a combination of positive and negative
electrode which helps to view electrical activity of heart in the form
of wave in ECG paper.
• TO RECORD ECG 12 DIFFERENT LEADS ARE PLACED ON THE BODY.
• TYPES OF LEAD:
o UNIPOLAR : positive electrode are active but negative electrodes are
at zero potential.
o BIPOLAR : both negative and positive electrode are active.
 CLASSIFICATION OF
LEADS :
• Leads I, II, and III are bipolar leads.
• Leads aVR, aVL, and aVF are unipolar leads.
• Leads V1- V6 are unipolar leads.

• Leads V1 to V6 are known as the anterior leads, meaning that they look at the front of the heart.
• Lead 1, aVL, V5, V6 – lateral leads shows lateral view (receive blood flow from left circumflex
artery).
• V1 and V2 look at the right ventricle an d interventricular septum,
• V3 and V4 look at the anterior surface of the ventricles.
• V5 and V6 look at part of the left ventricle. These views c a n b e remembered by thinking about
where the electrodes are pla ce d on the patient.
• Leads II, III and aVF are the inferior leads an d look at the bottom part of the left ventricle.
• Leads I, aVL, V5 and V6 are the lateral leads, a n d look at the side of the left ventricle.
 12 LEADS RESTING ECG
ELECTRODE
PLACEMENT

EINTHOVEN’S TRIANGLE
CORONARY ARTERIES AND
THEIR CORRESPONDING ECG
LEAD
 EINTHOVEN’S
• TRIANGLE
It is an imaginary formation of three bipolar limb leads ((I, II, and III) in
a triangle used in electrocardiography, formed by the two shoulders and
the pubis. The shape forms an inverted equilateral triangle with the heart
at the center.

BIPOLAR LIMB LEADS

Electrical connections between patients limbs
and electrocardiograph by using positive and
negative electrode.

EINTHOVEN LAW
Lead I potential + lead III potential = lead II
potential
GRAPHICAL REPRESENTATION BIPOLAR LIMB AUGMENTED
OF CHEST LEADS LEADS UNIPOLAR
LIMB LEADS
 HOW THE CONDUCTION SYSTEM
LOOKS ON AN ECG ???
• Before atrial depolarisation, the SA node depolarises but the signal is not enough to register on an
ECG so it appears as an isoelectric segment (flat line).
• Then there is atrial depolarisation which appears as an upward deflection as depolarisation
sp rea d s tow a rds the elec trod e. This is the P wave .
• The impulse reaches the AV node a n d is delayed after atrial depolarisation. This appears as
another isoelectric segment.
• The impulse spreads to the ventricles, a nd ventricular depolarisation is now seen as the QRS
complex.
• The depolarisation of the septum happens from right to left. This is seen as a downward deflection as it is
a w a y from the electrode, which is the Q aspect of the QRS complex.
• This is followed by an upwards deflection (R wave) as the depolarisation spreads d o w n the bundle of His.
• The negative deflection is the S w a v e a n d is the w a v e of depolarisation spreading up the walls of the
ventricles via the purkinje fibres a w a y from the positive electrode.
• There is then an isoelectric segment once ventricular depolarisation is complete.
• Finally ventricular repolarisation occurs which is seen as the T wave.
• An additional U wave c a n sometimes been seen in an ECG. This is a sign of pathology, e.g.
hypokalaemia.
12 LEADS ECG IN A HEALTHY
PERSON
 MYOCARDIAL INFARCTION
MI is defined as a
diseased condition which
is caused by reduced
blood flow in a coronary
artery due to
atherosclerosis &
occlusion of an artery by
an embolus or thrombus.
MI or heart attack is the
irreversible d a m a g e of
myocardial tissue caused
by prolonged ischaemia
& hypoxia.
PATHOPHYSIOLOGY
 ST SEGMENT ELEVATION MI , NON
STEMI AND DEPRESSION OF ST
SEGMENT IN MI
• ST-segment elevation myocardial infarction (STEMI) is the term cardiologists
use to describe a classic heart attack.
• It is one type of myocardial infarction in which a part of the heart muscle
(myocardium) has died due to the obstruction of blood supply to the area.
• Com p a red to the m ore c omm on typ e of hea rt a tta c k known a s STEMI,
a n NSTEMI is typically less damaging to your heart.
• ST- seg ment d ep ression MI - Just like ST elevation, not a ll ST
depression represents myocardial ischemia or an emergent condition.
There are multiple conditions associated with ST depression. Some of
these include hypokalemia, cardiac ischemia, and medications such as
digitalis.
GRAPH SHOWING ST ELEVATION IN
MI
GRAPH SHOWING ST DEPRESSION IN
MI
 EXACTLY WHAT HAPPENS IN ECG
WHEN A PERSON HAVE MI ???
• When there is a blockage of the coronary artery, there
will be lack of oxygen supply to all three layers
of cardiac muscle (transmural ischemia).
• The leads facing the injured cardiac muscle cells will
record the action potential as ST elevation
during systole while during diastole, there will be
d ep ression of the PR seg m ent a nd the PT seg m ent.
Sinc e PR and PT interval are regarded as baseline, ST
segment elevation is regarded as a sign of myocardial
ischemia.
The opposing leads (such as V3 and V4 versus posterior
lea d s V7-v9) a lw a ys show s rec ip roc a l ST seg m ent
changes (ST elevation in one lead is followed by ST
depression in the opposing lead).
• This is highly specific for myocardial infarction
12-lead electrocardiogram showing ST-segment elevation
(orange) in I, aVL and V1-V5 with reciprocal changes (blue) in
the inferior leads, indicative of an anterior wall MI
COMPLICATIONS OF MYOCARDIAL
INFARCTION
• CARDIOGENIC SHOCK
• ARRHYTHMIAS
• CONGESTIVE HEART FAILURE (CHF)
• RUPTURE
• MURAL THROMBUS
• FIBRINOUS PERICARDITIS WITH OR WITHOUT
EFFUSION
• VENTRICULAR ANEURYSM
• RIGHT VENTRICULAR AMI
CARDIOGENIC SHOCK

• About 10% of patients with acute MI develop cardiogenic shock

characterised by hypotension with systolic blood pressure of 80 mmHg or
less for many days.
• Shock may b e accompanied by peripheral circulatory failure, oliguria
and mental confusion.
• But revascularization c an improve the survival cases in the patients.
 ECG SHOWING CARDIOGENIC SHOCK
ECG parameters identified patients with cardiogenic shock who were at high risk. Emergency
revascularization eliminated the incremental mortality risk associated with cardiogenic shock in
patients with a prolonged QRS duration, or inferior AMI accompanied by precordial ST depression.
 ARRHYTHMIA
S
• Arrhythmias (or abnormalities in the normal heart rhythm) are the most
common complication in acute MI.
• These occur due to ischaemic injury or irritation to the conduction system,
resulting in abnormal rhythm. Other causes of arrhythmias include leakage of K+
from ischaemic muscle cells and increased concentration of lactate and free fatty
acids in the tissue fluid.
• premature ventricular contractions(PVC’s) – most common arrhythmia)
• Ventricular fibrillation – most common cause of death
• Frequently associated with cardiogenic shock
• Heart block
• Incidence of 5% of inferior AMI’s and 3% of anterior AMI’s
ECG Identification of Arrhythmias
 CONGESTIVE HEART FAILURE
(CHF)
• About half the patients with MI develop CHF which may
b e in the form of right ventricular failure, left ventricular
failure or both.
• CHF is responsible for about 40% of deaths from acute
MI.
• If the patient survives, healing may restore normal
cardiac function but in some CHF may persist and require
regular treatment later.
• Typical onset within 24 hours after infection
 RIGHT SIDED HEART FAILURE
AND TACHYCARDIA

from lead II across the bottom that this was atrial flutter.
 RUPTU
•
RE
Most likely to occur between days 3 and 7 (range,
1-10days) depending upon the patients.
• Rupture of the heart occurs in up to 5% cases of
acute MI causing death.
• ANTERIOR WALL RUPTURE
• Most common anterior or lateral ventricular walls.
• Results in cardiac tamponade
• Most commonly associated with the thrombosis of the
left anterior descending coronary artey (LADCA).
FREE WALL RUPTURE OF LEFT
VENTRICLE-
ECG showed an acute inferior STEMI
• POSTEROMEDIAL PAPILLARY MUSCLE
RUPTURE OR DYSFUNCTION
• Most often associated with inferior acute myocardial
infarction which is caused by thrombosis of the right
coronary artery.
• Presents with an acute onset of mitral valve
regurgitation and left sided heart failure (LHF).

INTERVENTRICULAR SEPTUM RUPTURE (IVS)

Most often associated with a thrombosis in the left
anterior descending coronary artery.
Which produces a left right shunt, causing RHF (right heart
failure
– because it overloads the R.V).
DIAGNOSIS : increased O2 saturation and pressure in the right
ventricle.
Rupture at any of these sites occurs usually in the first week and is
often fatal.
 RIGHT VENTRICULAR ACUTE
MI
• Associated with the right CA thrombosis.
• Occurs in one- third of inferior AMI’s clinically
significant significant in 30% of cases
• CLINICAL FINDINGS:
• Includes hypotension
• Right heart faiure
• Preserved left ventricular function (because there is no
problem in left ventricle at all).
• Inferior STEMI with STE in III > II
• Reciprocal ST depression in aVL and I
•Isoelectric / slightly elevated ST segment in V1 with ST depression in V2-3
These findings are consistent with inferior STEMI due to RCA occlusion, plus likely
associated RV infarction.
 MURAL
THROMBUS
• Occurs in approx. 10% of AMI,s.
• Most often associated with thrombosis of the LADCA.
• Danger of peripheral embolization. The incidence of
thromboembolism from intracardiac thrombi and from
thrombosis in the leg veins is 15-45% in cases of acute MI and
is the major cause of death in 12% cases.
• Mural thrombosis in the heart develops due to involvement
of the endocardium and subendocardium in the infarct and
due to slowing of the heart rate.
• Mural thrombi often form thromboemboli. Another source of
thromboemboli is the venous thrombosis in the leg veins due
to prolonged b e d rest. Thromboemboli from either source
may cause occlusion of the pulmonary, renal, mesenteric,
splenic, pancreatic or cerebral arteries and cause infarcts
in these organs.
 ➢ QRS is widening, with New Left Anterior Fascicular Block
Lots of precordial ST Elevation, now diagnostic of LAD occlusion.

❑ The thrombus in the LAD which was initially obstructing enough flow to result
in subendocardial ischemia has propagated and is now completely occluding
the LAD, resulting in STEMI (full subepicardial ischemia).
 FIBRINOUS PERICARDITIS WITH
OR WITHOUT EFFUSION
• Most likely to occur during days 1-7 post ST segment elevation MI.
• Presents with sub sternal chest pain (relieved by leaning
forward and aggravated by leaning backward)
• Precordial friction rub present on auscultation caused by
increased vessel permeability in the pericardium (exudate
of acute inflammation).
• AUTOIMMUNE PERICARDITIS ( Dressler syndrome)-
POST MYOCARDIAL INFARCTION SYNDROME
• Typically occurs 1 to 8 weeks after the STEMI (after the attack of
acute MI)
• Caused by autoantibodies directed against antigens within the
d a m a g e d pericardial tissue (type II hypersensitivity reaction).
• But these antibodies are also present in patients with acute MI who
d o not develop this syndrome.
• It is characterised by pneumonitis.
 How To Recognise 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).
• Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.
 VENTRICULAR ANEURYSM
(bulge or 'pocketing' of the wall or lining of a vessel commonly occurring in the blood vessels at the base of
the septum, or within the aorta.)

• Another 5% of patients of a c u t e MI develop aneurysm, often of the left

• ventricle.
Clinically recognized within 4 to 8 weeks after a STEMI begins to develop in the
48
firsthours.
• Precordial bulge synchronous with systole (on physical exam)
• Anterior chest wall movement ( blood fills u p the aneurysm in
systole).
• COMPLICATIONS:
• Development of systolic heart failure (SHF) – d u e to lack of contractile
tissue because it is completely replaced by the scar. It occurs in healed
infarcts through thin, fibrous, non-elastic scar tissue.
• Clot material whatever ma y b e present ma y embolize to distant sites a n d
c a n cause further life threatning complications
• An d the Rupture is extremely u n c o mmo n a n d scar tissue h a d a very
g o o d tensile strength that’s the reason rupture is u n c o mmo n in such
remember
cases but that CONGESTIVE HEART FAILURE is considered most c o m m o n
of d e a t h in such cases.
cause
➢ Rarely, calcification of the wall of aneurysm ma y occur.
❑ Anterior Left Ventricular Aneurysm:

Minimal ST elevation in V1-3 associated with deep Q waves and T-wave

inversion.
This is a LV aneurysm secondary to a prior anteroseptal STEMI.
▪IF YOU HAVE
ANY QUESTIONS
YOU CAN
ASK ?????
 O UR KI N D
U F OR Y
TH A N K YO
ATTE N TIO N