ARITMIA JANTUNG

Dr. dr. Taufik Indrajaya, SpPD, KKV, FINASIM

Divisi Kardiologi Departemen Penyakit Dalam
FK UNSRI / RSMH Palembang

Tingkat Kemampuan
Tingkat Kemampuan 1

Mengenali dan menempatkan gambaran-2 klinik

sesuai penyakit ketika membaca literatur

Tingkat Kemampuan 2

Membuat diagnosis klinik berdasarkan PF dan

pemeriksaan tambahan. Mampu merujuk
secepatnya

Tingkat Kemampuan 3

3a : (2) dan memutuskan dan memberi terapi

pendahuluan, merujuk kasus bukan emergensi
3b: (3a), merujuk kasus emergensi.

Level of Ability: 2 up to 3 B
Further reading :
1. Hursts: The Heart.

2. Harrissons. Principles of Internal

Medicine
3. Buku Ilmu Penyakit Dalam PAPDI
4. Buku Ajar Kardiologi FK UI
5. Internet, Others.

A gooD baSic KnOwlEdge

of the heart and cardiac function
is Essential in order
to Understand
the 12 lead ECG

Anatomy

Cardiovascular system works ..

Autoregulation
(Frank-Starling Law of the Heart)

CARDIAC OUTPUT = STROKE VOLUME x HEART RATE

Contractility
Sympathetic
Nervous System
Parasympathetic
Nervous System

Cardiac Cycle

Electrophysiology of The Heart

The different waveforms for each of the specialized cells.

Schematic representation of Normal ECG

CPR

TOPIK
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.

Manifestasi klinik
Penyebab aritmia
Kertas rekaman EKG
Lima jenis dasar aritmia
Aritmia asal sinus
Irama ektopik
Irama re-entrant
Empat Pertanyaan
Artimia Supraventrikuler
Aritmia Ventrikel
Aritmia Supraventrikuler vs Ventrikuler.

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.

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

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.

Causes ..
1. HHypoxia: Pulmonary disorders.
2. IIschemia and Irritability:
myocardial infarctions; angina,
myocarditis.
3. SSympathetic Stimulation:
hyperthyroidism, congestive heart
failure, nervousness, exercise).

Causes
DDrugs: Many drugs can cause
arrhythmias.
EElectrolyte Disturbances:
Hypokalemia, imbalances of calcium and
magnesium.
BBradycardia: to predispose to
arrhythmias ~ the sick sinus syndrome.
SStretch: congestive heart failure and
valvular disease can cause arrhythmias.

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.

These pre-existing heart conditions may

include:

Coronary artery disease (CAD).

Cardiomyopathy.
Valvular heart diseases.

Kertas Rekaman EKG

A typical rhythm strip

It can be as short or as long as you need

to decipher the rhythm.

ECG Paper

A systematic and complete approach

Check the patient details - correctly labelled?

What is the rate?
Is this sinus rhythm? If not, what is going on?
What is the mean frontal plane QRS axis ?
Are the P waves normal (look at II and V1)
What is the PR interval?
Are the QRS complexes normal?
Are the ST segments normal, depressed or
elevated?
Are the T waves normal? What is the QT
interval?
Are there abnormal U waves?

Heart Rate ( Regular Rhytm )

Heart Rate ( Irregular Rhytm ) ..

Principles of Rhythm Analysis

The standard 12-lead ECG and Rhythm
strips are the most easily accessible tools
for the diagnosis of a cardiac rhythm
disturbance.
Recognition of the P-wave and QRS
morphology and their relative timing may
be the only information needed to
diagnose the arrhytmia correctly.

The Five Basic Types of Arrhytmias

The heart is capable of only five basic types of
rhythm disturbances:
1. Arrhythmias of sinus origin.
2. Ectopic rhythms: focus other than the sinus.
3. Re-entrant arrhytmias.
4. Conduction blocks (another chapter).
5. Preexcitation syndromes ~ accessory
conduction pathways that bypass the normal
ones, providing an electrical shortcut, or short
circuit : WPW (another chapter).

Aritmia Asal Sinus

(A) Sinus tachycardia.

(B) Sinus bradycardia.

 Sinus arrhythmia. The heart rate

accelerates with inspiration and slows with
expiration.

Sinus arrhythmia.
The heart rate accelerates with inspiration and slows with expiration

Sinus arrest
occurs after the fourth beat.
The fifth beat, restoring electrical activity to the
heart, is a junctional escape beat. Note the
absence of a P wave before this last beat.

Non Sinus Pacemakers

Junctional escape.
The first two beats are normal sinus beats with a normal P
wave preceding each QRS complex.
There is then a long pause followed by a series of three
junctional escape beats occurring at a rate of 40 to 45 beats
per minute.

(A) Normal sinus

rhythm.
(B) Sinus arrest.
The sinus node
falls silent. No
current is
generated
The EKG shows
no electrical
activity.

(C) Sinus exit block.

The sinus node
continues to fire,
but the wave of
depolarization
fails to exit the
sinus node into
the atrial
myocardium.
EKG shows no
electrical activity.

Irama Ektopik

(A) Normally, the sinus node drives the heart.

(B) e.g., the AV junction

Irama Re-entrant
(1) Normally,
pathways A and B
(any two adjacent
regions of cardiac
function) conduct
current equally
well.
(2) Here, however,
conduction through
pathway B is
temporarily slowed.
Current passing
down A can then
turn back and
conduct in a
retrograde fashion
through B.
(3) The reentry loop is
established.

Normal sinus rhythm and

The Four Questions answered.

The Four Questions

1. Are normal P waves present ?
2. Are the QRS complexes narrow or
wide ?
3. What is the relationship between the
P waves and the QRS ?
4. Is the rhythm regular or irregular ?

Aritmia Supraventrikuler

(A) The third beat is an atrial premature beat.

(B) The fourth beat is a junctional premature beat. There
is no P wave preceding the premature QRS complex.

The third beat is an atrial premature beat.

The P wave is shaped differently from the other,
somewhat unusual-looking P waves, and the
beat is clearly premature.

(A)A junctional premature beat. .

(B)The third beat is a junctional escape beat

PSVT in 3 different
Patients :
Regular
P waves are retrograde if
visible
Rate 150-250 bpm
Carotid massage slows or
terminates

PSVT

Its onset is sudden,

Initiated by a premature
supraventricular beat,
its termination is just as
abrupt.

A ~ simultaneous
activation of the atria
and ventricles; the
retrograde P waves
are lost in the QRS
complexes.
B ~ a SVT mimicking a
more serious rhythm
called VT.
C here, retrograde P
waves can be seen.
D ~ Pseudo-R
configuration in lead
V1 representing the
retrograde P waves
(arrows) of PSVT.
(E) The AV node is
usually the site of the
reentrant circuit that
causes the arrhythmia.

The carotid sinus

contains baroreceptors
that influence vagal
input to the heart,
primarily affecting the
sinus node and AV
node.
Stimulation of the right
carotid baroreceptors
primarily stimulates
sinus node vagal input.

Stimulation of the left

carotid baroreceptors is
more likely to affect the
vagal input to the AV
node

 An episode of PSVT is broken almost at once by

carotid massage.
The new rhythm is a sinus bradycardia with a
rate of 50 beats per minute.

Regular, saw toothed

2:1, 3:1, 4:1 etc block

Atrial rate 250-350 bpm
Ventricular rate , 1/3,
etc of atrial rate

Carotid massage:
increases block !!

Atrial flutter.
Carotid massage increases the block from 3:1 to
5:1.

Irreguler

Undulating baseline
Atrial rate 350-500 bpm
Ventricular rate : variable
Carotid massage: may slow ventricular rate !!

Atrial fibrillation

Another example of atrial fibrillation. In the absence of

a clearly fibrillating baseline, the only clue that this
rhythm is atrial fibrillation is the irregularly irregular
appearance of the QRS complexes.

Regular
Rate 100-200 bpm
Characteristic warm up period in automatic form
Carotid massage :no effect, or only mild slowing

Paroxysmal Atrial Tachycardia.

P waves are not always visible, but here they can be seen easily.
Notice the varying distance between the P waves and the ensuing
QRS complexes; this reflects a varying conduction delay between
the atria and ventricles that often accompanies PAT.

Aritmia Ventrikel

(A) A premature ventricular contraction.

(B) Bigeminy. PVCs and sinus beats
alternate in a 1:1 fashion.

(A)Beats 1 and 4 are sinus in origin. The other

three beats are PVCs (multiform).
(B)A PVC falls on the T wave of the second sinus
beat, initiating a run of VT.

A run of three or more

consecutive PVCs
Rate 120-200 bpm

Ventricular tachycardia.
The rate is about 200 bpm.

Unlike PSVT, may be

slightly irregular

No true QRS complexes

No cardiac output
Need CPR and DC

Ventricular tachycardia degenerates into

ventricular fibrillation ( VF ).

Benign rhythm

Regular
50-100 bpm
< 50 bpm called Idioventricular rhytm

Accelerated idioventricular rhythm.

There are no P waves, the QRS complexes are
wide, and the rate is about 75 beats per minute.

= Twisting of the Point

In pt with Prolong QT interval
Congenital or electrolit imbalance

Torsades de pointes.
The QRS complexes seem to spin around the
baseline, changing their axis and amplitude

SUMMARY : Ventricular Arrhythmias

Rules of Malignancy for PVCs :

1.
2.
3.
4.
5.

Frequent PVCs
Consecutive PVCs
Multiform PVCs
R-on-T phenomenon
Any PVC occurring during an AMI
(or in any patient with underlying
heart disease)

 The heart rate of a 72-year-old woman is

rescued from VT by a shock delivered by
an implantable cardioverter-defibrillator.

Possible sites for conduction block

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

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.

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

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.

ECG
A mystery?
An enigma?
Confusing?
Difficult?

Interpretation

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

Summary
This Module introduced you to:
Abnormal ECG : ARRHYTMIA
Dont worry too much right now about
trying to remember all the details.
Youll focus more on advanced ECG
interpretation in your clinical years !!

Thanks for
attention