ELECTROCARDIOGRAM

Objectives:
At the end of the session every participant should be able to:
1. Define electrocardiogram and electrocardiogram.
2. Name uses of electrocardiogram.
3. Name indications for performing an electrocardiogram.
4. Name contraindications for performing an electrocardiogram.
5. Prepare patients for electrocardiogram.
6. Take electrocardiogram from patients.
7. Describe electrical conduction system of the heart.
8. Describe components of an electrocardiogram.

J.J. Kambona (M.B.Ch.B; M.Med)

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Definition:
 An electrocardiogram: (ECG)
It is a transthoracic interpretation of the electrical activity of the heart over time captured
externally by skin electrodes, amplifying by an electrocardiograph and recorded as a tracing
on a piece of paper.
 Electrocardiography:
It is the machine capable of detecting the pattern of distribution of electrical signals presented
on the surface of skin from the heart and prints them on the strip of paper.

General uses:
Evaluation of:
 Heart rate.  Myocarditis.
 Pericarditis.  Pericardial effusion.
 Pulmonary embolism.
 Patients with implanted defibrillators and pacemakers.
 Metabolic disorders e.g. hypokalaemia, hyperkalaemia etc.
 Conduction disturbances e.g. dysrrhythmias, heart block etc.
 Effects and side effects of pharmacotherapy e.g. digoxin toxicity.
 Ischaemic heart diseases e.g. angina pectoris and myocardial infarction.
 Primary and secondary cardiomyopathic processes e.g. ventricular hypertrophy and atrial
enlargement.

General indications:
 Seizures.  Syncope or collapse.
 Cardiac murmurs.  Pre-operative screening.
 A routine health check-up.
 Symptoms of myocardial infarction or angina pectoris.
 Perceived cardiac dysrrhythmias e.g. palpitation, skipped heart beats etc.

General contraindication:
No absolute contraindications to performing an electrocardiogram, other than patient refusal,
exist.

Preparation:
Positioning for resting ECG:
 The standard 12-lead electrocardiogram is generally performed with the patient lying quietly
in the supine position (on a bed or couch) while undress to the waist.
 Care should be taken to ensure that the skin is clean and is trimmed of excess hair in the
areas in which the leads are to be placed.

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 Placement of electrodes (leads):
A. Limb leads:

Electrode label Electrode (lead) placement

aVR On the right forearm, above the wrist joint. It is red coloured.
aVL In the same location that aVR was placed, but on the left forearm this time. It is yellow coloured
III On the right leg, above the ankle joint. It is black coloured.
II In the same location that III was placed, but on the left leg this time. It is green coloured.

B. Chest (precordial) leads:

Electrode label Electrode (lead) placement

V1 Fourth intercostal space, right sternal border.
V2 Fourth intercostal space, left sternal border.
V3 Equal distance between V2 and V4.
V4 Fifth intercostal space, left mid-clavicular line.
V5 Anterior axillary line, same level with V4.
V6 Mid axillary line, same level with V4 and V5.

Precordial electrode placement in women with large breasts can be problematic due to
obfuscation of bony landmarks. The current recommendations are that the electrodes should be
placed beneath, rather than overlying, the breast.

Frontal plane of the heart: (Longitudinal section view)

Transverse horizontal plane of the heart: (cross-section view)

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1. Resting ECG:
It is taken at resting position.

How to do it:
 Place sticky patches called electrodes onto arms, legs and chest.
 If a patient has a lot of hair on the chest, shave them to allow the electrodes to make
contact with skin.
 The electrodes are then attached to a recording machine by wires and switched on.
 When the heart beats, it produces electrical signals which spread on the surface of the
skin; electrodes pick up them and transmit to the recording machine. The machine then
prints a record of heartbeat onto a paper strip.
 A patient should lie still when the recording is being taken as moving can affect the
reading.

2. An exercise ECG: (a stress test or treadmill test)

Exercise testing is a cardiovascular stress test using treadmill or cycling on a stationary exercise
bike with ECG and blood pressure monitoring to show how the heart copes under stress.

 Uses:
o Assessment of the effects of therapy.
o Assessment of the probability and extent of coronary disease.
o Estimation of prognosis and determination of functional capacity of the heart.
 Indications:
It is indicated for diagnosis and prognosis of cardiovascular disease, specifically coronary
artery disease (CAD).
 Contraindications:
The guidelines according to American Heart Association (AHA) and American College
of Cardiology (ACC); 1997.
o Absolute contraindications:
 Acute aortic dissection.
 Acute myocarditis or pericarditis.
 Symptomatic severe aortic stenosis.
 Uncontrolled symptomatic heart failure.
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  Acute myocardial infarction (within 2 days).
 Acute pulmonary embolus or pulmonary infarction.
 Unstable angina not previously stabilized by medical therapy.
 Uncontrolled cardiac arrhythmias causing symptoms or haemodynamic
compromise.
o Relative contraindications:
Relative contraindications can be superseded if the benefits of exercise outweigh the
risks.
 Electrolyte abnormalities.
 Left main coronary stenosis.
 Tachyarrhythmia or bradyarrhythmia.
 Moderate stenotic valvular heart disease.
 Third degree (complete) atrioventricular (AV) block.
 Mental or physical impairment leading to an inability to exercise adequately.
 Hypertrophic cardiomyopathy and any other forms of outflow tract obstruction.
 Severe arterial hypertension (Systolic blood pressure of greater than 200 mmHg
and/or a diastolic blood pressure of greater than 110 mmHg).
 How to do it:
o Connect electrodes from the recording machine with wires in the same way as a
standard ECG.
The patient’s heart rate and blood pressure should be recorded during exercise.
Ask the patient to exercise, either by walking on a treadmill or cycling on a stationary
exercise bike.
o Pharmacological stress testing:
It is a diagnostic procedure in which cardiovascular stress induced by
pharmacological agents is demonstrated in patients with decreased functional
capacity or in patients who cannot exercise by using a drug called adenosine to
simulate the effect of exercise.
Pharmacological stress testing is used in combination with imaging modalities such
as radionuclide imaging and echocardiography.
o The exercise should start gentle and gradually becomes more strenuous, for example,
by increasing the speed or the slope of the treadmill. The doctor or technician should
monitor ECG along with blood pressure and heart rate, every few minutes while
exercise is on progress.
o The test will last between a few minutes to 15 minutes. Once ECG and blood pressure
have returned to normal, a patient is allowed to go home.
 Indications for terminating exercise testing:
According to the American Heart Association (AHA) and American College of
Cardiology (ACC) guidelines, the following are indications for termination of exercise
testing:
o Absolute indications:
 Subject's desire to stop.
 Moderate-to-severe angina.
 Sustained ventricular tachycardia.
 Signs of poor perfusion (cyanosis or pallor).
 When the doctor or technician has the readings he or she needs.

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 Technical difficulties in monitoring ECG tracings or systolic blood pressure.
Increasing nervous system symptoms such as ataxia, dizziness and near-syncope.
ST-segment elevation (1 mm) in leads without pathological Q-waves (other than
V1 or aVR).
 Drop in systolic blood pressure of greater than 10 mmHg from baseline blood
pressure, despite an increase in workload, when accompanied by other evidence
of ischemia.
o Relative indications:
 Increasing chest pain.
 Fatigue, shortness of breath, wheezing, leg cramps or claudication.
 Hypertensive response (systolic blood pressure of 250 mmHg and/or diastolic
blood pressure greater than 115 mmHg).
 Development of bundle branch block or intraventricular conduction delay that
cannot be distinguished from ventricular tachycardia.
 Drop in systolic blood pressure greater than or equal to 10 mmHg from baseline
blood pressure, despite an increase in workload, in the absence of other evidence
of ischemia.
 ST-segment changes such as excessive ST-segment depression (more than 2 mm
of horizontal or down-sloping ST-segment depression) or marked axis shift.
 Arrhythmias other than sustained ventricular tachycardia, including multifocal
premature ventricular contractions (PVCs), triplets of PVCs, supraventricular
tachycardia, heart block or bradyarrhythmia.

 A 24-hour ECG: (A Holter monitor or ambulatory ECG)

It is a test in which a patient wears an electronic recorder for 24 hours recording an electrical
activity of the heart.

How to do it:
o A patient is asked to wear a small portable recorder, attached to a belt around the waist.
Wires from the recorder are connected to three or four small electrodes (leads) onto the
chest.
o A patient can then undergo about her/his normal activities for the day, while keeping a
diary of everything that she/he does and noting when she/he feels symptoms.
o A patient should not have a bath or shower with the recorder on. At the end of the 24
hours, she/he can remove the electrodes and recorder and return it to the hospital for
analysis.

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 Cardiac event recorders:
It can record heartbeat over a longer period of time.
o Portable event recorders:
It is a small electrical device used when a patient has symptoms.
How to do it:
 When a patient has symptoms, such as palpitations, places the device on chest and
switches it on to record ECG.
 With most portable event recorders, a patient will be able to send the results of the
recording to the hospital by holding the device to a phone.
 The doctor or technicians at the hospital can then analyze results and tells the patient
what to do next.
o Implantable loop recorders: (ILR)
It is a subcutaneous, single-lead, electrocardiographic (ECG) continuously monitoring
device used for:
 Long-term monitoring in patients at risk for or with documented atrial fibrillation.
 Diagnosis of patients with recurrent unexplained episodes of palpitations or syncope.
 Risk stratification in patients who have sustained a myocardial infarction and those
who have certain genetic disorders.
The device is typically implanted in the left parasternal region.
Indications:
1. Syncope:
Definition:
Syncope is defined as a transient loss of consciousness due to global cerebral
hypoperfusion and is characterized by rapid onset, short duration and spontaneous
complete recovery.
Causes:
 Dysrhythmias:
– Tachyarrhythmia. – Bradyarrhythmia.
 Obstruction to blood flow:
– Aortic stenosis. – Pulmonary embolism.
– Aortic dissection. – Pericardial tamponade.
– Pulmonary hypertension.
 Chronic orthostatic intolerance:
– Postural orthostatic tachycardia syndrome (POTS).
– Orthostatic hypotension (secondary to volume depletion, systemic illness, use
of a vasoactive drug or pure autonomic failure/multiple system atrophy).
 Neurally-mediated syncope: (most common cardiovascular cause)
– Vasovagal syncope. – Situational syncope.
– Carotid sinus hypersensitivity.
2. Patients with palpitations.
3. Patients with or at risk for atrial fibrillation.
4. Risk stratification post-myocardial infarction.
Contraindications:
The presence of an active infection or a bleeding diathesis may preclude implantation.

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Electrical conduction system of the heart:
 The sinoatrial node, is situated at the junction of superior vena cava and the right atrium and
is the origin of electrical impulses responsible for heart rhythm under normal conditions
(sinus rhythm), it therefore called a pacemaker of the heart.
 At rest, each heart muscle cell has a charge across its outer wall or cell membrane. Reducing
this charge towards zero is called depolarization, which activates the mechanisms in the cell
that cause it to contract.
 The firing of the sinoatrial node sends out an electrical impulse via its neurons to the:
o Right atrium through the anterior, middle and posterior intermodal tract.
o Left atrium through Bachmann’s bundle.
From the right and left atrial, electrical impulse travel to atrioventricular node. Since the right
atrium is closer to the sinoatrial node, it depolarizes first, resulting in pumping action by the
right atrium before the left atrium. Conduction directly to ventricles is prevented by the
annulus fibrosus which insulates the atria from the ventricles.
 Atrioventricular node is situated beneath the right atrial endocardium at the lower end of the
interatrial septum. It conducts slowly and regulates the frequency of conduction of an
electrical impulse to the ventricles.
 At the atrioventricular node, the impulse is delayed to allow for the ventricles to fill up with
blood. After the delay, an electrical impulse from atrioventricular node passes through the
bundle of HIS, the annulus fibrosus and divides into two:
o The right bundle branch, which finally end with Purkinje fibres when come in contact
with the myocardium.
o Left bundle branch, which subdivides further into anterior, posterior and septal fascicles
and finally end with Purkinje fibres when come in contact with the myocardium.
 The anterior fascicle of the left bundle branch runs along the anterior surface of the
left ventricle.
 The posterior fascicle runs along the posterior surface of the right ventricle.
 The septal fascicle runs along and depolarizes the interventricular septum from left to
right direction.
This triggers the contraction of the ventricles, thus sending blood either to the lungs or out to
the body.

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Components of an electrocardiogram:

ECG terminologies:
 Duration:
Duration of the wave refers to the horizontal distance covered by the wave.
The standard paper speed is 25 mm/second i.e. in 1 second a stylus will move 25 mm (25

small squares) on the paper. Hence one small square on the ECG is equivalent to 0.04 second
and a one large square is 0.2 seconds.
1 mm = 1 small square = 0.04 seconds.
5 mm = 1 big square = 0.2 seconds (0.04 seconds x 5).
 Amplitude:
Amplitude of the wave refers to the vertical distance covered by the wave. It is measured in
mm or millivolts (mV) on ECG paper.
1 mm = 1 small square = 0.1 mV.
5 mm = 1 big square = 0.5 mV (0.1 mV x 5).
25 mm = 5 big squares = 2.5 mV = 1 seconds.

VAT = ventricular activation time

 Configuration: Configuration refers to the shape and symmetry of the wave.

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  Straight lines:
o Isoelectric line:
An isoelectric line is a baseline voltage of the electrocardiogram. Typically the isoelectric
line is measured as the portion of the tracing following the T-wave and preceding the
next P-wave.
o Segment: A segment is a straight line connecting two waves.
Example:
 ST-segment.  PR-segment.
 Intervals:
An interval is one that includes at least one wave plus a connecting straight line.
Examples:
o PR-interval. o RR-interval.
o QT-interval. o ST-interval.
 Waves:
A typical ECG tracing of the cardiac cycle (heartbeat) consists of a P-wave, a QRS-complex,
a T-wave and a U-wave which is normally visible in 50-75% of ECGs.

Feature Description Duration

 The ST segment connects the QRS complex and the T- wave.
 It measures the interval of time from the end of ventricular depolarisation to the
beginning of ventricular repolarisation (the interval of time from the end of
ventricular contraction to the beginning of ventricular relaxation).
 ST-segment represents the refractory period i.e. the interval of time during which a
normal cardiac impulse cannot re-excite an already excited area of cardiac muscle.
 Normal ST-segment: No elevation or depression.
 Differential diagnoses of elevated ST-segment:
o Hypothermia.
o Hyperkalaemia.
o Acute pericarditis.
o Prinzmental’s angina.
ST-segment o Ventricular aneurysm. 0.08-0.12 seconds
o Pulmonary embolism.
o Left bundle branch block.
o Acute myocardial infarction.
o Normal variant in athletic heart, Edeiken pattern and high-take off.
 Differential diagnoses of depressed ST-segment:
o Digoxin effect.
o Hypokalaemia.
o Pulmonary embolism.
o Ventricular hypertrophy.
o Left bundle branch block.
o Subendocardial ischaemia.
o Acute posterior myocardial infarction.
PR-segment  The PR-segment connects the P-wave and the QRS-complex. 0.05-0.12 seconds
 It is the interval of time when the electrical impulse is conducted from the AV node,
the bundle of His, bundle branches to the Purkinje Fibres.
This electrical activity does not produce a contraction directly and is merely travelling

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 down towards the ventricles and this shows up flat on the ECG.

Feature Description Duration

PR-interval  The PR-interval is measured from the beginning of the P-wave to the beginning of 0.12-0.2 seconds
the QRS complex.
 The PR-interval reflects the time the electrical impulse takes to travel from the sinus
node through the atrioventricular node and entering the ventricles.
 Differential diagnoses of short PR-interval:
o Duchenne muscular dystrophy.
o Lown-Ganong-Levine syndrome.
o Wolff-Parkinson-White syndrome.
o Hypertrophic obstructive cardiomyopathy.
o Type-II glycogen storage disease (Pompe’s disease).
 Differential diagnoses of prolonged PR-interval:
o Trifascicular block.
o First degree atrioventricular block.
 Differential diagnoses of variation in PR-interval:
o Mobitz type-I atrioventricular block.
o Multifocal atrial tachycardia.
 The QT-interval is measured from the beginning of the QRS complex to the end of
the T-wave.
QT-interval 0.30-0.43 seconds
 It measures the time from the beginning of ventricular depolarization to the end of
ventricular repolarisation.
Duration of QT-interval is inversely proportional to heart rate. The faster the heart beats,
the faster it must repolarise to prepare the next contraction and therefore the shorter the
QT-interval and vice versa.
QTc = QT-interval
√ RR-interval
 Differential diagnoses of long QTc:
o Hereditary:
 Romano-Ward syndrome (autosomal dominant).
 Jervill-Lange Nielson syndrome (autosomal recessive) associated with
sensorineural deafness.
o Myocarditis. Maximum:
The corrected
o Hypocalcaemia.  Males: 0.39
QT-interval for
o Hypothyroidism. seconds.
the heart rate
o Myocardial infarction.  Females: 0.44
(QTc)
o Diffuse myocardial disease. seconds.
o Intracerebral haemorrhage.
o Subarachnoid haemorrhage.
o Tricyclic antidepressants, Phenothiazines etc.
o Anti-arrhythmic drugs e.g. sotalol, amiodarone, quinidine etc.
 Differential diagnoses of short QTc:
o Digoxin.
o Graves disease.
o Hypercalcaemia.
o Hypermagnesaemia.

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 Feature Description Duration
P-wave  It represents the atrial depolarization in response to sinoatrial node triggering.  Configuration:
 Since the sinoatrial node is in the right atrial muscles, atrial contraction starts with the right – Smooth
atrium (first phase of P-wave) and then followed by the left atrium (second phase of P- contour.
wave). – Monophasic in
 Abnormal P-waves: lead II.
o Left atrial enlargement. – Biphasic in V1.
o Right atrial enlargement. – P-waves should
o Multifocal atrial tachycardia (MAT). be upright in
o Wandering atrial pacemaker (WAP). leads I and II,
o Premature atrial contractions (PACs). inverted in
 Absent P-waves: aVR.
o Atrial fibrillation.  Amplitude: < 0.25
o Severe hyperkalaemia. mV (< 2.5 mm) in
o Sinus node arrest or sinus exit block. limb leads and <
1.5 in precordial
 P-P interval variation: Sinus arrhythmia.
leads.
 Duration: 0.08-
0.12 seconds in
lead II.
QRS-  The QRS-complex reflects the rapid depolarization of the right and left ventricles. 0.08-0.11 seconds
complex  They have a large muscle mass compared to the atria and so the QRS-complex usually has
much larger amplitude than the P-wave.
 Definitions:
o Q-wave: The first negative deflection of the QRS-complex.
o R-wave: The first positive deflection of the QRS-complex.
o R’-wave (R-prime wave): Any positive deflection that follows an S wave.
o S-wave:
o The first negative deflection of the QRS-complex following a positive deflection.
o QS: If there is only a single negative deflection.
A negative deflection of the QRS-complex can only be Q-wave if it is the first wave of the
QRS-complex.
Capitalisation of the letter indicates tall or deep waves, with small waves notarised with
small letters.

 Normal QRS-complex:
o QRS-complex duration: 0.08-0.11 seconds.
o No pathological Q-waves.
o No evidence of left or right ventricular hypertrophy.
 Differential diagnoses of abnormally wide QRS-complex:
o Hyperkalaemia.
o Ventricular rhythm.

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 o Left bundle branch block.
o Right bundle branch block.
o Ventricular flutter or fibrillation.

Feature Description Duration

T-wave  The T-wave represents the repolarisation (recovery) of the ventricles. It usually takes 0.16 seconds
the same direction as the QRS complex (concordance); opposite polarity
(discordance) may indicate past or current infarction.
 Differential diagnoses of small, flattened or inverted T-waves:
o Aging.
o Anxiety.
o Pericarditis.
o Myocarditis.
o Hypokalaemia.
o Angina pectoris.
o Hyperventilation.
o Drugs e.g. digoxin.
o Pulmonary embolism.
o Drinking iced or hot drinks.
o Left ventricular hypertrophy.
o Intraventricular conduction delay e.g. right bundle branch block.
 Differential diagnoses of tall T-waves:
o Stroke.
o Hyperkalaemia.
o Ventricular hypertrophy.
o Left bundle branch block.
o Hyperacute myocardial infarction.
 Giant negative T-waves or at times upright T-waves associated with prolonged
QTc-interval:
Primary causes:
o Ischaemic heart disease.
o Subarachnoid haemorrhage.
o Following cardiac resuscitation.
o Hypertrophic obstructive cardiomyopathy.
o Complete heart block with marked bradycardia.
Secondary causes:
Secondary causes are due to alternation of timing or sequencing of depolarization or
both e.g. in left bundle branch block.
 Rate-related T-wave changes:
o Post extrasystolic T-wave changes are due to abnormal pathway of
repolarization, prolonged diastolic filling time and abrupt changes in the cycle
changes length.
o T-wave inversion occasionally seen in supraventricular or ventricular
tachycardia.
 Notched or bifid T-wave:
o Prolonged QT-syndrome.
o Alcoholic cardiomyopathy.
o Central nervous system disorders.
o ± Organic congenital heart disease.

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 o Notched or bifid T-wave is relatively common without heart disease especially
in children.
o Drug e.g. Phenothiazines, tricyclic antidepressants, lithium, digitalis, anti-
arrhythmic drugs etc.
Pathogenesis:
Mechanism of its formation is unclear probably by non-uniform repolarization
secondary to differential innervations of the anterior and posterior ventricular walls.

Feature Description Duration

 It is the interval between two successive R-waves of the QRS-complexes.
 It represents one cycle of cardiac activity.
 The interval between an R-wave and the next R-wave is the inverse of the heart rate.

RR-interval 0.6-1.2 seconds

ST-interval The ST-interval is measured from the J-point to the end of the T-wave. 0.32 seconds
 A point at which the QRS-complex ends and the ST-segment begins.
J-point  It is used to measure the degree of ST-elevation or depression present. Not applicable
The U-wave is normally visible in 50-75% of ECGs. It is typically low amplitude, and,
by definition, follows the T- wave.
 Differential diagnoses of U-waves:
U-wave o Ischaemia.
o Hypokalaemia.
o Hypomagnesaemia.
 The J-wave, elevated J-Point or Osborn Wave appears as a late delta wave following
J-wave the QRS or as a small secondary R-wave.
 It is considered pathognomic of hypothermia or hypocalcaemia.

 Wave deflections:
o A positive deflection:
It is an upward deflection of a wave. It means the current of depolarization is moving
towards the lead indicating the deflection.

o A negative deflection:

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 It is a downwards deflection of a wave. It means the current of depolarization is moving
away from the lead indicating the deflection.

o Biphasic waves:
It indicates that the current of depolarization is perpendicular to the leads.
 Biphasic QRS-complex: R- and S-waves are of nearly equal amplitude.

 Biphasic P-wave:
Amplitudes of the first and second phases of atrial contraction are of nearly equal
amplitude and faces oppositely.

P-waves deflections:
Atrial depolarization starts at the SAN in the right atrium, therefore the right atrium
depolarises first then the left atrium. The average vector of current flow is from the right to
the left and slightly inferiorly.
o In frontal plane:
In any lead that views the wave of atrial depolarization as moving towards it will record a
positive deflection on the ECG paper. These include:
 Left lateral leads: Lead I and aVL.
 Inferior leads: Lead II and aVF.
Lead III (inferior lead) due to its position i.e. The most rightward (orientation +120 o)
of the inferior leads, lies nearly perpendicular to the atrial current. Predictably, lead
III frequently records a biphasic P-waves.
 Lead aVR sees the current of atrial depolarization as moving away, so it records a
purely negative deflection.
o In horizontal plane:
 Leads V5 and V6 will record positive deflections.
 Leads V2, V3 and V4 are variable.
P-wave is most positive in lead II and most negative in aVR.
QRS-complex deflections:
Septal Q-wave:

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 Interventricular septum is the first to depolarize and it does so from left to right direction.
And this is normally not seen on ECG but when it is, it appears as a tiny negative deflection
or Q-wave in lead I, aVL, V5 and V6 (as the wave moving away from left to right); and some
people even inferior leads. These should be regarded as normal.
The rest of ventricular myocardium:
During ventricular depolarization, the vector points anywhere from 0o to +90o.
o In frontal plane:
 A large positive R-wave deflection may be seen in many of the left lateral and
inferior leads (as the wave moving towards it).
 Lead aVR, lying rightward, will record a deep negative deflection of S-wave.

o In horizontal plane:
 V1 and V2 will record deep S-waves, as the current moves leftwards from right to left
and they are overlying the right ventricle.
 V5 and V6, overlying left ventricle, will record tall R-waves.
 V3 and V4, represent the transitional zone and normally one of these record a
biphasic wave (R-wave and S-wave of nearly equal amplitude).
V1 has the smallest R-wave and V5 has the largest R-wave (V6 is a bit smaller than V5).
T-wave deflections:
o Since T-wave represents ventricular repolarisation, the vector of the current flow will be
opposite to that of depolarization i.e. backwards. The same electrodes that record a
positive deflection during depolarization (appearing as R-wave) will also record a
positive deflection during repolarisation (appearing as T-wave).
o It is therefore typical and normal findings to find a positive T-wave in the same leads that
have tall R-wave.
QRS-complex and T-waves tend to have the same general direction in the limb leads.
 Abnormal ECG in the absence of heart disease:
o QRS-complex:
 QS-complex in aVF, V1 and V2.
 QS- or QR-complexes in lead II and aVF.
 A tall R-wave over the left ventricle (V5, V6).
o T-wave:
 Persistence of juvenile T-wave inversion over right precordium (V1, V2).
 Isolated mid-precordial T-waves inversion (V3, V4) and terminal T-wave inversion
(V5, V6) associated with ST-segment elevation secondary to early repolarisation and
right precordial T-wave inversion in aged woman.

Blood supply to the heart:

The blood supply to the myocardium comes from the coronary artery with two main branches:
 The right coronary artery.  The left main coronary artery.
The right coronary artery:
The right coronary artery runs between the right atrium and right ventricle and supplies the:
 Right atrium.  Sinoatrial node.
 Right ventricle.  Posterior surface.
 Inferior surface (80%).

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  Atrioventricular node by its descending branch (posterior descending artery) in most
individuals.
The left coronary artery:
The left main coronary artery originates from the ostium of the left sinus of Valsalva. The left
main coronary artery supplies most of the left atrium, left ventricle and interventricular septum.
The left coronary artery divides into:
 Left circumflex coronary artery.
 Left anterior descending coronary artery.
Left anterior descending coronary artery:
It runs along the anterior interventricular sulcus and supplies the:
 Most of the interventricular septum.
 Anterior wall to the apex of both ventricles.
Left circumflex coronary artery:
It courses in the coronary groove around the left border of the heart to the posterior surface of the
heart to anastomose to the end of the right coronary artery:
 Left atrium.  Inferior surface (20%).
 Posterolateral walls of the left ventricle.

Localization of ischaemia and infarction:

Leads Site of myocardial ischaemia or infarction Occluded coronary artery
V1-V2 Anteroseptal wall Left anterior descending artery.
V3-V4 Anterior wall Left anterior descending coronary artery.
V5-V6 Anterolateral wall Left main coronary artery.
Right coronary artery (80%) or Left circumflex coronary artery
II, III and aVF Inferior wall
(20%).
I and aVL Left lateral wall Left circumflex coronary artery.
 Posterior wall infarction (reciprocal changes)*.
V1 and V2  Normal QRS-axis. Right coronary artery.
 Q-waves in V6.

Posterior wall infarction:

 Reciprocal changes*
o Poor R-waves progression i.e. R > S in V1 (normally, R-wave is < S-wave in V1 and
increases from V1-V6).
o ST-segment depression.
o Normal T-waves.
 Normal QRS-axis.
 Evidences of inferior myocardial infarction as the posterior wall shares blood supply with the
inferior wall.
Poor R-waves progression:
Differential diagnoses:
 Right bundle branch block.  Wolff-Parkinson-White syndrome.
 Right ventricular hypertrophy.  Posterior wall myocardial infarction.

References:
1. Swash M. Hutchison’s clinical methods.

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2. Dubin D. Rapid interpretation of EKG’s. Edition V.
3. Davidson’s principles practice of medicine; 17th edition.
4. Thaler M.S. The only EKG book you will even need; 2nd edition.
5. http://www.thelancetstudent.com/wp-content/uploads/2008/03/witham.pdf
6. Braunwald E. A textbook of cardiovascular diseases (heart disease); 4th edition, 1992.
7. Mittal S. Implantable loop recorder. www.emedicine.medscape.com last updated: March 29,
2011.
8. Levine E. Electrocardiography. www.emedicine.medscape.com last updated: August 10,
2011
-END-

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