Disritmia

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

Divisi Kardiologi Departemen Penyakit Dalam

FK UNSRI / RS dr. Muh Husin Palembang
FK UNSRI
2018
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 .

 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
1. Common : heart disease, high BP, DM,
smoking, excessive alcohol or caffeine, drug
abuse, stress
2. 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 ( HISDEBS ) …

1. H—Hypoxia :
>. Pulmonary disorders.

1. I—Ischemia and Irritability :

>. myocardial infarctions; angina, myocarditis.

3. S—Sympathetic Stimulation :
>. hyperthyroidism, CHF, nervousness,
exercise).
Causes …
• D—Drugs : Many drugs can cause arrhythmias.

• E—Electrolyte Disturbances : Hypokalemia,

imbalances of calcium and magnesium.

• B—Bradycardia : to predispose to arrhythmias

~ the sick sinus syndrome.

• S—Stretch : 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.
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 T waves normal ? What is the QT interval ?
• Are there abnormal U waves ?
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 Four Questions

1. Are normal P waves present ?

2. Are QRS complexes narrow or wide ?
3. What is the relationship between the P
waves and the QRS ?
4. Is the rhythm regular or irregular ?
 Normal sinus rhythm and
“The Four Questions” answered.
The 5 Basic Types of Arrhytmias

The heart is capable of only 5 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.
5. Preexcitation syndromes ~
WPW
1. Arrhythmias of sinus origin.

(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.
2. Irama Ektopik

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

(B) e.g., the AV junction
Relative
Refracter
3. Re-entry
3. 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.
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

•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.
PSVT in 3 different Pts
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 ½, 1/3, ¼ 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.

Ventricular Tachycardia.
The rate is about 200 bpm.
•A run of three or more
consecutive PVCs
•Rate 120-200 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. Frequent PVCs
2. Consecutive PVCs
3. Multiform PVCs
4. R-on-T phenomenon
5. 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
ICD ( Implantable cardioverter-defibrillator ).
4. 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.
5. W P W
 Summary

This Module introduced you to:

– Abnormal ECG : ARRHYTMIA

Don’t worry too much right now about

trying to remember all the details.
You’ll focus more on advanced ECG
interpretation in your clinical years !!
Thanks for
attention