ECG Interpretation

UNWAR Medical Student Lecture

A.A.Gede Budhitresna MD,Int,Ph.D,FINASIM

Objectives

The Basics
Interpretation
Clinical Pearls
Practice
Recognition

QUICK REVIEW OF HEART

Purpose
Pumps blood
Basic Anatomy
4 chambers
2 sides
4 valves

Circulatory System

Three basic components

Heart

Blood vessels

Serves as pump that establishes the pressure

gradient needed for blood to flow to tissues
Passageways through which blood is distributed
from heart to all parts of body and back to
heart

Blood

Transport medium within which materials being

transported are dissolved or suspended

Circulatory System

Pulmonary circulation

Closed loop of vessels

carrying blood between
heart and lungs

Systemic circulation

Circuit of vessels carrying

blood between heart and
other body systems

Functions of the Heart

Generating blood pressure

Routing blood

Heart separates pulmonary

and systemic circulations
Ensuring one-way blood flow

Regulating blood supply

Changes in contraction rate

and force match blood delivery
to changing metabolic needs

Blood Flow Through and Pump Action of the Heart

Blood Flow Through Heart

Sel otot jantung

2 macam sel :

Sel autoritmik (1%)

Potential pace maker

Hanya terdapat pada NSA NAV berkas his
cabang kanan dan kiri serabut purkinye

Sel kontraktil (99%)

Sel yang berkontraksi sebagai respon thd

impuls dari sel autoritmik

Muatan listrik sel otot jantung

Keadaan sel
otot jantung

Muatan listrik
intraseluler

ekstraseluler

Istirahat/repolari - (relatif lebih

sasi
negatif)

+ (relatif lebih
positif)

depolarisasi

- (relatif lebih
negatif)

+ (relatif lebih
positif)

Sel istirahat
+++++++
-- -- -- --- --- ----- --- --- --- --+++++++
Sel telah
depolarisasi
--- --- --- --- --+++++++
+++++++
--- --- --- ---

Sel sedang
depolarisasi
--- --- --++++
++++
++++
--- --- ---

--- --- ----- --- --+++++

Sel mulai
repolarisasi
--- --- --++++
++++
--- --- --++++
--- --- ----- --- --++++

Elektrokardiogram

Fase depolarisasi (SISTOLE)

Fase repolarisasi (DIASTOLE)

bagian yang terjadi akibat penyebaran

impuls
bagian yang terjadi bila sel otot jantung
kembali istrirahat

Arah defleksi , ditentukan :

Arah penyebaran impuls depolarisasi

Letak elektroda

Hubungan arah impuls defleksi

elektrokardiogram
Arah impuls
depolarisasi

Arah defleksi

Menuju
elektroda +

Positif (ke atas)

Menuju meninggalkan

Bifasik

Meninggalkan
elektroda +

Negatif (ke
bawah)

Gambar

The Normal Conduction System

CONDUCTION
SYSTEM

Normal Impulse Conduction

Sinoatrial node
AV node
Bundle of His

Bundle Branches
Purkinje fibers

RELATIONSHIP

18

Putting the A&P with the EKG

Normal Adult ECG

CARDIAC CYCLES

SANDAPAN (LEAD) EKG

Sandapan rutin 12 leads

3 bipolar standard leads ( I, II, III)

3 unipolar lead ekstremitas (aVR, aVL, aVF)
6 unipolar chest leads (V1, V2, V3, V4, V5, V6)

Bipolar standard lead & unipolar lead

ekstremitas menggambarkan keadaan medan
bioelektrik aktivitas jantung pada bidang
frontal
Chest lead Bidang horizontal

Lead Placement

aVF

All Limb Leads

12 Lead Placement

Precordial Leads

Precordial Leads

I and AVL
V3 & v4

V1 & v2
V5 & v6
II, III and AVF

Where the positive electrode is

positioned, determines what
part of the heart is seen!

Electrode Placement

Lead V1 is placed over the 4th intercostal space,

to the right of the sternum
Lead V2 is placed over the 4th intercostal space,
to the left of the sternum
Lead V4 is placed over the 5th intercostal space
in the mid-clavicular line
Lead V3 is placed midway between V2 and V4
Lead V5 is placed on the same horizontal level
as V4 but at the anterior axilliary line
Lead V6 is placed on the same horizontal level
as V4 and V5 but on the mid axilliary line

EKG Distributions

Anteroseptal: V1, V2, V3, V4

Anterior: V1V4
Anterolateral: V4V6, I, aVL
Lateral: I and aVL
Inferior: II, III, and aVF
Inferolateral: II, III, aVF, and
V5 and V6

The ECG Tracing: Waves

P- wave

Marks the beginning of the cardiac cycle and

measures the electrical impulse that causes atrial
depolarization and mechanical contraction

QRS- Complex

Measures the impulse that causes ventricular

depolarization

Q-wave- may or may not be evident on the ECG

R-wave- first upward deflection following P wave
S-wave- the first downward deflection following the Rwave

T- wave

Marks ventricular repolarization that ends the

2004 Anna Story
cardiac cycle

Intervals and Segments

P-R interval

QRS Interval

Time interval for impulse to go from AV node to stimulate

Purkinjie fibers
Less than 0.12 secs

QT Interval

Time interval for impulse to go from the SA to the AV node

normal 0.12-0.20 secs

Time interval from beginning of depolarization to the end of

repolarization
Should not exceed the length of the R-R

ST segment

end of the S to the beginning of the T

Waveforms

Interpretation

Develop a systematic approach to

reading EKGs and use it every time
The system we will practice is:

Rate
Rhythm (including intervals and blocks)
Axis
Hypertrophy
Ischemia

RATE

2 More Methods to Count Rate

When the rhythm is regular, the heart rate is 300
divided by the number of large squares between
the QRS complexes.

1.

For example, if there are 4 large squares between

regular QRS complexes, the heart rate is 75
(300/4=75).

The second method can be used with an irregular

rhythm to estimate the rate. Count the number of
R waves in a 6 second strip and multiply by 10.

2.

For example, if there are 7 R waves in a 6 second

strip, the heart rate is 70 (7x10=70).

Heart Rate: 300, 150, 100,

75, 60, 50, 43, 37 bpm

Rate

HR of 60-100 per minute is normal

HR > 100 = tachycardia
HR < 60 = bradycardia

Differential Diagnosis of Tachycardia

Tachycardia

Narrow Complex

Wide Complex

Regular

ST
SVT
Atrial flutter

ST w/ aberrancy

Irregular

SVT w/ aberrancy

VT

A-fib w/ aberrancy
A-fib
A-flutter w/ variable A-fib w/ WPW
conduction
VT
MAT

What is the heart rate?

www.uptodate.com

(300 / 6) = 50 bpm

Asystole

V-Tach to V-Fib

can lead to.

Asystole

Rhythm

Sinus

Originating from
SA node
P wave before
every QRS
P wave in same
direction as QRS

What is this rhythm?

Normal Sinus Rythm

Normal Intervals

PR

QRS

0.20 sec (less than one

large box)

0.08 0.10 sec (1-2

small boxes)

QT

450 ms in men, 460 ms

in women
Based on sex / heart rate
Half the R-R interval with
normal HR

Prolonged QT

Normal

Corrected QT (QTc)

Men 450ms
Women 460ms

QTm/(R-R)

Causes

Drugs (Na channel blockers)

Hypocalcemia, hypomagnesemia, hypokalemia
Hypothermia
AMI
Congenital
Increased ICP

Blocks

AV blocks

First degree block

Second degree block, Mobitz type 1

PR gradually lengthened, then drop QRS

Second degree block, Mobitz type 2

PR interval fixed and > 0.2 sec

PR fixed, but drop QRS randomly

Type 3 block

PR and QRS dissociated

What is this rhythm?

First degree AV block
PR is fixed and longer than 0.2 sec

What is this rhythm?

Type 1 second degree block (Wenckebach)

What is this rhythm?

Type 2 second degree AV block
Dropped QRS

What is this rhythm?

3rd degree heart block (complete)

Bundle Branch Block - BBB

The QRS Axis

Represents the overall direction of the hearts activity
Axis of 30 to +90 degrees is normal

The Quadrant Approach

QRS up in I and up in aVF = Normal

What is the axis?

Normal- QRS up in I and aVF

Hypertrophy
Add the larger S wave of V1 or V2 in
mm, to the larger R wave of V5 or V6.
Sum is > 35mm = LVH

Ischemia

Usually indicated by ST changes

Elevation = Acute infarction

Depression = Ischemia

Can manifest as T wave changes

Remote ischemia shown by q waves

Acute Coronary Syndrome

PEMBULUH DARAH KORONER

RCA
LM
LAD

LCx

Segmen ST
Diukur dari akhir QRS s/d awal gel T

Normal : Isoelektris
Kepentingan :

Elevasi
Depresi

Pada injuri/infark akut

Pada iskemia

NSTEMI dan STEMI

ECG Changes : Ischemia

T-wave inversion ( flipped T)

ST segment depression
T wave flattening
Biphasic T-waves
Baseline

ECG Changes: Injury

ST segment elevation of greater than 1mm in at least

2 contiguous leads
Heightened or peaked T waves
Directly related to portions of myocardium rendered
electrically inactive

Baseline

ECG Changes: Infarct

Significant Q-wave where none previously existed

Why?
Impulse traveling away from the positive lead
Necrotic tissue is electrically dead
No Q-wave in Subendocardial infarcts
Why?
Not full thickness dead tissue
But will see a ST depression
Often a precursor to full thickness MI
Criteria
Depth of Q wave should be 25% the height of the R wave
Width of Q wave is 0.04 secs
Diminished height of the R wave

Evolving MI and Hallmarks of AMI

Q wave
ST Elevation
1 year

T wave inversion

INFERIOR INFARCTION

Color Coding ECG- Inferior

Blue indicates leads II,

III, AVF

Inferior Infarct with ST

elevations
Right Coronary Artery
(RCA)
1st degree Heart Block
2nd degree Type 1, 2
3rd degree Block
N/V common, Brady

Inferior MI

Inferior myocardial infarction

Small inferior distal RCA occlusion

ECG changes in leads II, III, and aVF

ANTERIOR INFARCTION

ECG demonstrates large anterior infarction

Color Coding ECGs Anterior

Yellow indicates V1,

V2, V3, V4

Anterior infarct with ST

elevation
Left Anterior Descending
Artery (LAD)
V1 and V2 may also indicate
septal involvement which
extends from front to the
back of the heart along the
septum
Left bundle branch block
Right bundle branch block
2nd Degree Type2
Complete Heart Block

Anterior MI

Mid LAD occlusion

after the first septal
perforator (arrow)

ECG : large anterior MI

Color Coding ECG- Lateral

Red indicates leads

I, AVL, V5, V6

Lateral Infarct
with ST elevations
Left Circumflex
Artery
Rarely by itself
Usually in combo

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83

Lateral MI

Color Coding ECG- Posterior

Green indicates leads V1,

V2
Posterior Infarct with ST
Depressions and/ tall R wave
RCA and/or LCX Artery
Understand Reciprocal changes
The posterior aspect of the
heart is viewed as a mirror
image and therefore
depressions versus elevations
indicate MI
Rarely by itself usually in
combo

Posterior MI

Putting it ALL together

Practice 1

Click for
answer

Anterior MI with lateral

involvement

ST elevations V2, V3, V4

ST elevations II, AVL, V5

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89

Practice 2

Click for
answer

Anteroseptal MI

ST elevations V1, V2, V3, V4

Practice 3

Click for
answer

Inferior MI

ST elevation 2,3 AVF

Practice 4

Click for
answer

Inferior lateral MI

ST elevations 2, 3, AVF

ST elevations V5

Practice 5

Click for
answer

Acute inferior MI
Lateral ischemia

Cardiac Enzymes Indicating Infarct

Normals

CPK- 10-155u/liter

CPK-MB < than 5% IU/liter

LDH 85-200 IU/liter

begin rise 3-6 hours and peaks 12-24 with return to

norm 3-5 days

Begin rise 12 hours, peaks 36-72 and normal around 10

days

LDH 1- 18.1% - 29% of total

LDH 2- 27.4% to 37.5% of total

Cardiac Enzymes Indicating Infarct

Troponins- Now
the Gold Standard!

Rises after 3-6 hours

Negative Troponin
within 6 hours of
onset of S&S rules
out the MI
Peaks at about 20
hours
May be raised for 14
days

Cardiac Enzymes Indicating Infarct

Troponin T

84% sensitivity for MI 8 hours after onset of

symptoms
22% for unstable angina

Advantages

Highly sensitive for detecting myocardial ischemia

Levels may help to stratify risks

Disadvantages

Less specific than Troponin I

Increased in angina
Increased in chronic renal failure

Cardiac Enzymes Indicating Infarct

Troponin I

90% sensitivity for MI 8 hours after onset of S&S

and 95% specificity
Level greater than 1.2 suggest MI
Negative rules out MI
Obtain two negative troponin values 4 hours apart
Normally exceedingly low

Even a small elevation indicates

myocardial damage

DISKUSI KASUS

Normal Sinus Rhythm

Mattu, 2003

First Degree Heart Block

PR interval >200ms

Junctional Rhythm

Rate 40-60, no p waves, narrow complex QRS

Hyperkalemia

Tall, narrow and symmetric T waves

Premature Atrial Contractions

Trigeminy pattern

Atrial Flutter with Variable Block

Sawtooth waves Typically at HR of 150

Torsades de Pointes

Notice twisting pattern

Treatment: Magnesium 2 grams IV

Digitalis

Dubin, 4th ed. 1989

Lateral MI

Reciprocal changes

Inferolateral MI

ST elevation II, III, aVF

ST depression in aVL, V1-V3 are reciprocal changes

Anterolateral / Inferior Ischemia

LVH, AV junctional rhythm, bradycardia

Left Bundle Branch Block

Monophasic R wave in I and V6, QRS > 0.12 sec

Loss of R wave in precordial leads
QRS T wave discordance I, V1, V6
Consider cardiac ischemia if a new finding

Right Bundle Branch Block

V1: RSR prime pattern with inverted T wave

V6: Wide deep slurred S wave

First Degree Heart Block, Mobitz Type I (Wenckebach)

PR progressively lengthens until QRS drops

Supraventricular Tachycardia

Retrograde P waves

Narrow complex, regular; retrograde P waves, rate <220

Right Ventricular Myocardial Infarction

Found in 1/3 of patients with inferior MI

Increased morbidity and mortality
ST elevation in V4-V6 of Right-sided EKG

Ventricular Tachycardia

Second Degree Heart Block, Mobitz Type II

PR interval fixed, QRS dropped intermittently

Acute Pulmonary Embolism

SIQIIITIII in 10-15%
T-wave inversions, especially occurring in
inferior and anteroseptal simultaneously
RAD

Hypokalemia

U waves
Can also see PVCs, ST depression, small T waves

LVH with strain

Perempuan 26 th, MCU penerimaan karyawan

Sinus arrhythmia

Perempuan 46 th, DM, Nyeri dada 10 jam yg lalu, mendadak, Trop T (+)

Lateral myocardial infarction

Laki-laki 36 th, perokok, nyeri dada 1 jam yg lalu, mendadak, Trop T (-)

Acute inferoposterior myocardial infarction

Laki-laki 76 th, perokok, stroke ischemik berulang, nyeri dada memberat

Atrial fibrillation dan STEMI inferior

Laki-laki 76 th, perokok, keluhan (-), akan operasi reseksi kolon ok tumor

Atrial flutter

Laki-laki 32 th, gemuk, tidak nyaman di dada hilang timbul,

terutama kalau cape.

premature ventricular contraction

Laki-laki 66 th, perokok, DM, nyeri dada 8 jam yg lalu, tiba2 kolaps

Wide complex tachycardia

Perempuan 36 th, HT, berdebar-debar sejak 2 jam yll, hilang-timbul

Supraventricular tachycardia

Laki-laki 36 th, dyslipidemia, nyeri dada 6 jam yg

lalu, mendadak, Trop T (+), tiba-tiba kolaps di IGD

Ventricular flutter

KASUS 1

EKG

Interpretasi EKG ?

Jawaban: D

Kasus 2

Pria 50 thn, CAD post PTCA, Hipertensi

Berdebar & lemas 3 jam SMRS, hemodinamik stabil

Diagnosis EKG
A. Supraventricular Tachycardia (AVNRT)
B. Atrial Tachycardia
C. Atrial Flutter
D. Atrial Fibrillasi
Jawaban: A

KASUS 3

Pria 67 tahun, anggota DPR

Berdebar dan sesak nafas sejak 2 jam
Hipertensi dan PPOK
Tidak ada bukti klinis CAD

Apa diagnosis EKG ?

A.
B.
C.
D.

Atrial fibrillation
Atrial Tachycardia
Sinus arrhythmia
Atrial flutter
Jawaban: D

Kasus 4

Wanita 45 tahun
Lemas, lekas capek dan sesak nafas bila
aktivitas

Diagnosis EKG
A. Sick Sinus Syndrome
B. AV blok derajat 2 Mobitz II
C. Sinus arrest
D. AV blok derajat 3

Jawaban: D

Kasus 5 : Laki-laki, 50 thn. Chest pain

dengan Troponin T (+)

JAWABAN :
A.
B.
C.
D.

UAP
STEMI Anteroseptal (fase evolusi)
NSTEMI Anteroseptal
NSTEMI Anterior Ekstensif

Jawaban : B

KASUS 6

EKG

Interpretasi EKG ?

Jawaban : C

KASUS 7

EKG

Interpretasi EKG ?

Jawaban : D

KASUS 8

EKG

Interpretasi EKG ?

Jawaban : B

THANK YOU- ANY QUESTION?

151