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ELECTROCARDIOGRAPHY
(ECG / EKG)
Taufik Indrajaya
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Evaluasi Kardiovaskuler
Anamnesis
Tekanan darah
Nadi
Auskultasi
Foto Thoraks
EKG
Stress EKG
Scintigraphy Thallium
Ekhokardiografi
Angiografi
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C P R
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A good basic Knowledge
of the heart and cardiac function
is Essential in order
to Understand
the 12 lead ECG

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Anatomy
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Orientation of Cardiac Muscle Fibers


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1. Anastomosing muscular fibers of the heart.
2. Purkinjes fibers from the sheeps heart.

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Cardiovascular system works ..
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CARDIAC OUTPUT = STROKE VOLUME x HEART RATE
Autoregulation
(Frank-Starling Law of the Heart)
Contractility
Sympathetic
Nervous System
Parasympathetic
Nervous System
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The Conduction System of The Heart.

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Electrophysiology of The Heart
The different waveforms for each of the specialized cells.

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Apa itu Elektrokardiografi ?
Elektrokardiogram (EKG) merupakan
bagian dari kedokteran yang tidak bisa
digantikan.
Rutin dikerjakan, sederhana, tes yang
sangat berguna dan murah.
Akan mudah bila sering secara rutin
menginterpretasi EKG
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Bagaimana Merekam ?
Pasien dalam keadaan tenang / rileks.
Letakkan 12 lead dgn benar dan firm.
Limb lead
Lead I, II dan III
Augmented limb lead
aVR, aVL dan aVF
Precordial / Chest lead
V1 V6.
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Standard limb lead electrode placement
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Standard chest lead electrode placement
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The right-sided 12-lead ECG
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Apa yang direkam ?
Potensial listrik yang merupakan jumlah
keseluruhan dari arus listrik yang
dihasilkan oleh setiap sel otot jantung.
Tahun 1903 Willem Einthoven dengan
menggunakan string galvanometer
menghasilkan beberapa konvensi
mengenai kelistrikan ini.
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Ingat bahwa ke 12 lead tersebut akan
merekam secara sama persis dengan
kejadian / aktivitas listrik di dalam
jantung !!!

Posisi dan orientasi lead yang berbeda
akan memberikan hasil yang berbeda.
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Schematic representation of normal ECG

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Pokok Bahasan :

1. Overview
2. Cara membuat rekaman EKG
3. Melaporkan rekaman EKG :
1. Deskripsi EKG
2. Interpretasi EKG
4. EKG Normal
5. EKG Variasi Normal
6. EKG Abnormal :
1. Takikardi dan bradikardi
2. Gangguan konduksi (SA node origin)
3. Hipertropi (atrium dan ventrikel)
4. Aritmia (non SA node origin).
5. Kondisi tertentu
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A systematic and complete approach

a. Check the patient details - correctly labelled?
b. Rate ?
c. Rhythm ?
d. QRS Axis ?
e. P wave ? (look at II and V1)
f. PR Interval ?
g. QRS Complexes ? Specifically, are there:
1. Significant Q waves ?
2. Voltage criteria for LVH ?
3. Predominant R wave in V1 ?
4. Widened QRS complexes ?
h. ST Segment (normal, depressed or elevated ? )
i. T waves ? QT interval ?
j. Abnormal U waves ?
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a. Heart Rate ( Regular Rhytm )
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Heart Rate ( Irregular Rhytm ) ..
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b. Rhythm
Irama Normal : Sinus Rhytm

1. Gelombang P berasal dari SA node, Positif di II
dan Negatif di aVR.
2. Setiap gelombang P selalu diikuti gel QRS dan T.
3. Bentuk gel P pada satu lead sama & konstan.
4. Interval P-P konstan.
5. Interval PR normal : 0,12 0,20 detik
6. Frekuensi Jantung (HR) : 60 100 /menit
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c. Cardiac Axis
Transformation of leads I, II, and III from
Einthovens triangle into the axial reference system.
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Normal Axis
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How to determine the axis
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Perhitungan praktis axis jantung

Lead

NORMAL AXIS

RIGHT AXIS

LEFT AXIS
I Positif Negatif Positif
II Positif Positif atau negatif Negatif
III Positif atau negatif positif Negatif
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INTERPRETASI
= DIAGNOSIS

Bila sesuai dgn KRITERIA NORMAL
maka EKG tsb adalah NORMAL
dan sebaliknya
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Pokok Bahasan :

1. Overview
2. Cara membuat rekaman EKG
3. Melaporkan rekaman EKG :
1. Deskripsi EKG
2. Interpretasi EKG
4. EKG Normal
5. EKG Variasi Normal
6. EKG Abnormal :
1. Takikardi dan bradikardi
2. Gangguan konduksi (SA node origin)
3. Hipertropi (atrium dan ventrikel)
4. Aritmia (non SA node origin).
5. Kondisi tertentu
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Ciri EKG
yang normal
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Pokok Bahasan :

1. Overview
2. Cara membuat rekaman EKG
3. Melaporkan rekaman EKG :
1. Deskripsi EKG
2. Interpretasi EKG
4. EKG Normal
5. EKG Variasi Normal
6. EKG Abnormal :
1. Takikardi dan bradikardi
2. Gangguan konduksi (SA node origin)
3. Hipertropi (atrium dan ventrikel)
4. Aritmia (non SA node origin).
5. Kondisi tertentu
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Normal variance or
ECG in healthy peoples
Always normal:
Sinus arrhythmia
Supraventricular extrasystoles
Incomplete RBBB
'High take-off' ST segment
T wave inversion in lead III but not VF
T wave inversion in leads VR and V1.

Not necessarily indicative of heart disease:
Ventricular extrasystoles
Left or right axis deviation
RBBB
T wave inversion in leads other than III, VR and V1
Nonspecific ST segment changes
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Sinus arrhythmia
Although the R-R interval varies markedly, the shape of the
P waves and the duration of the PR intervals are constant.
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Supraventricular extrasystole
The QRS complex and the T wave are the same as in the sinus beat
The 4th beat has an abnormal P wave (Early abnormal P wave) and
therefore an atrial origin.
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Incomplete RBBB
RSR1 pattern in lead V1
Notched S wave in lead V2
QRS complex duration 100 ms
Partial RBBB pattern
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Ventricular extrasystole
Sinus rhythm, with one VES
Extrasystole has a wide and abnormal QRS
complex and an abnormal T wave
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Pokok Bahasan :

1. Overview
2. Cara membuat rekaman EKG
3. Melaporkan rekaman EKG :
1. Deskripsi EKG
2. Interpretasi EKG
4. EKG Normal
5. EKG Variasi Normal
6. EKG Abnormal :
1. Takikardi dan bradikardi
2. Gangguan konduksi (SA node origin)
3. Hipertropi (atrium dan ventrikel)
4. Aritmia (non SA node origin).
5. Kondisi tertentu
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Possible sites for conduction block

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Sinoatrial (SA) block
Sinus rhythm for three beats, then a 'sinus pause'
P waves arrowed
The expected P wave is not seen, but the SA node must
have been depolarized because the next P wave
appears at the predicted time
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Any rhythm other than sinus rhythm is
called an 'arrhythmia'.
The term 'dysrhythmia' - which means
essentially the same thing
Properly speaking,
conduction disorders are not
arrhythmias.
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RBBB
Sinus rhythm with a normal PR interval
RSR1 pattern in V1
The dominant R wave is characteristic of RBBB, and does not
indicate RV hypertrophy
Wide and slurred S wave in V6
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LBBB
Sinus rhythm
Broad QRS complexes with notch in the R wave in I, VL, V5, V6
Inverted T waves are associated with bundle branch block, and
have no other significance.
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LVH
Kriteria LVH

1. Gel R di V5 atau V6 26 mm
2. R di V5 atau V6 + S di V1 35 mm
3. R di lead I 15 mm
4. R di lead I + S di lead III 25 mm
5. R di aVL 13 mm atau R II,III, atau aVF
20 mm
6. Perubahan sekunder T di V5-6 (strain)
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A. Normal Rhytm ?
B. Disrhytmias ? (Arrhytmias ?)
and Conduction Disturbances

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Dis- /Arrhythmias :

disorders of the regular rhythmic beating of the
heart.
Common 2.2 million Americans are living with
AF(one type of rhythm problem).
Can occur in a healthy heart and be of minimal
consequence.
Also may indicate a serious problem and lead to
heart disease, stroke or sudden cardiac death.
The goal : ultimately reduce disability and death
from heart disease and stroke.

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Signs or Symptoms
May not cause any signs or symptoms.
A fluttering in your chest
A racing heartbeat
A slow heartbeat
Chest pain
Shortness of breath
Lightheadedness
Dizziness
Fainting (syncope) or near fainting
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Causes
Common~ heart disease, high BP, DM, smoking,
excessive alcohol or caffeine, drug abuse, stress
Scarring most commonly, from a previous
heart attack disrupt the initiation or conduction
of electrical impulses.
In a healthy person with a normal, healthy heart, a
sustained arrhythmia to develop caused by
outside trigger: an electrical shock or the use of
illicit drugs.
However, in a heart with some evidence of
disease or deformity, the initiation or conduction
of the heart's electrical impulses may be
destabilized, making arrhythmias more likely to
develop.
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Any pre-existing structural heart condition
can lead to arrhythmia development due to:
Inadequate blood supply.
It can alter the ability of heart tissue
including the cells that conduct electrical
impulses to function properly.

Damage or death of heart tissue.
This can affect the way electrical impulses
spread in the heart.

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These pre-existing heart conditions may
include:

Coronary artery disease (CAD).
Cardiomyopathy.
Valvular heart diseases.

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Complication
Stroke.
When your atrial chambers fibrillate, they're unable to
pump blood effectively. Stagnant blood in the atria can
form blood clots. If a clot breaks loose, it can travel to
and obstruct a brain artery, causing an ischemic stroke.
This may damage or kill a portion of your brain or lead to
death.

Congestive heart failure.
This can result if your heart is pumping ineffectively for a
prolonged period due to a bradycardia or tachycardia,
such as atrial fibrillation. Sometimes, controlling the rate
of an arrhythmia that's causing congestive heart failure
can lead to improved heart function.
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ST Segmen
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LVH
LBBB
RBBB
ISCHEMIA
ST segment depression
David Arnall, Ph.D., P.T. (2000)
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The 12-Lead ECG
This contains a wealth of information.
ST segment elevation in two leads is
suggestive of an AMI.
In this session will only cover:
ST Elevation and non-ST Elevation
MIs
Left Ventricular Hypertrophy
Bundle Branch Blocks
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ST Elevation
and
non-ST Elevation MIs
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ST Elevation and non-ST Elevation MIs
When myocardial blood supply is abruptly
reduced or cut off to a region of the heart, a
sequence of injurious events occur beginning
with Ischemia (inadequate tissue perfusion),
followed by Necrosis (infarction), and
eventual Fibrosis (scarring) if the blood
supply isn't restored in an appropriate period
of time.

The ECG changes over time with each of
these events
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ECG Changes
Ways the ECG can change include:
Appearance
of pathologic
Q-waves
T-waves

peaked flattened inverted
ST elevation &
depression
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ECG Changes & the Evolving MI
There are two
distinct patterns
of ECG change
depending if the
infarction is:

ST Elevation (Transmural or Q-wave), or
Non-ST Elevation (Subendocardial or non-Q-wave)
Non-ST Elevation
ST Elevation
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ST Elevation Infarction
ST depression, peaked T-waves,
then T-wave inversion
The ECG changes seen with a ST elevation infarction are:
Before injury Normal ECG
ST elevation & appearance of
Q-waves
ST segments and T-waves return to
normal, but Q-waves persist
Ischemia
Infarction
Fibrosis
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ST Elevation Infarction
Heres a diagram depicting an evolving infarction:
A. Normal ECG prior to MI

B. Ischemia from coronary artery occlusion
results in ST depression (not shown) and
peaked T-waves

C. Infarction from ongoing ischemia results in
marked ST elevation

D/E. Ongoing infarction with appearance of
pathologic Q-waves and T-wave inversion

F. Fibrosis (months later) with persistent Q-
waves, but normal ST segment and T-
waves
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ST Elevation Infarction
Heres an ECG of an inferior MI:
Look at the
inferior leads
(II, III, aVF).
Question:
What ECG
changes do
you see?
ST elevation
and Q-waves
Extra credit:
What is the
rhythm? Atrial fibrillation (irregularly irregular with narrow QRS)!
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Non-ST Elevation Infarction
Heres an ECG of an inferior MI later in time:
Now what do
you see in the
inferior leads?
ST elevation,
Q-waves and
T-wave
inversion
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Non-ST Elevation Infarction
ST depression & T-wave inversion
The ECG changes seen with a non-ST elevation infarction are:
Before injury Normal ECG
ST depression & T-wave inversion
ST returns to baseline, but T-wave
inversion persists
Ischemia
Infarction
Fibrosis
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Non-ST Elevation Infarction
Heres an ECG of an evolving non-ST elevation MI:
Note the ST
depression
and T-wave
inversion in
leads V
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-V
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Question:
What area of
the heart is
infarcting?
Anterolateral
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Normal R wave progression
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Normal 12-lead ECG
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Anterior MI
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Inferior MI
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Lateral MI
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Septal MI
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Posterior MI
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ECG Interpretation
A mystery?

An enigma?

Confusing?

Difficult?
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ECG INTERPRETATION

If the normal
ECG is known
then
interpretation
of abnormals
becomes
easier
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Summary

This Module introduced you to:
Normal and Abnormal ECG

Dont worry too much right now about
trying to remember all the details.
Youll focus more on advanced ECG
interpretation in your clinical years !!
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Thanks for
attention