ARRHYTHMIA

Prof. Hardi Darmawan, MD, MPH&TM.,FRSTM

Department of Physiology & Biophysic

Definition of Arrhythmia:
The Origin, Rate, Rhythm, Conduct
velocity and sequence of heart
activation are abnormally.

Arrhythmia
ARRHYTHMIA VARIATION IN NORMAL
RHYTHM

DYSRHYTHMIA ABNORMAL,
DISTURBED RHYTHM
RESULTS FROM IMPULSE
FORMATION DISTURBANCE OR
CONDUCTION DISTURBANCE
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AXIOM
ALL RHYTHM INTERPERTATION MUST
BE CORRELATED WITH SIGNS &
SYMPTOMS AND PATIENT
CONDITION

TREAT THE PATIENT,

NOT THE MONITOR

Dysrhythmia
Impulse formation
(site of impulse origin)

SA Node

Ectopic

AV Node

Premature
Beat

Ventricle
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Anatomy of the conducting system

Normal Sinus Rhythm

NORMAL SINUS RHYTHM IS PRODUCED BY

THE SA NODE
P WAVE FOLLOWS QRS COMPLEX IN A

PREDICTABLE RELATIONSHIP
ALL P WAVES LOOK ALIKE, ALL QRS
COMPLEXES ARE NARROW
R R INTERVAL IS REGULAR
RATE: 60 100 bpm

Normal Sinus Rhythm

Normal Sinus Rhythm

Sinus / Atrial dysrhythmia

ORIGINATE FROM SA NODE OR ATRIA

(ABOVE VENTRICLES)
CONDUCTION WITH VENTRICLE IS
UNDISTURBED
USUALLY BENIGN & SYMPTOMATIC
RHYTHM MAY BE IRREGULAR

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Sinus / Atrial dysrhythmia

SINUS TACHYCARDIA
SINUS BRADYCARDIA
ATRIAL FIBRILLATION
ATRIAL FLUTTER
Premature atrial contractions
Paroxysmal atrial tachycardia
Supraventricular Tachycardia
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Dysrhythmia
Bradycardia / Tachycardia
Flutter / Fibrillation
Heart blocks

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Pathogenesis and Inducement

of Arrhythmia

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Some physical condition

Pathological heart disease
Other system disease
Electrolyte disturbance and acid-base
imbalance
Physical and chemical factors or
toxicosis

Occurrence/Incidence
80 % of patient AMI
50 % of anesthetized patient
25 % of digitalis patient

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Etiology

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Physiological
Pathological:
Valvular heart disease.
Ischemic heart disease.
Hypertensive heart diseases.
Congenital heart disease.
Cardiomyopathies.
Carditis.
RV dysplasia.
Drug related.
Pericarditis.
Pulmonary diseases.
Others.

Mechanism of Arrhythmia
Abnormal heart pulse formation
1. Sinus pulse
2. Ectopic pulse
3. Triggered activity

Abnormal heart pulse conduction

1. Reentry
2. Conduct block
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Classification of Arrhythmia
Abnormal heart pulse formation
1.
2.
3.
4.

Sinus arrhythmia
Atrial arrhythmia
Atrioventricular junctional arrhythmia
Ventricular arrhythmia

Abnormal heart pulse conduction

1.
2.
3.
4.

Sinus-atrial block
Intra-atrial block
Atrio-ventricular block
Intra-ventricular block

Abnormal heart pulse formation and

conduction

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Classification of Arrhythmia
1. Characteristics:

a. flutter very rapid but regular contractions

b. tachycardia increased rate
c. bradycardia decreased rate
d. fibrillation disorganized contractile activity

2. Sites involved:

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a. ventricular
b. atrial
c. sinus
d. AV node
e. Supraventricular (atrial myocardium or AV node)

Common Arrhythmias
Atrial
AF
A Flutter
Paroxs. SVT
AVNRT
AVRT (WPW)
Multifocal atrial

tachycardia

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Ventricular
VT
VF
Torsades

Bradyarrhytmia
Medication
AV block
SSS

Ventricular fibrillation

Basic Rhythm Strip Interpretation

1.
2.
3.

4.
5.
6.

7.

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Determine the rate. Does the atrial rate equal the

ventricular rate.
Is the rhythm regular/irregular?
Find the P wave. Is there a P wave for every QRS?
Determine the PRI (Normal 0.12-0.20 sec)
Find the QRS (Normal <0.12seconds)
Any ectopic beats?
Find the T wave.

Diagnosis of Arrhythmia
Medical history
Physical examination

Laboratory test

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Therapy Principal
Pathogenesis therapy
Stop the arrhythmia immediately if the

hemodynamic was unstable

Individual therapy Personalized Medicine

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Arrhythmia Assessment
ECG

24h Holter monitor

Echocardiogram
Stress test

Coronary angiography
Electrophysiology study

Arrhythmia Presentation
Palpitation.

Dizziness.
Chest Pain.
Dyspnea.

Fainting.
Sudden cardiac death.

Strategy of Antiarrhythmic Agents

Suppression of dysrhythmias
A. Alter automaticity
i. decrease slope of Phase 4
depolarization
ii. increase the threshold potential
iii. decrease resting (maximum
diastolic) potential

B. Alter conduction velocity

i. mainly via decrease rate of
rise of Phase 0 upstroke
ii. decrease Phase 4 slope
iii. decrease membrane resting
potential and responsiveness

C. Alter the refractory period

i. increase Phase 2 plateau
ii. increase Phase 3 repolarization
iii. increase action potential duration

antiarrhythmic agents:
There are five main classes in the Vaughan
Williams classification of antiarrhythmic agents:
1.Class I agents interfere with the sodium (Na+)
channel.
2.Class II agents are anti-sympathetic nervous
system agents. Most agents in this class are beta
blockers.
3.Class III agents affect potassium (K+) efflux.
4.Class IV agents affect calcium channels and the
AV node.

5.Class V agents work by other or unknown

mechanisms

Anti-arrhythmia Agents
Anti-tachycardia agents
Anti-bradycardia agents

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Anti-tachycardia agents
Modified Vaugham Williams classification
1. I class: Natrium channel blocker
2. II class: -receptor blocker
3. III class: Potassium channel blocker
4. IV class: Calcium channel blocker
5. Others: Adenosine, Digital

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Anti-bradycardia agents
1. -adrenic receptor activator
2. M-cholinergic receptor

blocker
3. Non-specific activator

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