BASICS OF ECG READING

BY MATOVU JOHN PAUL

SUPERVISOR: DR ELEKU
OBJECTIVES
• INTRODUCTION
• SIGNIFICANCE AND INDICATIONS
• ELECTROPHYSIOLOGY
• NORMAL 12 LEAD ECG
• CARDIAC AXIS
• HEART RATE
• RHYTHM
• DIFFERENT PRESENTATIONS OF ARRHYTHMIAS, BBB, ELECTROLYTE
IMBALANCES
INTRODUCTION
• The electrocardiogram (ECG) is a recording of wave forms reflecting the

electrical activity of the heart or

• It’s a graphic record of electrical impulses generated by depolarization and

repolarization of the cardiac muscle

• A good quality ECG is essential for the evaluation of all cardiac patients
SIGNIFICANCE OF ECG
• To determine the rate and rhythm of the heart

• To determine the physical orientation of the heart

• To aid in diagnosis of heart pathologies e.g. ischemia, infarction, arrhythmias

and conduction abnormalities

NB; It does not measure the electrical activity of the heart

INDICATIONS OF AN ECG
• Cardiac arrhythmias

• Coronary artery disease

• Inflammatory disease of the heart e.g. myocarditis, pericarditis

• Electrolyte imbalances like hypokalemia, hyperkalemia

• Drug toxicity e.g. digoxin

• Congenital heart disease

• Heart blocks e.g. AV blocks, BBB

• pulmonary embolism , cor pulmonale etc

PREPARATION FOR ECG
1. Create rapport. Explain procedure and reassure patient of no possibility of
electrocution
2. Clear the room of bystanders to prevent them from touching the patient.
Ensure patient privacy and protection. Remove all ornaments.
3. Patient should lie flat and relaxed with no muscle twitching or movements
which may alter tracings.
4. Ensure proper placement of leads and good contact between client skin and
electrodes by applying electrode jelly to skin where electrode is attached.
5. Proper standardization of the machine and proper grounding to prevent
interference with the recording.
ELECTROPHYSIOLOGY
• During sinus rhythm, the SA node triggers atrial depolarization

• This produces the P wave

• Depolarization proceeds slowly through the AV node

• The Bundle of His, bundle brunches and purkinje system are the activated, initiating
ventricular myocardial depolarization which produces the QRS complex

• QRS complex is larger than the P wave due to differences in muscle mass

• Ventricular repolarization produces the T wave

NORMAL 12 LEAD ECG
• Leads I – III are standard bipolar leads that measure the potential difference
between two limbs
Lead I: left arm to right arm
Lead II: left leg to right arm
Lead III: left leg to left arm
• The remaining leads are unipolar and are connected to a limb (aVR, aVL and
aVF) or to the chest wall ( V1 – V6)
• The wave of depolarization is different for each lead due to the different
orientation
• The direction and magnitude of the ECG deflections is also different in each
lead
AUGMENTED LIMB LEADS
• These are unipolar leads

• Because there is a single positive electrode

that is referenced against a combination of
the other limb electrodes.

• The positive electrodes for these

augmented leads are on the left arm (aVL),
the right arm (aVR), and the left leg (aVF).
EINTHOVEN TRIANGLE
• Einthoven's triangle is an imaginary
formation of three limb leads in a triangle
used in the electrocardiography
• It serves as a reference system for
Einthoven's triangle is an imaginary
formation of three limb leads in a triangle
used in the
electrocardiography,measuring the
electrical activity of the heart
• By placing electrodes on these three
points, an ECG can record the hearts
electrical signals and display them in
wave form
CHEST LEADS
• V1- electrode positioned in the 4th ICS in the right sternal border

• V2- 4th ICS in the left sternal border

• V3- midway between V2 and V4

• V4- 5th ICS in the left midclavicular line

• V5- 5th ICS in the anterior axillary line

• V6- 5th ICS in the mid axillary line

ECG WAVE BASIC DEFINITIONS
Baseline – flat, straight and isoelectric line

• Wave form deviation or movement away from the baseline may be upward or
downward

Segment – a line between two waves

Interval – a wave form plus a segment: this shows time duration

Complex – a combination of several waves without a segment

WAVE INTERPRETATION
P WAVE PR INTERVAL
• Its duration should not exceed 0.10 s
• Normal duration is 0.12 – 0.20 s
• Prolongation indicates left atrial
• Prolongation indicates delayed AV
enlargement which could be due to mitral
conduction (1st degree heart block)
valve disease or left ventricular failure
• Shortening indicates rapid conduction
• Tall peaked ‘pulmonary’ P waves indicate
through accessory pathway by-passing the
right atrial enlargement caused usually by
AV node (Wolff-Parkinson-White syndrome)
pulmonary HTN and right ventricular failure
WAVE INTERPRETATION
QRS COMPLEX
• Should not exceed 0.12 s
• Prolongation indicates: slow ventricular depolarization due to BBB, pre-
excitation (WPW syndrome), ventricular tachycardia or hypokalemia
• Exaggerated QRS deflections may indicate ventricular hypertrophy
• Right ventricular hypertrophy causes tall R waves in V1 and V2
• Dominant R wave in lead V1 may be due to Right BBB, WPW syndrome and
dextrocardia
• Diminished QRS deflections occur in myxedema, also when pericardial
effusions or obesity electrically insulate the heart
• Presence of pathological Q waves (duration > 0.04 s) usually indicates
previous myocardial infarction
WAVE INTERPRETATION
QT INTERVAL
• Represents the duration of electrical systole (mechanical systole starts
between the QRS complex and T wave)

• Abnormal prolongation of the QT interval predisposes to ventricular

arrhythmias

• It could also be congenital or occur in response to hypokalemia, rheumatic

fever or drugs e.g. quinidine, amiodarone, tricyclic antidepressants

• shortening of the QT interval is caused by hyperkalemia or digoxin therapy

WAVE INTERPRETATION
ST SEGMENT

• Minor ST segment showing early repolarization is a normal variant more so in

some Africans or west Indians

• Pathological elevation (>2.0mm above the baseline) occurs in: acute

myocardial infraction, variant angina and pericarditis

• Horizontal ST depression indicates myocardial ischemia, digoxin therapy and

hypokalemia
T WAVE
• It represents the ventricular repolarization • T wave inversion is seen in the following
but shows the upward deflection because circumstances:
the part depolarized in the last is the first to  Normality
be repolarized that is the base of heart
depolarized in the last but is first to be Ischaemia
repolarized Ventricular hypertrophy
• T wave should not be more than one third of Bundle branch block
R wave
Digoxin treatment.
Leads adjacent to those showing inverted T
INVERSION OF THE T WAVE ;The T wave is waves sometimes show ‘biphasic’ T waves –
normally inverted in leads VR and V1, initially upright and then inverted.
sometimes in leads III and V2, and also in
lead V3 in some black people.
CARDIAC AXIS
This is the average direction of the spread
of depolarization through the ventricles as
seen from the front
Its direction can be derived most easily from
the QRS complex in leads I, II and III
RIGHT AXIS DEVIATION
• If the right ventricle is hypertrophied
• Its has more effect on the QRS complex
than the left ventricle
• Therefore the axis will swing towards the
right
• Deflection in lead I becomes negative
(predominantly downwards) because
depolarization is leaving it
• Deflection in lead III becomes more positive
(predominantly upward) because
depolarization is spreading towards it.
• This is associated with pulmonary condition
that strain the right side of the heart and
congenital heart disorders
RIGHT VENTRICULAR HYPERTROPHY
LEFT AXIS DEVIATION
• If the left ventricle becomes hypertrophied
• It exerts more influence on the QRS
complex than the right ventricle
• Hence the axis may swing to the left
• the QRS complex becomes predominantly
negative in lead III
• LAD is not significant until the QRS
complex deflection is predominantly
negative in lead II
LEFT VENTRICULAR HYPERTROPHY
HEART RATE
There are 2 methods
Method 1
The ECG is usually recorded at a paper speed of 25 mm/s
Each large square (5mm) represents 0.20 s
The heart rate is conveniently calculated by counting the number of large squares between
consecutive R waves
Then dividing this into 300
This method assumes the heart rate is regular and the distance between the successive
QRS complexes is constant
HEART RATE
Method 2
A quicker method to use is the rhythm strip
that is printed at the bottom of most
standard ECG recordings
This is the longer recording of a particular
lead
A rhythm strip is a 10 second recording
Count the number of QRS complexes in a
10 second rhythm strip
Multiply by 6 which will give you the heart
rate in beats per minute
RHYTHM
• In the normal sinus rhythm, P waves
precede each QRS complex and the rhythm
is regular
• Absence of the P waves and an irregular
rhythm shows atrial fibrillation
• A slow sinus rhythm (sinus bradycardia) can
be associated with athletic training,
hypothermia or myxedema and also
immediately after a heart attack
• A fast sinus rhythm (sinus tachycardia) can
be associated with exercise, fear, pain,
hemorrhage or thyrotoxicosis
COMMON ARRHYTHMIAS
ATRIAL ARRHYTHMIAS: these include atrial rates of 150, 100 or 75/min)
ectopic beats, atrial fibrillation and atrial flutter
ATRIAL FLUTTER
Less common than atrial fibrillation
ECG characteristically shows sawtooth
flutter waves that are mostly seen when the
block is increased by carotid sinus pressure
it is characterised by a large (macro) re-
entry circuit, usually within the right atrium
encircling the tricuspid annulus.
 The atrial rate is approximately 300/min,
and is usually associated with 2 : 1, 3 : 1 or
4 : 1 AV block (with corresponding heart
ATRIAL FIBRILLATION
• This is a complex arrhythmia characterized • This increases with age and most common
by both abnormal automatic firing and with hypertensive heart disease, mitral valve
presence of multiple reentering circuits disease, LVF, Thyrotoxicosis
looping around the atria
• The atrial activity is chaotic and
mechanically ineffective
• P waves are therefore absent and replaced
by irregular fibrillatory waves (rate 400-
600/min)
• The ECG shows normal but irregular QRS
complexes and the ventricles are activated
irregularly at a rate determined by
conduction through the AV node
ATRIAL ECTOPIC BEATS
• These rarely indicate heart disease resetting of the SA node.
• They could be spontaneously provoked
by toxic stimuli e.g. caffeine, alcohol and
cigarette smoking
• Caused by premature discharge of an
atrial ectopic focus
• Seen as an early and often bizarre P
wave which is essential for dx but
otherwise shows a normal QRS complex
• The premature impulse enters and
depolarizes the sinus node such that a
partially compensatory pause occurs
before the next sinus beat during
NODAL ARRHYTHMIAS
• Also known as supraventricular tachycardias (SVTs)
• Usually paroxysmal with out obvious cardiac and extrinsic causes
• Are reentry arrhythmias caused either by an abnormal pathway between the atrium
and the AVN or by an accessory AV pathway (Bundle of Kent) as seen in WPW
syndrome
AV nodal re-entry tachycardia
• The abnormal atrionodal pathway provides the basis for a small re-entry circuit
• This arrhythmia is self limiting
• The sinus rhythm shows normal ECG findings and a occasionally a short PR interval
(Lown –Ganonglevine syndrome)
• During tachycardia, the rate is 150 -250 bpm
WOLFF-PARKINSON-WHITE SYNDROME
• This congenital disorder caused by an arrival of the impulse conducted through the
accessory pathway (bundle of Kent) atrioventricular node rapidly completes
between the atria and the ventricles. ventricular depolarization by normal His-
• In sinus rhythm, atrial impulses conduct Purkinje pathways.
more rapidly through the accessory pathway
than the AVN
• Therefore the initial phase of ventricular
depolarization occurs early (preexcitation)
and spreads slowly through the ventricles by
abnormal pathways.
• This produces a short PR interval and
slurring of the initial QRS deflection (δ
wave).
• The remainder of ventricular depolarization,
however, is rapid because the delayed
VENTRICULAR ARRHYTHMIAS
VENTRICULAR PREMATURE BEATS-
• These may occur in normal individuals, either spontaneously or in response to toxic
stimuli such as caffeine or sympathomimetic drugs.

• They are caused by the premature discharge of a ventricular ectopic focus that
produces an early and broad QRS complex

• The premature impulse may be conducted backwards into the atria, producing a
retrograde P wave, but penetration of the sinus node is rare.

• Thus, resetting of the sinus node does not usually occur and there is a fully
compensatory pause before the next sinus beat.
VENTRICULAR TACHYCARDIA
• It’s always pathological. complex, including an ‘rSR’ complex in V1
• 3 or more consecutive ventricular beats at a and a QS complex in V6.
rate above 120 per minute.
• Ventricular depolarization inevitably occurs
slowly by abnormal pathways, producing a
broad QRS complex.
Support for the diagnosis is provided by;
Very broad QRS complex (>140 ms)
Extreme left or right axis deviation
Concordance of the QRS deflections in V1–
V6 (either all positive or all negative)
Configurational features of the QRS
TORSADES DE POINTES
• This is a broad complex tachycardia with
changing wave fronts
• This form of polymorphic VT is a
complication of prolonged ventricular
repolarisation (prolonged QT interval).
• It may be inherited as an autosomal
dominant (Romano- ward syndrome) or as
autosomal recessive (Lange Nielsen
syndrome) trait when it is associated with
congenital deafness
• Other causes include the use of drugs ( anti-
arrhythmic and anti-psychotic therapy) that
cause prolongation of the QT interval
TORSADES DE POINTES
VENTRICULAR FIBRILLATION

• This occurs most commonly in severe myocardial ischaemia, either with or

without frank infarction.

 It is a completely disorganized arrhythmia characterized by irregular

fibrillatory waves with no discernible QRS complexes.

 There is no effective cardiac output and death is inevitable unless

resuscitation with direct current cardioversion is instituted rapidly
ATRIOVENTRICULAR BLOCK
• Conduction is delayed or completely • Third-degree AVN block, complete failure of
interrupted, either in the AVN or in the conduction and continuing ventricular
bundle branches. activity depends on the emergence of an
• Delayed conduction is e.g. first-degree escape rhythm.
atrioventricular block, bundle branch block,
the heart rate is unaffected.
• Completely interrupted conduction, the heart
rate may slow sufficiently to produce
symptoms.
• Second-degree AVN block, failure of
conduction is intermittent, and if sufficient
sinus impulses are conducted to maintain
an adequate ventricular rate, symptoms
may be avoided.
FIRST-DEGREE ATRIOVENTRICULAR BLOCK

• Delayed atrioventricular conduction

causes prolongation of the PR interval

(>0.20 s).

• Ventricular depolarization occurs

rapidly by normal His-Purkinje
pathways and the QRS complex is
usually narrow
SECOND-DEGREE ATRIOVENTRICULAR BLOCK
MOBITZ TYPE I (WENCKEBACH)- occurs in MOBITZ TYPE II
inferior myocardial infarction. • This indicates advanced conducting tissue
• Successive sinus beats find the AVN disease affecting the bundle branches.
increasingly refractory until failure of • The ECG typically shows a normal PR
conduction occurs. interval with bundle branch block in
• The delay permits recovery of nodal conducted beats
function, and the process may then repeat • Intermittent block in the other bundle branch
itself. results in complete failure of AVN
• The ECG shows progressive prolongation of conduction and dropped beats.
the PR interval, culminating in a dropped
beat. Block is within the AVN and ventricular
depolarization occurs rapidly by normal
pathways. Thus the QRS complex is usually
narrow.
 THIRD-DEGREE (COMPLETE) AVN BLOCK
• In third-degree AV block, conduction fails • AVN block (e.g. inferior myocardial
completely and the atria and ventricles beat infarction, congenital atrioventricular block),
independently a junctional escape rhythm with a reliable
• The atrial and ventricular rhythms are rate (40-60 bpm) takes over.
‘dissociated’ because none of the atrial • Ventricular depolarization occurs rapidly by
impulses are conducted. normal pathways, producing a narrow QRS
• Ventricular activity is maintained by an complex.
escape rhythm arising in the AV node or • However if the block is with in bundle
bundle of His (narrow QRS complexes) or branches (e.g. in idiopathic fibrosis), there is
the distal Purkinje tissues (broad QRS always extensive conducting tissue disease
complexes)
• The ECG shows regular P waves (unless
the atrium is fibrillating) and regular but
slower QRS complexes occurring
independently of each other.
BUNDLE BRANCH BLOCKS
RIGHT BUNDLE BRANCH BLOCK Prominent S waves in leads I and
• may be a congenital defect but is V6.
more commonly the result of organic
conducting tissue disease.

• Right ventricular depolarization is

delayed, resulting in;

A broad QRS complex with an ‘rSR’

pattern in lead V1
BUNDLE BRANCH BLOCKS
LEFT BUNDLE BRANCH BLOCK
• This always indicates organic
conducting tissue disease.

• The entire sequence of ventricular

depolarization is abnormal,

• This results in a broad QRS complex

with large slurred or notched R waves
in leads I and V6.
DIGOXIN THERAPY
• The administration of digoxin causes T wave inversion
• Characteristically with sloping depression of the ST segment
NB) It is helpful to record an ECG before giving digoxin, to save later confusion about the
significance of T wave changes.
ELECTROLYTE IMBALANCES
• Abnormalities of the plasma levels of potassium, calcium and magnesium affect the
ECG, though changes in the plasma sodium level do not.
• The T wave and QT interval (measured from the onset of the QRS complex to the
end of the T wave) are most commonly affected.
• A low potassium level (hypokalemia) causes T wave flattening and the appearance
of a hump on the end of the T wave called a ‘U’ wave.
• A high potassium level (hyperkalemia) causes peaked T waves with the
disappearance of the ST segment and the QRS complex may be widened.
• The effects of abnormal magnesium levels are similar.
• A low plasma calcium level causes prolongation of the QT interval, and a high
plasma calcium level shortens it.
REFERENCES

Davidson’ principles and practices of medicine

Hutchinsons clinical methods

The ECG made easy