The electrocardiogram (EKG) is a
graphical representation of the
electrical events of the cardiac cycle.
1895 - William Einthoven, credited for
the invention of EKG
1924 - William Einthoven got the Noble
prize for the same
SA node is the pacemaker where the electrical
impulse is generated.
Located along the posterior wall of the right
atrium right beneath the opening of the SVC.
It is crescent shaped and about 3 mm wide
and 1 cm long.
The impulse travels from the SA node through
the internodal pathways to the
atrioventricular node (AV node).
The AV node is responsible for conduction of
the impulse from the atria to the ventricles.
The impulse is delayed slightly at this point to
allow complete emptying of the atria before
the ventricles contract.
The impulse continues through the AV bundle
and down the left and right bundle branches
of the Purkinje fibers.
The Purkinje fibers conduct the
impulse to all parts of the
Turn on machine
Calibrate to 10mm/ mV
Rate at 25mm/ s
Record and print
Label the tracing - Name, DOB, Hospital
number, date and time
10 electrodes in total are placed on the
The 10 leads are lubricated with jelly
then placed over the respective sites
Chest leads are labelled “V”(vector) and are
numbered from 1 to 6.
The placement of these electrodes needs to
be exact to give the optimum information.
V1 fourth intercostal space, right sternal edge
V2 fourth intercostal space, left sternal edge
V4 at the apex (fifth ICS mid clavicular line)
V3 midway between V2 and V4
V5 same level as V4 but on the anterior
V6 same level as V4 and V5 but on the mid
Electrical impulse (wave of depolarisation) picked up
by placing electrodes on patient
The voltage change is sensed by measuring the
current change across 2 electrodes – a positive
electrode and a negative electrode
If the electrical impulse travels towards the positive
electrode this results in a positive deflection
If the impulse travels away from the positive
electrode this results in a negative deflection
P wave: Activation (depolarization) of the
right and left atria
QRS complex: right and left ventricular
T wave: ventricular repolarization
PR interval: time interval from onset of atrial
depolarization (P wave) to onset of ventricular
depolarization (QRS complex)
QRS duration: duration of ventricular muscle
QT interval: duration of ventricular depolarization and
RR interval: duration of ventricular cardiac cycle (an
indicator of ventricular rate)
PP interval: duration of atrial cycle (an indicator of
Symtoms Palpitation, cyanosis, chest pain, syncope, seizure, poisoning
Signs tachycardia, bradycardia, hypothermia, murmur, Shock
Evaluation of rheumatic heart disease, congenital heart diseases
Evaluation of suspected electrolyte imbalance
Evaluation of cases like drowning, electrocution
During cardiopulmonary resuscitation (CPR).
Evaluation of patients with implanted defibrillators and pacemakers
To detect myocardial injury, ischemia, and the presence of prior
infarction as well.
Effects and side effects of pharmacotherapy
Evaluation of metabolic disorders processes among others.
No absolute contraindications
patient refusal, exist.
patients allergies to adhesive used to affix the leads
Limb leads Poles E.g.
Bipolar Positive and
I, II, III
Unipolar Positive and zero
aVL, aVR, aVF, chest
◦ One small box - 0.04 s
◦ One large box - 0.20 s
◦ One large box - 0.5 mV
◦ 25mm = 1s
Height 10mm = 1mV
Half standardisation 5mm=1mV
One fourth standardisation 2.5mm= 1mV
(only amplitude is changed not speed)
Paper speed = 25mm/ s
25 mm (25 small squares / 5 large squares)
equals one second
If the heart rate is regular
Count the number of large squares
between R waves i. e. the RR interval
in large squares
Rate = 300/RR(no. of large boxes)
= 1500/RR(no. of small boxes)
If the rhythm is irregular it may be better to estimate
the rate using the rhythm strip at the bottom of the
ECG (usually lead II)
The rhythm strip is usually 25cm long (250mm i. e.
Count the number of R waves on that strip and
multiple by 6 you will get the rate
Regular slow 300/RR (large square)
Regular fast 1500/RR (small square)
Irregular R wave in rhythm strip X 6
Normal rhythm must have a P wave before each QRS
The easiest way to tell is to take a sheet of paper and
line up one edge with the tips of the R waves on the
Mark off on the paper the positions of 3 or 4 R wave
Move the paper along the rhythm strip so that your
first mark lines up with another R wave tip
See if the subsequent R wave tips line up with the
subsequent marks on your paper
If they do line up, the rhythm is regular. If not, the
rhythm is irregular
Absent P wave – indicate non sinus rhythm
AV rhythm (may be present)
Multiple P waves
◦ Atrial flutter
◦ Atrial fibrillation
◦ 2nd ar 3rd degree block
Changing P wave shape
◦ Wandering atrial pacemaker
The axis is the overall direction of
the cardiac impulse or wave of
depolarisation of the heart
An abnormal axis (axis deviation)
can give a clue to possible
= R-S amplitude
Lead I = 4-0 = 4mm
Lead aVF = 13-2 = 11mm
Lead I = 5+ (-10)= -5mm
Lead aVF = 17-4 = 13mm
Right Axis Deviation - Right ventricular hypertrophy,
Anterolateral MI, Left Posterior Hemi-block, COPD,
pulmonary arterial hypertension or large pulmonary
Left Axis Deviation- Ventricular tachycardia, Left
ventricular hypertrophy, Left Anterior hemi-block
Wolff-Parkinson-White syndrome can cause both
Left and Right axis deviation
1. up in all leads
< 2.5 mm.
< 2.5 mm.
1. Inverted P-wave
2. Wide P-wave (P- mitrale)
3. Peaked P-wave (P-
4. Saw-tooth appearance
5. Absent normal P wave
Definition: the time
beginning of P-
wave to beginning
of QRS complex.
Normal PR interval
<3yrs – 0.08sec
3-16 yrs – 0.10sec
>16 – 0.12sec
1. Short PR interval
2. Long PR interval
First degree heart
If the PR interval is constant with a missed
QRS complex: 2nd degree heart block,
Mobitz type II, each QRS followed after P
If there is no relationship between the P
waves and the QRS complexes: 3rd degree
Block Relation Electrical origin
1st degree Each P has QRS SA node
2nd degree Each QRS has P SA node
3rddegree No Relation Fasciular,Ventricular, or other
Q waves <0.04 second.
That’s is less than one small square duration.
Present commonly in I,II,III,aVF, and always
present in V5 and V6 (lateral leads)
Absent in V1
Height < 1/4 of R wave height.
The width of the QRS complex should be
less than 0.12 seconds (3 small squares)
Height of R wave is (V1-V6) >8 mm in at
least one of chest leads.
Morphology: progression from Short R and
deep S (rS) in V1 to tall R and short S in V6
New born +125
1 month +90
3 years +60
Full term 0.0.5s
1 -3yrs 0.06s
>3 years 0.07s
like - BBB,
complex – limb lead
less than 5mm
◦ Pericardial effusion
Right axis deviation of +110° or more.
Dominant R wave in V1
Dominant S wave in V5 or V6
Right atrial enlargement (P pulmonale).
Right ventricular strain pattern = ST
depression / T wave inversion in the right
precordial (V1-4) and inferior (II, III, aVF)
Left axis deviation
Increased R wave amplitude in the left-sided ECG leads (I, aVL and
Increased S wave depth in the right-sided leads (III, aVR, V1-3).
The thickened LV wall leads to prolonged depolarisation and delayed
repolarisation (ST and T-wave abnormalities) in the lateral leads.
Left atrial enlargement (P mitrale).
Left ventricular strain pattern = ST depression / T wave inversion in
the lateral (I, aVL,V5-V6) leads.
In RBBB, activation of the right ventricle is delayed as depolarisation
has to spread across the septum from the left ventricle.
The left ventricle is activated normally, meaning that the early part of
the QRS complex is unchanged.
The delayed right ventricular activation produces a secondary R wave
(R’) in the right precordial leads (V1-3) and a wide, slurred S wave in
the lateral leads (V5-6)
Delayed activation of the right ventricle also gives rise to secondary
repolarization abnormalities, with ST depression and T wave inversion
in the right precordial leads (V1-3)
QRS duration ≥ 120ms
rSR’ pattern or notched R wave in V1-3 along with
T wave inversion
Wide S wave in I and V6
Normally the septum is activated from left to right, producing small Q waves
in the lateral leads.
In LBBB, the normal direction of septal depolarisation is reversed (becomes
right to left), as the impulse spreads first to the RV to the LV via the septum.
Eliminates the normal septal Q waves in the lateral leads.
The overall direction of depolarisation (from right to left) produces tall R
waves in the lateral leads (I, V5-6) and deep S waves in the right precordial
As the ventricles are activated sequentially (right, then left) rather than
simultaneously, this produces a broad or notched (‘M’-shaped) R wave in the
QRS duration ≥ 120ms
Broad R wave in I, aVL, and V5-6
Prominent QS wave in V1-3
Absence of q waves (including physiologic q waves) in I and V6
The ST segment should sit on the isoelectric
line (at least in the begining)
It is abnormal if there is planar (i.e. flat)
elevation or depression of the ST segment
1. ST elevation:
More than one small
More than one small
T wave is best measured in left
In V5 <1yr 11mm
1. Peaked T-wave:
Posterior wall MI.
2. T- inversion:
The normal range for QT is 0.38-0.42 (≤ 11mm )
Definition: Time interval between beginning of
QRS complex to the end of T wave.
QT interval varies with heart rate - As the heart
rate gets faster, the QT interval gets shorter
It is possible to correct the QT interval with
respect to rate by using the following formula:
Bazzet’s formula QTc = QT/ √RR
(QTc = corrected QT)
Long QTc – causes
◦ Drugs – procanamide, quinidine
Jerwell and Lange-Neilsen syndrome
Romano- Ward syndrome
Short QT interval: hypercalcemia, digitalis
U waves occur after the T wave and
are often difficult to see
They are thought to be due to
repolarisation of the atrial septum
Prominent U waves can be a sign of