ECG

Abnormalities

The ECG Paper (cont)

3 sec

3 sec

Every 3 seconds (15 large boxes) is

marked by a vertical line.
This helps when calculating the heart rate.
NOTE: the following strips are not marked
but all are 6 seconds long.

Determining the Rate

Frekuensi Denyut Jantung

FDJ normal : 60 100 x/menit
Takikardi : > 100 x / menit
Bradikardi : < 60 x / menit
Takikardi abnormal : 140 250 x / menit
Flutter : 250 350 x / menit
Fibrilasi : > 350 x / menit

DISRITMIA
Aritmia terdiri dari aritmia yang
disebabkan oleh terganggunya
pembentukan impuls atau aritmia
yang terjadi karena gangguan
penghantaran impuls.

ECG Diagnosis
The trajectory of the
electric vector
resulting from the
propagating
activation wavefront
can be traced by the
ECG and used to
diagnose cardiac
problems

Gangguan pembentukan
impuls
1 Nodus SA ;
SINUS TACICARDIA

Factors associated with Sinus Tachycardia:

Physiologic
Exercise
Strong emotion
Pain
Anxiety states

Pathologic
Fever
Hyperthyroidism
Hemorrhage
Shock
Anemia
Infection
Congestive heart failure
Myocarditis
Hypoxia

Other factors
Drugs
Epinephrine
Atropine
Food,etc
Tea coffee
Alcohol
Tobacco

SINUS BRADICARDIA
Rate

40-59 bpm

P wave

sinus

QRS

normal (.06-.12)

Conduction

P-R normal or slightly prolonged at slower

rates

Rhythm

regular or slightly irregular

I. Sinus Bradicardia

Common causes
Physiologic bradycardia
Laborers and trained athletes
Emotional states leading to syncope
Carotid sinus pressure, eyeball
pressure,intracranial pressure
Sleep

Pathologic

Systemic disease
Obstructive jaundice
Obstructive diseases of the intestine,kidney or bladder
During convalescence after some diseases marked by
fever(e.g.influenza)
myxedema
myocardial infarction(inferior wall or atrial infarction)
high intracranial pressure
Drug
Digitalis
Morphine
Quinidine
Propranolol

Rate

45-100/bpm

P wave

sinus

QRS

normal

Conduction

normal

Rhythm

regularly irregular

The rate usually increases with inspiration and decreases with expiration.
This rhythm is most commonly seen with breathing due to fluctuations in parasympathetic vagal tone. During inspiration
stretch receptors in the lungs stimulate the cardioinhibitory centers in the medulla via fibers in the vagus nerve.
The non respiratory form is present in diseased hearts and sometimes confused with sinus arrest (also known as "sinus
pause").
Treatment is not usually required unless symptomatic bradycardia is present.

Sinus arrhythmia

Sinus arrest
There is no sinus P wave in ECG
suddenly.The long interval is not times of P-P
interval.

Premature beat
The terms premature beat,premature
contraction,premature systole,or
extrasystole indicate that the atria ,AV
junction, or ventricle are stimulated prematurely.
These premature beats are called atrial
premature beatswhen they arise in some
portion of the atria .AV junctional premature
beats arise in the AV junction. Ventricular
premature beats arise in one of the branches
of the bundle of His ,the Purkinje network ,or
the ventricular muscle.

Atrium
Ekstrasistol
Atrial premature beats

1).A premature P wave is present .It may be

surperimposed on the preceding T wave
because it is premature.The premature P wave
is usually followed by a QRS complex and a T
wave.Occasionally, it is not followed by a QRS
complex and a T wave .(blocked atrial premature
beat).
2).The QRS and T waves that follow the
premature P waves usually resemble the other
QRS and T waves in the lead

II.Premature beat
2. Ventricular premature beats
1)The QRS complex is premature ,is 0.12second
or more wide ,and is aberrant,notched ,or
slurred .It is associated with a T wave that
usually point in a direction opposite to the main
deflection of the QRS complex.
2).The premature QRS complex is not preceded
by a P wave.

II.Ventricular Premature beat

3).A ventricular premature beat is often followed
by a fully compensatory pause(the sum of the RR intervals including the pre-premature beat and
the post-premature beat interval equals the
sum of two normal R-R intervals)
4).Multiply, ventricular premature beats that arise
from a single focus show a similar shape and
usually a similar coupling intervals (distance
from the preceding normal QRS complex to the
premature ventricular beat) in any one lead.

II. VentricularPremature beat

5).occasionally, a ventricular premature beat will
occur simultaneously with the apex of the
preceding T wave,This is R on T phenomenon.
When this occurs ,it may be a precursor of a
ventricular tachycardia.

Note: multifocal ventricular prematyre beat

(VPB) and multiformed VPB

PREMATURE VENTRICULAR CONTRACTION

A single impulse originates at right ventricle

Time interval between normal R peaks

is a multiple of R-R intervals

Causes of PVCs
Heart failure

Mitral valve prolapse

Electrolyte imbalances

Thyroid disease

Caffeine

Acute MI

Hypoxia

II.Premature beat
3. AV Junctional premature beats
1).A premature AV junction P wave is followed by a QRS
and T wave.
2).The AV junction P waves in aVR become upward .The
P waves in II,III, and aVF is downward.The PR interval is
usually less than 0.12second ,if the P waves is before
the QRS complexes. The P waves may appear after the
QRS complexes or may be hidden within the QRS
complex.
3).An AV junctional premature beat is followed by a fully
compensatory.

.Ectopic tachycadia
It is more common to paroxysmal tachycardia.
The paroxysmal tachycardia can be divided
into two main groups.
Paroxysmal Supraventricular tachycardia
Paroxysmal ventricular tachycardia

.Ectopic tachycadia
1.paroxymal supraventricular tachycardia
ECG
1).Heart rate is regular rhythm with a rate
o f 160-250/minute.
2).The QRS complex in form is usually
normal.
3).The P wave in not easy to see.
4).With abrupt onset and abrupt terminal.

Supraventricular tachycardia

Rate

atrial 160-250/min: may conduct to

ventricles 1:1, or 2:1, 3:1, 4:1 into the
presence of a block.

P wave

morphology usually varies from sinus

QRS

normal (unless associated with

aberrant ventricular conduction).

Conduction

P-R interval depends on the status of

AV conduction tissue and atrial rate:
may be normal, abnormal, or not
measurable.

PAT also known as Paroxysmal Supraventricular Tachycardia

This rhythm is often transient and usually requires no treatment.
However, it can usually be terminated with vagal maneuvers.
Digoxin, antiarrhythmics, adenosine and cardioversion may be used.
Frequent symptomatic episodes may require surgical intervention. When an accessory conduction pathway can be
demonstrated, interventional surgery to ablate the accessory conduction pathway can be curative

.Ectopic tachycadia
2. paroxysmal ventricular tachycardia
1).The QRS complex are 0.12 second or more
wide ,are aberrant ,and are followed by aberrant
ST segments and T waves.
2) Ventricular rate is between 140 and 200/minute
and regular rhythm or slightly irregular.
3).The P waves have no relation to the QRS
complexes.
4).Fusion beats or ventricular capture are present.
5).Sometimes, P-P interval >R-R interval.but the
P-R is no relation.

Ventricular tachycardia (VT)

Rapid rate, 100 to 250 beats per minute
Wide, bizarre, QRS complex followed by large T
wave
Patient may be unconscious, pulseless, apneic-initiate CPR
If patient awake, treat as medical emergency

Cardiac Rhythm: Ventricular

VENTRICULAR FIBRILLATION

Chaotic ventricular depolarization ineffective at pumping blood death within minutes

Rapid, wide, irregular ventricular complexes

PACER RHYTHM

Impulses originate at transvenous pacemaker

Wide ventricular complexes preceded by pacemaker spike

Rate is the pacer rhythm

VDD PPM

.Flutter and Fibrillation

The flutter and fibrillation arise from excitable
ectoptic focus in the atria and ventricle and with
a rapid rate and appropriate conduction block.
Thus ,They are easily caused by a reentry.

.Flutter and Fibrillation

1. Atrial Flutter
ECG:
1).There are no P waves in ECG
2).Presence of saw-tooth flutter wave.
3).F waves always uniform in size ,shape and
frequency.
4).Regular atrial rhythm with a rate of 250-350
5).Ventricular response of 1:1,2:1,3:1,4:1,or
higher.
6).Absence of isoelectric line.

Rate

atrial 250-350/min; ventricular

conduction depends on the capability
of the AV junction (usually rate of 150175 bpm).

P wave

not present; usually a "saw tooth"

pattern is present.

QRS

normal

Conduction

2:1 atrial to ventricular most common.

Rhythm

usually regular, but can be irregular if

the AV block varies.

Atrial flutter almost always occurs in diseased hearts. It frequently precipitates CHF.
The treatment depends on the level of hemodynamic compromise.
Cardioversion, vagal maneuvers and verapamil are used when prompt rate reduction is needed.
Otherwise, digoxin and other antiarrhythmic drugs can be used.

Atrial flutter

.Flutter and Fibrillation

2. Atrial Fibrillation
ECG:
1).Absence of P waves
2).P waves replaced by f waves.
3).f waves : irregular in size ,shape ,and
spacing.
Rate between 350 and 600
4). Irregularly irregular ventricular rhythm, best
seen in ,,Avf,V1 or V2.

Rate

atrial rate usually between 400650/bpm.

P wave

not present; wavy baseline is seen

instead.

QRS

normal

Conduction

variable AV conduction; if untreated

the ventricular response is usually
rapid.

Rhythm

irregularly irregular. (This is the

hallmark of this dysrhythmia).

Atrial fibrillation may occur paroxysmally, but it often becomes chronic. It is usually associated with COPD, CHF or other heart disease.

Treatment includes:
Digoxin, diltiazem, or other anti-dysrhythmic medications to control the AV conduction rate and assist with
conversion back to normal sinus rhythm.
Cardioversion may also be necessary to terminate this rhythm.

Atrial fibrillation

Causes of AF
Atrial enlargement due to COPD

Stress

Other lung diseases

Fatigue

Thyroid disease
Acute MI
Ischemic heart disease

Alcohol
Caffeine
Cigarettes

About AF
Two hallmarks of AF:
irregularly irregular rhythm
f waves

If patient unstable or symptomatic: administer

oxygen and obtain I.V. access
All patients with AF lasting longer than 48 hours
are at increased risk for thrombus

Cardiac Rhythm: Supraventricular

ATRIAL FLUTTER

Impulses travel in circular course in atria No interval between T and P

Rapid flutter waves, ventricular response irregular

ATRIAL FIBRILLATION

Impuses have chaotic, random pathways in atria

Baseline irregular, ventricular response irregular

Electrical Conducting system

.Atrio ventricular block(AVB)

AV block, or heart block, exists when conduction
of the stimulus from the atria to the ventricle
through the AV node is slowed or blocked.The
AV block may be transient ,intermittent ,or
permanent .It may be incomplete or complete. A
patient may show various types of AV block in
one ECG.

AVB
1. First degree heart block( AVB)
I AVB is prolongation of the atrio-ventricular
conduction time and is also referred to as first
degree A-V block.
ECG:prolonged P-R interval:longer than
0.20sec in adults and >0.22s in old adults.
The difference of P-R interval between two times
is more than 0.04 second.
Note:P-R interval varies with heart rate and age.

First- degree AV block

P-R interval is > 0.2 seconds (greater than one big box)

A-V BLOCK, FIRST DEGREE

Atrio-ventricular conduction lengthened

P-wave precedes each QRS-complex but PR-interval is > 0.2 s

Atrio-Ventricular (AV) Block

Possible sites of AV block:

AV node (most common)

His bundle (uncommon)

Bundle branch and fascicular divisions (in presence of already
existing complete bundle branch block)

1 Degree AV Block: PR interval > 0.20 sec; all P waves conduct to the ventricles
st

Type I (Wenckebach) AV block (note the RR intervals in ms duration):

Type I AV block is almost always located in the AV node, which means

that the QRS duration is usually narrow, unless there is preexisting
bundle branch disease.

Activation Sequence Disorders

A-V BLOCK, FIRST DEGREE

Atrio-ventricular conduction lengthened

P-wave precedes each QRS-complex but PR-interval is > 0.2 s

A-V BLOCK, SECOND DEGREE

Sudden dropped QRS-complex

Intermittently skipped ventricular beat

2nd Degree A-V Block

Cardiac conduction system disorder where some
P waves fail to conduct to the ventricle to
generate a QRS complex.
Progressive prolongation of the PMobitz I
R interval causing progressive R-R
AV block
interval shortening until a P wave
(Wenckebach) fails to conduct to the ventricle.
Mobitz II
AV block

Sudden unexpected blocked P

waves without variation or
prolongation of the PR interval.

Second- degree type I AV Block

Second-degree type I AV block

AVB
2).II II type(mobity type II AV block)
Mobity II is characterized by failure of conduction of one
or more sinus beats to the ventricle .There is a fixed
numerical relationship between atrial and ventricular
impulses,which may be 2:1 or 3:1 or 4:1 .Mobitz II blocks
become progressive worse until a complete heart block
is established.Thus ,mobitz Type II require a
pacemaker,whereas mobitz I does not require a
pacemaker,since it does not progress to complete heart
block.

Second-degree type II AV block

2nd Degree A-V Block

Pathophysiology:
Mobitz I (Wenckebach) block is most often caused by
conduction delay in the AV node. A narrow QRS complex
makes the site of delay even more likely to be the AV node.
Wenckebach block with a wide QRS complex may be due to
AV nodal or infranodal conduction delay.
EP studies demonstrate that Mobitz II block is due to an
infranodal His-Purkinje system conduction delay an is often
associated with a wide QRS complex.

2nd-degree AV block
Mortality/Morbidity:
Most investigators believe that Mobitz I block localized to
the AV node is not significantly associated with morbidity
or death in the absence of organic heart disease. Type I
block localized to the His-Purkinje system has the same
risks as type II block.
Mobitz II block carries a high risk of progression to
complete heart block, often with associated
cardiovascular collapse

www.emedu.org/ecg/

2nd Degree Type I

www.emedu.org/ecg/

www.emedu.org/ecg/

2nd Degree Type II

Too
Bad
www.emedu.org/ecg/

Type II (Mobitz) AV block(note there are two consecutive constant PR intervals before the blocked P wave):

Type II AV block is almost always located in the bundle branches, which means that the QRS
duration is wide indicating complete block of one bundle; the nonconducted P wave is
blocked in the other bundle. In Type II block several consecutive P waves may be blocked as
illustrated below:

AVB
3.III AVB(Complete heart block)
(Third degree A-V Block)
ECG:
1).The atrial and the ventricular rhythms are absolutely
independent of one another .
2).There is no P-R to QRS relationship.
3).The atrial rate is more rapid than the ventricular rate.
4).regular P-P interval .
5).rugular R-R interval

AVB
6).QRS is 0.12sec or greater.
VR is 36 beats per minute or less.(20-40
beats/mim)
QRS is less than 0.12sec.
VR is 36 to 60 beats per min(40-60beats/min)

AV Block
Third-degree AV block

High-grade atrioventricular block

Complete (3 Degree) AV Block

Usually see complete AV dissociation because the atria and ventricles are each controlled by
separate pacemakers.
rd

Narrow QRS rhythm suggests a junctional escape focus for the ventricles with block above the
pacemaker focus, usually in the AV node.
Wide QRS rhythm suggests a ventricular escape focus (i.e., idioventricular rhythm). This is seen in
ECG 'A' below; ECG 'B' shows the treatment for 3 degree AV block; i.e., a ventricular pacemaker.
The location of the block may be in the AV junction or bilaterally in the bundle branches
rd

AV Dissociation (independent rhythms in atria and ventricles):

Not synonymous with 3 degree AV block, although AV block is one of the causes.
rd

May be complete or incomplete. In complete AV dissociation the atria and ventricles are always
independent of each other. In incomplete AV dissociation there is either intermittent atrial capture
from the ventricular focus or ventricular capture from the atrial focus.
There are three categories of AV dissociation (categories 1 & 2 are always incomplete AV
dissociation):
1. Slowing of the primary pacemaker (i.e., SA node); subsidiary escape pacemaker takes over by
default:

Bradycardia Guidelines

Treat only symptomatic bradycardias

Symptomatic bradycardia means that heart rate is slow

(<60bpm), patient has symptoms, and symptoms are due
to the slow HR
Symptoms: chest pain, SOB, decreased consciousness,
weakness, fatigue, lightheadedness/dizziness, syncope
Signs: hypotension, orthostatic hypotension, diaphoresis,
pulmonary congestion on exam/CXR, CHF or pulmonary
edema, bradycardia-related PVCs or VT

Bradycardia Guidelines
Recognize bradycardias that are likely to deteriorate,
even if asymptomatic:
2nd degree AV block type II
3rd degree AV block
Overall treatment approach
Atropine (1st line treatment in absence of
immediately reversible causes)
Transcutaneous pacing
Dopamine infusion
Epinephrine infusion

Transcutaneous Pacing

Pacing delivers electrical stimulus causing electrical depolarization and

subsequent cardiac contraction
TCP delivers impulses through the skin using cutaneous electrodes
Most manual defibrillators now have a pacing mode
Set rate to 60/min to begin
Start at low milliamp and increase until capture. Set it at 2
milliamps above what achieves consistent capture.
Indications for emergent TCP:
Hemodynamically symptomatic bradycardia unresponsive to
atropine, particularly if high degree block (Mobitz II or 3 rd degree
block)
Sx: SBP <80 mmHg, mental status changes, pulmonary edema

More on Pacing

Following initiation of pacing, confirm electrical and

mechanical capture. Reassess patient for
improvement/stability.
Analgesics and sedatives for pain control during pacing
if time allows
If TCP is ineffective (inconsistent capture), prepare for
transvenous pacing and obtain expert consulation

.Bundle branch block

The ventricular conduction system is composed
of two major divisions.
the right bundle branch
the left bundle branch

.Bundle branch block

1. Right Bundle Branch Block(RBBB)

ECG:
1).QRS 0.12 sec or wider
2).Rsr(M)pattern in V1 and V2 and deep ,wide S wave in
,V5-6.
3).The ST segment is slight depressure with negative T
waves
When incomplete RBBB is present ,the pattern is similar,
but the QRS width is less than 0.12sec.

Right bundle-branch block (RBBB)

Impulse conduction to right ventricle is blocked
Examine lead V1 to
RBBB

identify

ECG show delayed or positive R wave

Key identifier is QRS complex wider than 0.12
second, with positive R wave in V1

Bundle-branch Block
RIGHT BUNDLE-BRANCH BLOCK
QRS duration greater than 0.12 s
Wide S wave in leads I, V5 and V6

Right bundle branch block

.Bundle branch block

2. Left Bundle Branch Broch,(LBBB)

ECG: 1).
QRS 0.12sec or more .
2)absent q waves in I,V5 and V6
3).wide ,notched,or slurred R waves in V5-6 with
depressed ST segments,downward T waves.
4).wide QS or rS patters with elevated ST
segments and upward T waves in V1-2.
When incomplete LBBB in present ,the pattern is
similar ,but the QRS width is less than 0.12
second.

Left bundle branch block (LBBB)

Electrical impulses dont reach left side of
the heart
QRS wider than 0.12 second
Key to recognizing LBBB
is a
wide downward
S wave or
rS wave in
leads V1 and V2

Left bundle branch block

.Bundle branch block

3. Left anterior fascicular block (LAH)

ECG criteria
1).Left axis deviation (-30 to -45 or greater)
2).Small q wave in lead I
3).Deep s wave in lead II
4).Decper S wave in lead III
5).S wave in aVF and V6

ECG
Abnormalities
Associated with ischaemia

Coronary Artery Circulation

Coronary Artery Circulation

Right Coronary Artery
right atrium
right ventricle
inferior wall of left
ventricle
posterior wall of left
ventricle
1/3 interventricular
septum

Coronary Artery Circulation

Left Main Stem Artery divides in two:
Left Anterior Descending
Artery
antero-lateral surface of
left ventricle
2/3 interventricular
septum
Circumflex Artery
left atrium
lateral surface of left
ventricle

Surfaces of the Left Ventricle

Inferior - underneath
Anterior - front
Lateral - left side
Posterior - back

Inferior Surface
Leads II, III and avF look UP from below to the
inferior surface of the left ventricle
Mostly perfused by the Right Coronary Artery

Inferior Leads
II
III
aVF

Anterior Surface
The front of the heart viewing the left ventricle and
the septum
Leads V2, V3 and V4 look towards this surface
Mostly fed by the Left Anterior Descending branch
of the Left artery

Anterior Leads
V2
V3
V4

Lateral Surface
The left sided wall of the left ventricle
Leads V5 and V6, I and avL look at this surface
Mostly fed by the Circumflex branch of the left
artery

Lateral Leads
V5, V6,

I, aVL

Posterior Surface
Posterior wall infarcts are rare
Posterior diagnoses can be made by looking at the
anterior leads as a mirror image. Normally there are
inferior ischaemic changes
Blood supply predominantly from the Right
Coronary Artery

RIGHT

Inferior
II, III, AVF

Posterior
V1,
V2, V3

LEFT

Antero-Septal
V1,V2, V3,V4

Lateral
I, AVL, V5,
V6

Anatomic region of heart & associated

coronary artery
Inferior MI----------------RCA
Antero-septal MI---------LAD
Antero-lateral MI---------Circumflex
Posterior MI--------------RCA
----------------------------------------------------------Inferior leads-------------II, III, aVF
Antero-septal leads------V1,V2,V3&V4
Antero-lateral leads------I,aVL,V2-V6

Myocardial Ischemia and Infarction

Oxygen depletion to heart
can cause an oxygen debt in
the muscle (ischemia)
If oxygen supply stops, the
heart muscle dies (infarction)
The infarct area is
electrically silent and
represents an inward facing
electric vectorcan locate
with ECG

Ischaemic Changes
S-T segment elevation
S-T segment depression
Hyper-acute T-waves
T-wave inversion
Pathological Q-waves
Left bundle branch block

ST Segment Elevation
The ST segment lies above the isoelectric line:
Represents myocardial injury
It is the hallmark of Myocardial Infarction
The injured myocardium is slow to repolarise
and remains more positively charged than the
surrounding areas
Other causes to be ruled out include pericarditis
and ventricular aneurysm

ST-Segment Elevation

Recognizing
myocardial infarction (MI)
Series of predictable ECG changes occur in MI
ST-segment-elevation MI
(STEMI)-serious type
of MI, associated
with
more complications,
higher risk of death

NOTE: The Q wave is the first downward stroke of the QRS complex, and it is never preceded by anything in the
complex. In the QRS complex, if there is any positive wave - even a tiny spike - before the downward wave, the
downward wave is an S wave (and the upward wave preceding it is an R wave).

Sequence of changes in
evolving AMI
R

R
T

ST

ST

QS

1 minute after onset

1 hour or so after onset

A few hours after onset

R
ST

P
T

A day or so after onset

ST

P
T

Later changes

A few months after AMI

Anterior infarction
Anterior infarction

I II III

Left
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Inferior infarction
Inferior infarction

I II III

Right
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Lateral infarction
Lateral infarction

I II III

Left
circumflex
coronary
artery

aVR aVL aVF

V1 V2 V3

V4 V5 V6

Location of infarct combinations

aVR

LATERAL
aVL

II

V1
ANT
POST
V2

V4

ANT
SEPTAL

V5
ANT

V3
III

INFERIOR

aVF

V6 LAT

T waves
The T wave represents ventricular
repolarisation
Should be in the same direction as and
smaller than the QRS complex
Hyperacute T waves occur with S-T
segment elevation in acute MI
T wave inversion occurs during ischaemia
and shortly after an MI

Hyperacute T waves

T wave inversion in an evolving

MI

Wide QRS (LBBB)

Q Waves
Non Pathological Q waves
Q waves of less than 2mm are normal

Pathological Q waves
Q waves of more than 2mm
indicate full thickness myocardial
damage from an infarct
Late sign of MI (evolved)