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 Other factors

Fever Drugs
Hyperthyroidism
Hemorrhage Epinephrine
Shock Atropine
Anemia Food,etc
Infection Tea coffee
Congestive heart failure
Myocarditis Alcohol
Hypoxia 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 beats”when 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 R-
R 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.
 Ⅲ.Ectopic tachycadia
It is more common to paroxysmal tachycardia.
The paroxysmal tachycardia can be divided
into two main groups.
① Paroxysmal Supraventricular tachycardia
② Paroxysmal ventricular tachycardia
 Ⅲ.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
 atrial 160-250/min: may conduct to ventricles
Rate 1:1, or 2:1, 3:1, 4:1 into the presence of a
block.

P wave morphology usually varies from sinus

normal (unless associated with aberrant

QRS
ventricular conduction).

P-R interval depends on the status of AV

Conduction 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
 Ⅲ.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

VT
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
 Ⅳ.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.
 Ⅳ.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.
 atrial 250-350/min; ventricular conduction
Rate depends on the capability of the AV junction
(usually rate of 150-175 bpm).

not present; usually a "saw tooth" pattern is

P wave
present.

QRS normal

Conduction 2:1 atrial to ventricular most common.

usually regular, but can be irregular if the AV

Rhythm
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
 Ⅳ.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 Ⅱ,Ⅲ,Avf,V1 or V2.
 Rate atrial rate usually between 400-650/bpm.

P wave not present; wavy baseline is seen instead.

QRS normal

variable AV conduction; if untreated the

Conduction
ventricular response is usually rapid.

irregularly irregular. (This is the hallmark of

Rhythm
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

• Alcohol
• Thyroid disease

• Caffeine
• Acute MI
• Cigarettes
• Ischemic heart disease
 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
 Ⅴ.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(Ⅰ゜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.

Mobitz I Progressive prolongation of the P-R

interval causing progressive R-R
AV block interval shortening until a P wave fails
(Wenckebach) to conduct to the ventricle.
Sudden unexpected blocked P waves
Mobitz II
without variation or prolongation of the
AV block 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
rd

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

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.
rd

The location of the block may be in the AV junction or bilaterally in the bundle branches
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 3rd 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
 Ⅵ.Bundle branch block

The ventricular conduction system is composed

of two major divisions.
①the right bundle branch
②the left bundle branch
 Ⅵ.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
Ⅰ,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 identify

RBBB

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
Ⅵ.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 don’t 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
Ⅵ.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 LEFT

Inferior Antero-Septal
II, III, AVF V1,V2, V3,V4

Lateral
Posterior I, AVL, V5,
V1, V2, V3 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
vector…can 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 R
ST ST
T
P P P

T
QS Q
Q

1 minute after onset 1 hour or so after onset A few hours after onset

ST T
P P ST
P

T T
Q Q Q

A day or so after onset Later changes A few months after AMI

 Anterior infarction
Anterior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left
coronary
artery
 Inferior infarction
Inferior infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Right
coronary
artery
 Lateral infarction
Lateral infarction

I II III aVR aVL aVF V1 V2 V3 V4 V5 V6

Left
circumflex
coronary
artery
Location of infarct combinations

I aVR V1 V4

ANT
LATERAL
POST ANT
II aVL V2
SEPTAL
V5

ANT
V3 V6 LAT
III aVF
INFERIOR
 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)