BASIC

ELECTROCARDIOGRAPHY
Kardiovaskular Udayana
OUTLINES

Brief History of
ECG

The Science
Behind the Waves
ECG Systematic
Reading
 BRIEF HISTORY OF ECG
Matteuci record Bayliss & Starling
(UK) demonstrated
electrical activity
triphasic cardiac
from the heart of
electrical activity using
frog
capillary electrometer
Willem Einthoven

1786 1842 1887 1891 1893

Luigi Galvani Waller record Willem Einthoven

(Italian)
Notes that electrical electrical activity (Netherland) first used
current could be the term ECG during a
recorded from from the human
muscle scientific meeting in
heart
Netherland
 BRIEF HISTORY OF ECG
Einthoven build
string galvanometer
based 3 lead ECG
Machine

1895 1901 1908

Einthoven
Why PQRST & not ABCD?
Publish a paper in
which he refined the
Einthoven decided follow
Descartes’ mathematical
ECG enter
capillary electrometer, tradition (where “Q” is used the US
demonstrated five for the origin of cartesian
coordinates → “P” is the
initial reflection
next letter)
 BRIEF HISTORY OF ECG
Wilson AHA standardized
invented the central 12 leads ECG as
terminal precordial
we know now
leads are born

1924 1934-
1938
1942 1954

Golberg
Einthoven
used the central terminal
won Nobel prize
with augmentation &
for ECG thus augmented
unipolar leads
THE SCIENCE BEHIND THE WAVES

◼ Elektrokardiogram adalah grafik yang merekam

perubahan potensial listrik jantung yang
dihubungkan dengan waktu

◼ Elektrokardiografi adalah ilmu yang mempelajari

perubahan-perubahan potensial atau perubahan
voltage yang terdapat dalam jantung.
 THE SCIENCE BEHIND THE WAVES

1. ACTION
POTENTIAL
2. CARDIAC CELL
PROPERTIES
3. CONDUCTION
SYSTEM
 ACTION POTENTIAL

Polarization
◦ Intracellular is more negative than extracellular
Depolarization
◦ Intracellular becomes more positive
◦ Influx of Na+
Repolarization
◦ Intracellular restores to its resting potential
◦ Efflux of K+

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ACTION POTENTIAL
 CARDIAC CELLS PROPERTIES

Automaticity
Excitability
Conductivity
Contractility
CONDUCTION SYSTEM
 CONDUCTION SYSTEM

Sinoatrial Node (SA Node)

◦Rhythmic rate : 60 – 100 bpm
Internodal Pathway
◦Anterior, middle, posterior pathways
Atrioventricular Node (AV Node)
◦Regions : atrionodal (AN), nodal (N),
nodal-His (NH)
◦Delays the impulse
 CONDUCTION SYSTEM
Bundle of His
◦Rate : 40 – 60 bpm
Bundle Branches
◦LBB & RBB
◦LBB : anterior, posterior, septal fascicles
Purkinje Fibers
◦Rate : 20 – 40 bpm

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CONDUCTION SYSTEM
ECG SYSTEMATIC READING

KERTAS EKG
◦ Identitas
◦ Urutan Lead
◦ Kalibrasi

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URUTAN LEAD EKG

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 LEADS

Standard Limb Leads

◦Lead I, II, III
Augmented Limb Leads
◦aVL, aVR, aVF
Precordial Leads
◦V1, V2, V3, V4, V5, V6
◦V1R, V2R, V3R, V4R, V5R, V6R
◦V7, V8, V9

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 LEADS

The extremity leads are:

◼ I from the right to the left arm
◼ II from the right arm to the left leg
◼ III from the left arm to the left leg

Augmented Limb leads are:

◼ AVL points to the left arm
◼ AVR points to the right arm
◼ AVF points to the feet

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 LEADS
PRECORDIAL LEADS

- Lead V1 is placed in the fourth intercostal space to the right

of the sternum.
- Lead V2 is placed in the fourth intercostal space to the left
of the sternum.
- Lead V3 is placed directly between leads V2 and V4.
- Lead V4 is placed in the fifth intercostal space in the
midclavicular line (even if the apex beat is displaced).
- Lead V5 is placed horizontally with V4 in the anterior
axillary line
- Lead V6 is placed horizontally with V4 and V5 in the
midaxillary line.

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 LEADS
PRECORDIAL LEADS

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LEADS

LEADS VIEW OF HEART

I, aVL Lateral

II, III, aVF Inferior

V1, V2 Antero-Septal

V3, V4, V5, V6 Antero

V1-V6 Whole Anterior

I, aVL, V5, V6 High Lateral

 KALIBRASI EKG

• Kalibrasi
• Waktu
• Amplitudo

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KALIBRASI EKG

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 QRS complex = ventricular
depolarization
VENTRICULAR NECROSIS
→ NO R WAVE
T wave = ventricular
P wave = atrial depolarization Repolarization
VENTRICULAR ISCHEMIA
ABNORMAL ATRIAL →
→ ABNORMAL T WAVE OR
ABNORMAL P WAVE ST SEGMENT

Horizontal length describe electrical Amplitude/Height describe how

conduction much electrical produce by myocyte
LONGER → BLOCK HIGHER → MORE CELL PRODUCE
SHORTER → ACCESSORY ELECTRICITY/ENLARGEMENT
PATHWAY SHORTER → LESS CELL
PRODUCE ELECTRICITY
 HOW TO READ ECG?

Rhytme
Normal ECG
AXIS
 
Sinus Rhytme 90 x/minutes normal axis Left ventricular Hypertrophy

 
RATE Abnormal ECG
 RUMUS BACA EKG
Irama
Rate
Axis
Gelombang P
Interval PR
Gelombang QRS
Rasio R/S di V1
Jumlah amplitudo R di precordial
kanan dan S di precordial kanan // SV2 + RV5
Perubahan segmen ST-T
Gelombang Q , Gelombang U
Rhytme

SINUS OR NOT
Except sinus. It could be no P
wave, abnormal or etc.

P Followed by QRS complex

Go to arrhytmia chapter

✓ 
SINUS ?
 P?

qrs qrs qrs qrs

✓ p p p p

✓
qrs qrs qrs

p p p

 P?
 Irama / Rhythm
Sinus (normal) :
◦ Ada gelombang P diikuti QRS
◦ Reguler
◦ Rate 60 -100 x per menit
◦ P wave Normal
◦ PR interval normal
◦ QRS complex normal
Ventrikel :
• Tidak ada gelombang P
• Reguler
• QRS lebar dan morfologi “aneh”
• Rate 20- 40 x per menit
Junctional:
• Tidak ada P didepan QRS (tidak
terlihat) atau retrograde P
(inverted / normal)
• Reguler
• Rate 40 - 60 x per menit
Atrial :
• Tidak ada P (fibrilasi) / terbalik,
morfologi aneh berubah – ubah
(wandering) , gergaji / sawtooth
(flutter)
• Mayoritas ireguler
Sinus (normal) :
• Ada gelombang P diikuti
QRS
• Reguler
• Rate 60 -100 x per menit

Junctional:
• Tidak ada P didepan QRS
(tidak terlihat) atau
retrograde P (inverted /
normal)
• Reguler
• Rate 40 - 60 x per menit

Ventrikel :
• Tidak ada gelombang P
• Reguler
• QRS lebar dan morfologi
“aneh”
• Rate 20- 40 x per menit
Sinus (normal) : > 100 x : sinus
takikardi
• Ada gelombang P diikuti
QRS
< 60 x : sinus
bradikardi
• Reguler
• Rate 60 -100 x per menit

Junctional:
• Tidak ada P didepan QRS >100x : junctional
(tidak terlihat) atau takikardi
retrograde P (inverted / > 60 x : accelerated
normal) junctional

• Reguler < 40 x : junctional

bradikardi
• Rate 40 - 60 x per menit

Ventrikel : >100x : ventrikular

• Tidak ada gelombang P takikardia

• Reguler > 40 x : accelerated

ventricular
• QRS lebar dan morfologi
“aneh”
< 20 x : ventricular
bradikardia
• Rate 20- 40 x per menit
Atrial :
• Tidak ada P (fibrilasi) / terbalik, morfologi
aneh berubah – ubah (wandering) , gergaji /
sawtooth (flutter)
• Mayoritas ireguler FIBRILASI
P sulit dibedakan (dianggap tidak ada P yang
sebenarnya)

WANDERING PACEMAKER
P berubah ubah, lebih dari 3 morfologi
Bila lebih dari 100x dapat disebut multifocal
atrial takikardi

ATRIAL FLUTTER
P seperti gergaji
 RATE MEASUREMENT
Large Boxes → 300/R-R interval
Small Boxes → 1500/R-R interval
Six-Second Method → count the number of complete QRS
complexes in 6 seconds multiply by 10 → for irreguler rhythm

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 RATE MEASUREMENT

jumlah gel QRS dalam 6 detik dikali 10

(HR : 10 x 10 = 100x/ mt)
AXIS
Axis frontal

II III
HEART AXIS
NORMO AXIS AXIS DEVIATION

RAD LAD

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AXIS DEVIATION

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Axis horizontal
ECG WAVEFORMS

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ECG WAVEFORMS

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ECG WAVEFORMS

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 RUMUS BACA EKG
Irama
Rate
Axis
Gelombang P
Interval PR
Gelombang QRS
Rasio R/S di V1
Jumlah amplitudo R di precordial
kanan dan S di precordial kanan // SV2 + RV5
Perubahan segmen ST-T
Gelombang Q , Gelombang U
 P Wave
Morfologi
• Monofasik di lead II P wave
• Bifasik di leadV1 ◦No more than 2.5 mm in
Axis
height
• Normal P wave axis antara 0° dan
+75° ◦No more than 0.11 sec in
• P waves harus tegak di lead I dan II, duration
inversi di aVR ◦Positive : I,II,aVF,V2-6
Durasi
• < 120 ms ◦May be positive, negative,
Amplitudo or
• < 2.5 mm pada limb lead, biphasic : III,aVL,V1
• < 1.5 mm pada lead precordial
P MITRALE
Di lead II
Total durasi gelombang P >0.11 s
Bentukan gelombang P damat
menyerupai huruf M yang cembung,
ataupun hanya melebar tanpa // Biasanya didapat pada:
bentukan spesifik Mitral stenosis
Di Lead V1 Hipertensi
Gelombang P bifasik dengan Aortic stenosis
terminal force gelombang P ≥0.04 (1 Mitral regurgitasi
kotak kecil) Hypertrophic cardiomyopathy
Gelombang P bifasik dengan
amplitudo terminal force gelombang
P ≥1 mm (1 kotak kecil)

P PULMONAL // Biasanya didapat pada

• Pembesaran atrium kanan akan
menimbulkan P wave yang tinggi
(peaked P wave) dengan amplitudo
• > 2.5 mm di lead inferior (II, III dan
AVF)
• > 1.5 mm di V1 dan V2
HIPERTENSI PULMONAL karena:
PPOK (cor pulmonale)
Tricuspid stenosis
Congenital heart disease
(pulmonary stenosis, Tetralogy of Fallot)
Hipertensi pulmonal primer
 ATRIAL ENLARGEMENT
Left Atrial Enlargement
Notched P wave

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 ATRIAL ENLARGEMENT
Right Atrial Enlargement
Peaked P wave

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ATRIAL ENLARGEMENT

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 PR interval

◦ 0.12 – 0.20 sec (3-5

small boxes) in adult,
◦ may be shorter in
children and longer in
elders
INTERVAL PR
PR interval normal 0.12 – 0.2 s (3-5 kotak kecil)

< 0.12 s : PRE EKSITASI > 0.2 : BLOK

Jalur aksesoris yang mempercepat konduksi
(keterlambatan konduksi pada AV node)
dari atrium ke ventrikel

Preeksitasi dan degree dari blok tidak dijelaskan lebih jauh dalam slide ini
 QRS Complex
◦ 0.06 – 0.10 sec
◦ Q : 1st negative deflection after P
◦ R : 1st positive deflection after P
◦ S : negative deflection after R

Types Of QRS Complex

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KOMPLEKS QRS

• Rotasi
• Durasi (sempit / lebar)
• Morfologi
• Amplitudo
ROTASI ?

Horizontal axis
 DURASI
Durasi normal 0.07 – 0.1 s , dibawah 0.12 s masih dapat dianggap normal

<0.12 s >0.12 s
Kompleks sempit
Kompleks lebar
biasanya berasal dari
biasanya dapat
supraventrikel (atrium,
disebabkan oleh
SA node, junctional)
- irama ventrikel
- aberansi (gangguan
konduksi) berupa
bundle branch block,
gangguan depolarisasi
(karena elektrolit dsb)
MORFOLOGI (pada bundle branch block)

KANAN KIRI
AMPLITUDO

R/S V1 SV2 + RV5

Rasio gelombang R dan S di V1 Total voltage gelombang S di lead
precordial kanan dan gelombang R di
< 1 normal precordial kiri
> 1 abnormal
<35 normal
>35 abnormal
 VENTRICULAR HYPERTROPHY

Right Ventricular Hypertrophy

◦ RAD
◦ Reversed R-wave progression (taller R
waves and smaller S waves in V1 & V2;
deeper S waves & small R waves in V5 &
V6

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VENTRICULAR HYPERTROPHY

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VENTRICULAR HYPERTROPHY

Right Ventricular Hypertrophy

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 VENTRICULAR HYPERTROPHY

Left Ventricular
Hypertrophy
◦ S wave in V1/V2 + R wave in
V5/V6 ≥ 35 mm (mV)
◦ R wave in aVL ≥ 12 mm (mV)
◦ Strain pattern in V5 and V6
◦ May be accompanied by LAD

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VENTRICULAR HYPERTROPHY

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VENTRICULAR HYPERTROPHY

LVH Strain

Left Ventricular Hypertrophy

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 ST Segment

◦Isoelectric (flat)
SegmenST-T
Normal : Segment ST isoelektrik, gelombang T
upward

Berkaitan dengan kelainan repolarisasi : baik primer maupun

sekunder
PRIMER :
paling sering karena penyakit jantung koroner (iskemik /
infark)
Kelainan elektrolit , efek obat, sekunder karena kelainan
neurologi
SEKUNDER :
Perubahan segmen ST mengikuti kelainan preeksitasi
(WPW), bundle branch block, hipertrofi, IVCD, ventrikular
ekstrasistol
ST – T segment
penyakit jantung iskemik

Harus contiguous lead

Segmen ST
Dikaitkan paling sering terhadap kelainan jantung iskemik
Apabila disertai klinis chest pain / discomfort akan makin
menambah kecurigaan klinis
Pada pasien curiga ACS , ada baiknya dilakukan serial EKG
untuk membuktikan iskemik / infark → adanya evolusi
merupakan tanda khas penyakit iskemik akut

ST depresi ST elevasi
Infark
iskemik
Sumbatan total
 ST ELEVASI

Pada laki – laki Wanita semua

Laki – laki
>40 tahun usia Pada lead posterior dan
< 40 tahun
- ST elevasi > 2 mm - ST elevasi > RV , ST elevasi >0.5mm
- ST elevasi > 2,5mm di
di lead V2 –V3 1,5mm di lead V2 dianggap signifikan
lead V2 – V3
- ST elevasi 1mm –V3
- ST elevasi >1mm di
lead lain - 1 mm di lead lain
lead lainnya
ST ELEVASI
ST ELEVASI
jenis lain
 ST DEPRESI

ST depresi horisontal / downsloping > 0,5mm pada ≥ 2 lead

contiguous menandakan iskemik miokard (sesuai dari Guideline
AHA, 2007 Task Force Criteria).
ST depresi ≥ 1 mm lebih spesifik dan punya prognosis lebih buruk
ST depresi ≥ 2 mm pada ≥ 3 lead dihubungkan dengan high
probability NSTEMI dan punya nilai prediksi mortalitas signifikan
(35% mortalitas pada 30 hari).
 ST DEPRESI
Types of ST-segment depression

UPSLOPING – very nonspecific for the diagnosis of

ischemia. Associated with a lot of false positive
exercise tests.

HORIZONTAL – likely associated with ischemia.

DOWNSLOPING – almost certainly associated with an

ischemic myocardium

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 T wave

◦Limb lead : no more

than 5 mm (height)
Precordial lead : no
more than 10 mm
(height)
Gelombang T
Kelainan gelombang T yang berkaitan dengan iskemik
Hiperakut T T inversi
 ABNORMAL WAVEFORMS

T wave : peaked/tall, inverted, flattened

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Gelombang T
T inversi dapat ditemukan pada
Temuan normal pada anak2 (juvenile T wave pattern)
Iskemi dan infark miokard
Bundle branch block
Hipertrofi ventrikel (‘LVH strain’)
Pulmonary emboli
Hypertrophic cardiomyopathy
Peningkatan TIK
ABNORMAL WAVEFORMS

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Gelombang Q
 MYOCARDIAL INFARCTION

Ischemia
Injury
Necrosis

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 MYOCARDIAL INFARCTION
Evolution of the ECG during a myocardial infarct
Time See Figure Change
Minutes A Normal
B S-T Elevation
C S-T elevation with Negative T Waves

Hours D Negative T Waves with Pathologic Q Waves

Day E Pathologic Q Waves

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MYOCARDIAL INFARCTION

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 MYOCARDIAL INFARCTION
Evolutionary changes in
anteroseptal myocardial
infarction

A. At admission
B. At 24 hours
C. At 48 hours

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 MYOCARDIAL INFARCTION
Localization of a Myocardial Infarction

LOCALIZED S-T ELEVATION CORONARY ARTERY

Anterior MI V1-V6 LAD

Septal MI V1-V4 LAD

Lateral MI I, aVL, V5, V6 RCX or MO

Inferior MI II, III, aVF RCA (80%) RCX (20%)

Posterior MI V7, V8, V9 RCX

Vascularization of the Heart

N.B :
LAD → Left Anterior Descending Artery
Left Coronary Artery
RCX → Ramus Circumflexa
LM → Left Main Artery
RCA → Right Coronary Artery

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ANTERIOR INFARCTION

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INFERIOR INFARCTION

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POSTEROLATERAL
INFARCTION

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Acute inferior myocardial
infarction

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Septal wall myocardial infarction

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 MYOCARDIAL INFARCTION

Extensive (whole) anterior myocardial infarction

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• Irama → sinus / atrial / junctional / ventrikel
• Rate → bradikardi / normal / takikardi
• Axis → normal / LAD / RAD / ekstrim
• Gelombang P → amplitude / durasi / mitral ? Pulmonal ? Inversi ?
• Interval PR → normal / blok / preeksitasi
• Gelombang QRS → rotasi / durasi / morfologi
• Rasio R/S di V1 → <1 (normal) / >1 / RVH?
• S di V2 + R di V5 →Jumlah amplitudo R di precordial
kanan dan S di precordial kanan? <35 / > 35
• Perubahan segmen ST-T → normal / T inversi / ST depresi / ST
elevasi
• Gelombang Q
ECG WAVEFORMS

Normal ECG Waveforms in all the Leads

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 ABNORMAL WAVEFORMS
P : tall, notched
PR interval : prolonged, shortened
Q : pathologic Q (>0.04 sec, 25% of the R wave)
QRS complex : widened (>0.10 sec)
ST segment : depression (>1 mm), elevation (>1 mm in limb
leads or >2mm in precordial leads)
T : peaked/tall, inverted, flattened
QT interval : prolonged, shortened

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 ABNORMAL WAVEFORMS
Poor R-wave progression :
Infarction (anteroseptal)
LBBB
LVH
Severe COPD (emphysema)

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thank you!

“ Change will not come if we wait for some other

person or some other time. We are the ones we’ve
been waiting for. We are the change that we seek

- Barack Obama
Soal #1
Soal #8
Soal #9
Soal #12