ECG Interpretation

Basics & Quick Guide

Waseem Jerjes
 Cardiac conduction system
 Sinoatrial (SA) node:
Located in the right atrium
Heart’s main pacemaker
Initiates 60-100 beats/minute

 Internodal tracts and Bachmann’s bundle

In the R atrium, the impulse travel along three
internodal tracts
In the L atrium, the impulse travel via Bachmann’s
bundle
 Atrioventricular (AV) node
Positioned in the R atrium
Doesn’t posses pacemaker cell, but the junctional tissue
around it does
Conducts atrial impulse to the ventricles with 0.04sec
delay (filling time of ventricles)

 Bundle of His
Divides into R & L bundle branches
The L bundle branch splits into two branches or
fascicles
Impulse travel faster down the left bundle branch
Pacemaker site, firing rate 40-60 beats/minute
 Purkinje fibers
Transmit impulses quicker than any other part of the
conduction system
Usually fires when SA, AV nodes fail or when normal
impulse is blocked in both bundle branches
Firing rate 15-40 beats/minute

 Accessory pathways
Plays role in some arrhythmias (i.e. Bundle of Kent)
 Electrocardiography
 Heart electrical activity produces currents
radiates to the surroundings (skin)
 Skin leads
 Corresponds to the heart’s depolarization and
repolarization
 The resulting graph is called
Electrocardiogram
(ECG)
 ECG uses
 Identify rhythm disturbances, conduction
abnormalities and electrolytes imbalances
 Contributes information about the size of the
heart chambers and relative position of the
heart in the chest
 Diagnosis and progression of MI, ischaemia
and pericarditis
 Monitoring recovering from MI
 Monitoring drug effects
 Evaluates the function of artificial pacemakers
 Types of ECGs
 Resting: primary conduction disorders, arrhythmias, cardiac
hypertrophy, pericarditis, electrolyte imbalances, site and
extent of MI, recovery from MI, evaluate pacemaker
performance and the effect of cardiac glycosides and
antiarrhythmics
 Exercise: heart functional capacity and the origin of chest
pain, screen for asymptomatic CAD, arrhythmias that develop
during exercise, effect of antiarrhythmics and antianginal,
chnges in CV function after exercise
 Ambulatory: cardiac arrhythmias, effect of antiarrhythmic
drugs, evaluate chest pain and cardiac status after MI or
pacemaker implantation, assessment of SOB, syncope, light-
headedness and palpitations and evaluation of ST-segment
changes in ischemia
 Leads & planes
 A lead provide particular view of the heart
electrical activity
 When current flow towards the positive pole,
the waveform deflects upwards - positive
deflection
 Away from the positive pole, downwards -
negative deflection
 Absent electrical activity, straight line -
isoelectric deflection
 Leads & planes
Standard 12-lead ECG

 Limb leads (I, II, III, aVR, aVL, aVF): frontal

plane (bipolar and unipolar)
 Precordial (chest) leads (V1 to V6): unipolar
(from the centre of heart to electrode)
 Leads & planes
Single lead ECG

 Rhythm strip
 Continuous information about the heart’s
electrical activity
 Three bipolar leads (I, II, III) and two others
(MCL1, MCL6)…modified versions of V1 and
V6
 Leads I, II, III
 Standard limb leads or bipolar limb leads
 R arm, L arm, L leg and R leg (stabilize ECG
tracing)
 Lead I: records electrical activity between R
and L arm
 Lead II: R arm and L leg
 Lead III: L arm and L leg
 Einthoven’s triangle
 The sum of the electrical potentials at any
specific moment as recorded in leads I and III
equals the electrical potential recorded in lead
II ( error in electrode placement)
 Leads aVR, aVL, aVF
 Augmented unipolar leads
 Same electrode locations as (I, II, III)
 No need for R leg electrode
 Measure electrical potential between the limbs
and the centre of the heart (neutral)
 aVR: right shoulder
 aVL: left shoulder
 aVF: left foot
 Leads V1 to V6
 V1: 4th IS, R sternal border
 V2: 4th IS, L sternal border
 V3: midway between V2 and V4
 V4: 5th IS in L midclavicular line
 V5: 5th IS in L anterior axillary line
 V6: 5th IS in L mid axillary line
 V1, V2 (R precordial leads); V3, V4 (mid
precordial); V5, V6 (L precordial leads)
 Electrodes and heart walls
 Leads I, II and VL: lateral surface of the heart
 Leads III and VF: inferior surface of the heart
 VR: right atrium
 V1- V2: right ventricle
 V3-V4: septum & anterior left ventricle
 V5-V6: anterior & lateral left ventricle
 Graph paper
 Horizontal axis: length of particular event and
duration (small block 0.04 sec, large block 0.2
sec)
 Vertical axis: electrical voltage (amplitude) in
millivolts (small block 0.1 mV, large block 0.5
mV)
 ECG waveform
 Wave forms: P wave, QRS complex, T wave
 Segments and intervals: PR interval, ST
segment, QT interval

 U wave: may appear sometimes

 J point: marks the end of the QRS complex
and the beginning of ST segment
 P wave
 Atrial depolarization
 Originates in SA node, atria or AV junctional
tissue
 P wave normal (originates in the SA node)

 If a P wave precedes each QRS, the impulse

are being conducted from the atria to the
ventricles
 P wave -characteristics
 Location: precedes the QRS complex
 Amplitude: not more than 0.25mV (< ( 2.5 small
squares)
 Duration: 0.06 to 0.11sec (<
( 3 small squares)
 Configuration: usually rounded and upright
 Deflection: +ve leads I, II, aVF, V2-6; -ve in
lead aVR; biphasic lead V1; variable lead III,
aVL
 P wave -variations
 Peaked: R atrial abnormality
 Broad, notched: L atrial abnormality
 Inverted: SA node isn’t the pacemaker
(junctional arrhythmias)-except in aVR
 Varying (shapes and sizes vary): pulses
originating at various sites
 Missing: third degree AV block, sinus exit
block, atrial flutter or AF
 PR interval
 Beginning of atrial depolarization to the
beginning of ventricular depolarization
 Time taken from SA node-atria-AV node to
the bundle branches
 Any variation in the PR interval suggests a
conduction delay (AV block)
 PR interval-characteristics
 Location: extends from the beginning of P to
the beginning of QRS
 Amplitude:
 Duration: 0.12 to 0.2sec (<
( 1 big square)
 Configuration:
 Deflection:
 PR interval-variations
 Short: impulse is originating in an area other
than SA node (junctional arrhythmias)
 Prolonged: impulse is delayed as it passes
through the AV node (1st degree or 2nd degree
AV block)
 Depressed: pericarditis
 QRS complex
 Ventricular depolarization

 If the P wave doesn’t appear before the QRS

complex, then the impulse probably originated
in the ventricles (ventricular arrhythmia)
 Q wave: Any initial negative deflection
 R wave: Any positive deflection
 S wave: Any negative deflection after an R
wave
Depolarization
Depolarization is
is moving
moving towards
away from
thethe
leadlead
 The transition point
 Normal position: leads V3/V4

 Can detect hypertrophy (RV hypertrophy, the

transition point will be at leads V4/V5 or
V5/V6)… “clockwise rotation of the heart”
 QRS complex -characteristics
 Location: follows the PR interval
 Amplitude: differs for the 12 leads

 Duration: 0.06 to 0.10sec (<

( 3 small squares)
 Configuration: 3 waves ( Q: -ve, R: +ve S: -ve)

 Deflection: +ve (complex above the baseline);

-ve (complex below the baseline); biphasic
(complex above and below the baseline)
+ve: I,II,III,aVL,aVF,V4-6
-ve: aVR,V1-2
Biphasic: V3
 QRS complex -variations
 Widened: bundle branch block, premature
ventricular contractions, ventricular
tachycardia
 Configuration variation: bundle branch block,
WPW syndrome
 Varying complexes: ectopic impulse
 Missing: AV block, ventricular standstill
 ST segment
 End of ventricular depolarization and the
beginning of ventricular repolarization

 The point that marks the end of the QRS

complex and the beginning of the ST segment
is known as the J point

 A change in ST segment may indicate

myocardial damage
 ST segment -characteristics
 Location: from the end of S wave to the
beginning of T wave
 Amplitude:
 Duration:
 Configuration:
 Deflection: usually isoelectric, if elevated no
more than 0.1mV
 ST segment-variations
 Elevation: myocardial injury
 Depression: myocardial injury or ischemia
 Changes: pericarditis, myocarditis, L
ventricular hypertrophy, pulmonary embolism,
electrolyte disturbances and antiarrhythmic
(amiodarone)
 T wave
 Ventricular repolarization
 T wave-characteristics
 Location: follows S wave
 Amplitude: 0.5mV or less in I,II,III; 0.1 or less
in V1-6
 Duration:
 Configuration: typically rounded and smooth
 Deflection: +ve leads I, II, V3-6; -ve in lead
aVR; variable lead III, aVL, aVF, V1-2
 T wave -variations
 Inverted: in I,II, V3-6 may indicate myocardial
ischemia
 Peaked: hyperkalemia, myocardial ischemia
 Heavily notched: children (normal), adults
(pericarditis)
 Large or small: electrolyte imbalance
 With bumps: (P wave hidden within T wave)
impulse originated above the ventricle
 QT interval
 The time needed for the ventricular
depolarization-repolarization cycle

 Abnormal duration may indicate myocardial

irregularity

 Shouldn’t be greater than half the distance

between consecutive R wave (R-R interval)
when the rhythm is regular
 QT interval -characteristics
 Location: extends from the beginning of the
QRS complex to the end of the T wave
 Amplitude:
 Duration: varies according to age, sex, and
heart rate, usually (0.36-0.44 sec)
 Configuration:
 Deflection:
 QT interval -variations
 Prolonged: antiarrhythmics, myocardial
ischemia, MI, life threatening ventricular
arrhythmia
 Shortened: hypercalcemia, digoxin toxicity
 U wave
 Theory:
repolarization
of the His-
Purkinje fibres
 U wave -characteristics
 Location: follow T wave
 Amplitude:
 Duration:
 Configuration: typically rounded and upright
 Deflection: upright
 U wave -variations
 Prominent: hypokalemia, healthy people
 Inverted: heart disease
 Applying your knowledge
 Rate
 Rhythm
 Cardiac axis

 Abnormalities
 Heart Rate
 Locate the QRS complex that is closest to a
dark vertical line
 Count either forward or backwards to the next
QRS complex
 300-150-100-75-60-50-43
 2 lines means HR=150 beat/minute
 Heart Rhythm
 Source and its Regularity
 Source of the rhythm is the SA node or an
ectopic pacemaker
 Relationship of the P-wave to the QRS-
complex
 P wave before each QRS and the P is in the
same direction (sinus).
 Heart Axis
 Sum of the vectors
 The same direction (down-left) for a normal
heart: SA node (top right) to the purkinje fibers
(bottom left)

 I and AVF = +ve = normal axis

The normal range for the cardiac axis is
between - 30° and 90°
R axis deviation: long thin individuals, RV hypertrophy,
pulmonary conditions (PE), congenital heart disease, conduction
defect

L axis deviation: short fat individuals, LV hypertrophy,

conduction defect
The 3 pathways of Normal axis: effect of
the depolarization normal conduction
wave
L anterior fascicular L posterior fascicular
block block
RBBB RBBB+L ant hemi
block
 Normal axis
or
Slight L
axis deviation
Conduction and its
problems
 SA node block
 Seen as a complete pause of 1 beat - "skipped
beat"
 Can occur occasionally in normal patients
 AV nodal blocks (heart block)
 AV Node Block is a block which delays the
electrical impulse as it travels between the
atria and the ventricles in the AV node
o
 1 AV node block:

One P wave per QRS complex

PR interval > 1 large box
 2oAV Block is when sometimes excitation
fails to pass through the AV node or the
bundle of His
 Mobitz type II:

Constant PR interval
One P wave is not followed by QRS complex
 Wenckebach type:

Progressive lengthening of the PR interval

One non-conductive P wave
Next conductive P wave has a shorter PR
interval
 Second degree heart block (2:1 type)
Two P waves per QRS complex
Normal and constant PR interval
 Second degree heart block (3:1 type)
 3˙ Block is a complete block of signals from
the atria to the ventricles
P waves 90/min, QRS complex 36/min
No relationship between P & QRS (lack of
synchronization)
Abnormal shape of QRS (abnormal spread of
depolarization)
 Morphology (QRS complex): narrow complex
(origin is likely to be nodal), wide complex
(ventricular)
 Bundle branch block
 The key to recognizing a bundle block is to
find a R-S-R' pattern
 The criteria consist of a QRS wider than 0.12
seconds and the 2 R waves
 In a left bundle block, the left ventricular firing
is delayed, while in right bundle block, the
right ventricular firing is late
 RBBB
 Remember to consider what precordial lead the
block is presenting in
 V1-V2: RBBB, V5-V6: LBBB
 The axis will be hard to accurately determine
Diagnostic criteria RBBB:

QRS duration >0.12 s

RSR in V1-V2

Wide slurred S wave in leads I,

V5, and V6
 LBBB
 Note the R-S-R' pattern repeating as well as
the QRS complex being wider than (0.12sec).
 In the LBBB, the R wave is the right ventricle
and the R' is the left ventricle
 “W” pattern in V1 & “M” pattern in V6
Diagnostic criteria LBBB:

QRS duration of >0.12 s

“W” pattern in V1 & “M” pattern

in V6

Absence of Q waves in leads V5

and V6
 Fascicular (hemi) blocks
 L ant fascicular block (L ant hemiblock): L
axis deviation
 L post fascicular block (L post hemiblock): R
axis deviation
 RBBB: normal cardiac axis
 Bifascicular block (RBBB+L ant hemiblock):
L axis deviation
 Bifascicular block (RBBB+L post hemiblock):
R axis deviation
 Fascicular blocks
 RBBB with L ant hemiblock is the commonest type
of bifascicular block.
 The left posterior fascicle is fairly stout and more
resistant to damage

 Trifascicular block: bifascicular block + first degree

heart block
 RBBB+ L ant hemiblock + L post hemiblock =
complete heart block (as if the His bundle is
damaged)
Trifascicular block:

right bundle branch

block

left anterior hemiblock

first degree heart block

 Useful information
 First degree block: normal people, acute MI,
rheumatic fever
 Second degree block: acute MI; Mobitz type II
& Wenckebach type require no treatment, but
2:1 type block may need temporary or
permanent pacemaker
 Third degree block: fibrosis more than
ischemia; temporary or permanent pacemaker
 Useful information
 RBBB: ASD
 LBBB: aortic stenosis, ischemia, acute MI

 L axis deviation: LV hypertrophy

 L axis deviation + RBBB: severe conducting
tissue disease; may need pacemaker
The rhythm of the heart
 Sinus bradycardia
 Unusually slow heartbeat
 Sinus Tachycardia
 Increased in demand for cardiac output, which
is successfully met by the heart and whose
rhythm originates in the SA node.
 Remember that if the rate is high enough, the
P-wave can be obscured in the ST-segment,
but is still present
 Sinus arrhythmia
 The normal increase in heart rate that occurs
during inspiration
 Sinus arrhythmia is generally a good thing
 Absence of any sinus arrhythmia suggests an
autonomic neuropathy
 Tachycardia
 The source of a tachycardia, if ventricular, is
always pathologic, while non-ventricular
tachycardias can be thought of as "sinus" and
supraventricular (SVT) rhythms, and may or
may not be pathologic
 The most common cause of pathologic
tachycardias and arrhythmias results from
reentry
 Tachycardia-reentry
This is due to a signal splitting around a defect
and one side of that split being conducted
significantly slower than the other
If the slow signal meets the fast side ready to be
depolarized it can cause both normal and
retrograde depolarization
 SVT-Paroxysmal Atrial Tachycardia
 This arrhythmia is seen with reentry in the atria
 Causing reentry to give a rapid tachycardia
 There is a single ectopic pacemaker , which can even
be the AV node itself
 Inverted P-waves (source being lower down in the
atria)
 Can be differentiated from sinus tachycardia by vagal
maneuvers (if the rhythm slows and then resumes
after cessation of the maneuvers, sinus rhythm is
present. If the rhythm terminates abruptly or there's
no change, then it's PAT).
 SVT- Multifocal Atrial Tachycardia
 Ectopic pacemaker somewhere in the atria
 This causes there to be 2 or more
asynchronous pacemakers for the heart
 The hallmark of this form of SVT is the 2 or
more P-wave morphologies you see (one P-
wave from each pacemaker)
 Each of the pacemakers is not tachycardia, it is
the sum of their rates that produces the
tachycardia
 Atrial extrasystoles
These arise from ectopic atrial foci
Commonly, the ectopic beat always arises at
about the same time after the sinus beat

 Distinguish between an atrial extrasystole, and

an atrial escape beat, where the SA node
falters, and a subsidiary pacemaker takes over
 Regular SVT-Atrial flutter
 Undulating saw-toothed baseline F (flutter)
waves
 Atrial rate 250-350 beats/min
 Regular ventricular rhythm
 Ventricular rate typically 150 beats/min (with
2:1 atrioventricular block)
 4:1 is also common (3:1 and 1:1 uncommon)
 Irregular SVT-Atrial
SVT fibrillation
 P waves absent; oscillating baseline f
(fibrillation) waves
 Atrial rate 350-600 beats/min
 Irregular ventricular rhythm
 Ventricular rate 100-180 beats/min
 Ventricular extrasystoles
 The QRS complex is wide, bizarre, and
unrelated to a preceding P wave
 There is usually a constant relationship
(timing) between the preceding sinus beat and
a subsequent ventricular beat, because the
preceding beat influences the ectopic focus
 Ventricular extrasystoles
 Because the intrinsic rate of an ectopic focus
often tends to be slow-ish, extrasystoles will
tend to arise more commonly with slower
rates.
 In addition, if the rate is varying, extrasystoles
will tend to `squeeze in' during long RR
intervals. Some have called this the "rule of
bigeminy".
 Ventricular Tachycardia
 When there is ischemic, infarcted or necrotic
conductive tissue around the bundles, there can be a
reentry of the downward propagating depolarization,
that causes the signal to repeat itself
 This causes the Ventricular Tachycardia; this can
be a life threatening condition.
 The hallmark of ventricular rhythms is the wide QRS
complex
 Ventricular flutter
 Ventricular 'flutter' is a bizarre sine-wave like
rhythm, and usually degerates into ventricular
fibrillation
 Ventricular Fibrillation
 complete breakdown in the synchronization of
the myocardial conduction system; ranging
from course (large amplitude) to fine (close to
asystole) in amplitude. The only "cure" for V-
fib is electrical cardioversion (defibrillation).
Abnormalities of:
P waves
QRS complexes
T waves
 Atrial hypertrophy
 V1, which is mostly over the right atrium,
 tall P wave (3 blocks or more) signifies right
atrial enlargement; widened bifid one, left
atrial enlargement
 P-wave can become biphasic in bilateral atrial
hypertrophy
Large P waves
in leads II, III,
and aVF
(P pulmonale)
Biphasic P wave in V1. The large
negative deflection indicates left
atrial abnormality

P mitrale in lead II
It is commonly seen in association
with mitral valve disease,
particularly mitral stenosis
 Ventricular hypertrophy
 Large S wave in V1 and a large R wave in V5
The actual criteria, are to add the height of S in
V1 and the height of R in V5 (in mm) and if
the sum is greater than 35mm, then LVH is
probable.
Left ventricular
hypertrophy in patient
who had presented with
chest pain and was given
thrombolytic therapy
inappropriately because
of the ST segment
changes in V1 and V2
 Ventricular hypertrophy
 V1 (and less so in V2 and V3) and notice that
there is a large R-wave (the normal V1 has a
small R with a large S)
Right ventricular hypertrophy
secondary to pulmonary stenosis
(note the dominant R wave in
lead V1, presence of right atrial
hypertrophy, right axis deviation,
and T wave inversion in leads V1
to V3)
 Ischemia, Infarct and Injury
 the QRS is not the most affected part of the
EKG waveform in ventricular ischemia
 ST segment is most often affected in ischemic
conditions
 Transmural Ischemia: elevation of the ST
segment (unstable angina, acute MI)
 As the ischemia becomes more extensive the
ST segment elevation becomes more
pronounced
 Ischemia, Infarct and Injury
 The lead in which the ST elevation appears,
allows you to accurately locate the ischemic or
infarcted area of ventricular myocardium. If
the elevation appears in inferior leads, this
indicates an inferior
 ischemic/infarcted myocardium; the lateral
leads, likewise indicate lateral wall
ischemia/infarction
 Ischemia, Infarct and Injury
 It is important to differentiate pathologic ST segment
elevation from non-pathologic J-point
 elevation. J-point elevation is identified by an
elevation of the terminal portion of the QRS which
then dips back down towards the baseline before
rising back up to the ST segment. This is opposed to
the pathological ST-elevation which is visualized as
the terminal portion of the QRS going directly up to
the T-wave
 Ischemia, Infarct and Injury
 After the ischemia has progressed to an infarct,
and the tissue has scarred, the ECG will show
an inverted T wave
 A pronounced Q-wave (not normally present)
and loss of all or part of the R wave may also
present
 Ischemia, Infarct and Injury
 Sub-Endocardial Ischemia: ST-segment depression
(stable-angina)
 Unlike elevation, the ST-segment depression is not
localizable to a specific lead, but is seen in the leads
with the tallest R waves, which are the inferior leads
(II, III and AVF and leads V4-V6). Typically, stable
angina will self-resolve, however, like elevation, the
depression is increased as the myocardial demand
increases
 Prinzmetal's angina
 The simple (and possibly even correct)
explanation of why you see ST segment
elevation with this variant form of angina is
that the predominant area of ischaemia is
epicardial. This disorder is thought to be
related to vascular spasm, and angiography
shows coronaries without a significant burden
of atheroma. Many other morphological
abnormalities have been described with this
disorder
 Hyperkalemia

 The most prominent feature of an ECG of a

hyperkalemic patient is the peaked-T wave

 The other feature of the hyperkalemic EKG is

a stretching of entire waveform
ECG in hyperkalaemia
5.5-6.5 Tall peaked T waves
6.5-7.5 Loss of P waves
7.0-8.0 Widening of QRS complexes
8.0-10 Sine wave, ventricular arrhythmias, asystole

Serial changes in hyperkalaemia

Broad complex tachycardia

with a potassium
concentration of 8.4 mmol/l
(A); after treatment,
narrower complexes with
peaked T waves (B)
 Hypokalaemia
 The T waves flatten, U waves become
prominent (this may be falsely interpreted as
QT prolongation), and there may even be first
or second degree AV block.
ECG in hypokalaemia
Broad, flat T waves
ST depression
QT interval prolongation
Ventricular arrhythmias (premature
ventricular contractions, torsades
de pointes, ventricular tachycardia,
ventricular fibrillation)

Electrocardiogram showing prominent

U wave, potassium concentration 2.5
mmol/l (A) and massive U waves with
ST depression and flat T waves,
potassium concentration 1.6 mmol/l (B)
 Digitalis Toxicity
 Overdoses of digitalis (Digoxin or Digitoxin) can
have effects ranging from mild 1 ˙ AV block to
junctional rhythms through fatal arrhythmias.
 The most noticeable change to the ECG is the
"swooping" ST-segment depression, extended PR
intervals or 1˙ block, although this alone is
indistinguishable from primary 1˙ AV Block.
Others
 Wolff-Parkinson-White syndrome
 PR interval under 0.12s
 A delta wave
 QRS duration of 0.12s (or more)
 A normal P-wave axis
 Acute pulmonary embolism
 Patients who present with a small pulmonary embolus
are likely to have a normal electrocardiogram or a
trace showing only sinus tachycardia.

 If the embolus is large and associated with pulmonary

artery obstruction, acute right ventricular dilatation
may occur. This may produce an S wave in lead I and
a Q wave in lead III. T wave inversion in lead III may
also be present
S1, Q3, T3
Sinus tachycardia and S1,
Q3, T3 pattern in patient
with pulmonary embolus
COPD ECG

P pulmonale
low amplitude QRS complexes
poor R wave progression)
 Left ventricular hypertrophy
Hypertrophic Left atrial enlargement
cardiomyopath Abnormal inferior and anterior
y ECG and/or lateral Q waves
Bizarre QRS complexes
masquerading, for example, as
pre-excitation and bundle branch
block
Dilated
cardiomyopathy ECG

Left bundle branch block

Left atrial enlargement
Abnormal Q waves in leads
V1 to V4
Left ventricular hypertrophy
Arrhythmias—ventricular
premature beats, ventricular
tachycardia, atrial
fibrillation
 Restrictive
cardiomyopathy
ECG

Low voltage QRS complexes

Conduction disturbance
Arrhythmias—supraventricular,
ventricular
 Hypothermia ECG

Tremor artefact from shivering

Atrial fibrillation with slow
ventricular rate
J waves (Osborn waves)
Bradycardias, especially junctional
Prolongation of PR, QRS, and QT
intervals
Premature ventricular beats,
ventricular tachycardia, or
ventricular fibrillation
Asystole
 Most common
Sinus tachycardia
Increased QRS voltages
Atrial fibrillation

Less common
Supraventricular arrhythmias
(premature atrial beats, paroxysmal
supraventricular tachycardia,
multifocal atrial tachycardia, atrial
flutter)
Non-specific ST and T wave
Thyrotoxicosis changes
(ECG) Ventricular extrasystoles
 Hypothyroidism
(ECG)

Most common Less common

Sinus bradycardia Heart block
Prolonged QT interval Low QRS voltages
Flat or inverted T waves Intraventricular
conduction defects
Ventricular extrasystoles
Simple test
2:1 AV block
Acute anterior myocardial infarction
Acute inferior myocardial infarction
Acute myocardial infarction in the presence of left bundle
branch block
Acute posterior myocardial infarction
Acute pulmonary embolus
Atrial fibrillation and complete heart block
Atrial fibrillation with pre-existing left bundle branch block
Atrial fibrillation with rapid ventricular response
Atrial flutter
Atrial flutter with 2:1 AV conduction
Atrial Premature Beat (APB)
Complete Heart Block
Hyperkalaemia
Implantable cardioverter defibrillator
Left anterior hemiblock & L atrial & ventricular hypertrophy
Left atrial & ventricular hypertrophy
Mitral Stenosis
Normal
Old inferior myocardial infarction
Pericardial effusion with electrical alternans
Right atrial hypertrophy
Right Bundle Branch Block
Sinus bradycardia
Sinus tachycardia
'Trifasicular' block
Ventricular bigeminy
Ventricular fibrillation
Ventricular pacemaker
Ventricular tachycardia
Ventricular tachycardia
Wolf-Parkinson-White syndrome with atrial fibrillation
Hypokalaemia
Digitalis effect
I hope you can read ECG now

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