TACHYARRHYTMIA SERIES

Mechanism of arrhytmia
Arrhytmia
Arrhythmia

Changes in electrical impulses that cause

abnormalities of heart rhythm, speed and
electrical waveform of the heart

Impulse formation disorders

Impulse delivery disorders
Arrhythmia
 Bradiarrhythmia
• SA Node automaticity failure
•The most common cause of bradycardia
•When the slowdown increases symptoms appear
• Failure of impulse propagation
•Second cause of arrhythmia bradikaridia
•Conduction or refractory speed abnormalities in the conduction system
•Heart block or AV block
•Failure of electrical impulses generated by SA Node to AV Node
•Study required on EP
•Insufficient amount of electrical impulses
Bradyaarrhytmia mechanism
• Reduced automaticity
•SA node
•AV node
•Drugs
• Block conduction
•SA BLOCK
•AV BLOCK
Block conduction
Tachycardia
• Arrhythmias; Heart rate > 100x per minute.
• Tachycardia causes clinical symptoms in extreme conditions (heart
rate ≥ 150x per minute)
• Tachycardia is based on QRS complex, heart rate and regularity.
Tachycardia by location

• Atrial :
•AT, AF, Afl
• AV Nodal
•JT, AVNRT
• Resiprok / AV
•AVRT
• Ventrikel
•VT, VF, Torsade de pointes
Mechanism of tachyarrhytmia
• Impulse formation
•Increased automaticity
•Physiological normal automaticity (sympathetic nerve: ST, AT)
• Triggered activity
•Abnormal AP (EADs, DADs: AT, MAT, VT, Torsade de pointes)
• Reentry
•Macroreentry : AVRT, Afl, VT
•Microreentry : AVNRT, Afib, AT
•Abnormal automaticity (ectopic pace maker : Atrial tachycardia, accelerated
idioventricular rhytm)
AUTOMATICTY
• The normal condition of atrial and ventricular muscle cells is non-pacemaker.
• Automaticity is the ability to initiate impulses spontaneously (no stimulation is required).
• Abnormal automaticity is the abnormal acceleration of phase 4 AP.
•Due to the increased potential of resting membranes
• Increased levels of extracellular potassium, decreased intracellular pH and excessive catecholamines
• uncommon, < 10 % from mechanism tachyarrhythmia

• Constant depolarized non-pacemaker cells -10 to -60 mv

• Spontaneous action potential (depolarization induced automaticity)
• The greater the condition of the depolarization stimulus the faster the frequency of
automation..
• Tissue damage to the heart muscle can cause atrial and ventricular muscle cells
to secrete spontaneous impulses.
• Shift of non-pacemaker cell MDP toward potential threshold
Automaticity
Abnormal automaticity
• Warm-up & warm down, peak rates< 200 bpm
• Often seen in acute pain
•Ischaemia, hypokalemia, lung disease, electrolyte disorder, high sympathetic tone
•Transient arrhythmia (only present when substrate active)
• Spontaneous induction and termination
• Cannot be triggered or stopped with PES ( EP lab)
• The most common abnormal focus
•A: CT, RAA, LAA, PV, CS, AV Valves, Triangle of Koch
•V: His-Purkinje, Ventricular muscle, RVOT, LVOT
• Long RP tachycardia
• No reliable initiation or termination in EP lab
•Transient suppression by overdrive pacing, Often spontaneous induction

• It often arises from metabolic causes.

Abnormal focus
Automatic Tachycardias
• Atrial
•Sinus tachycardia
•Inappropriate sinus tachycardia
•Incessant atrial tachycardia
•Multifocal atrial tachycardia
• Junctional
•Focal junctional tachycardia
• Ventricular
•Accelerated idioventricular rhythm
•PVC's
Normal automaticity
Abnormal automaticity
Automaticity
Reentry
• The most common mechanism of tachyarrhythmia
• Reentry occurs when the spreading impulse fails to dissipate and then reeks of the heart that
has finished its refractory period..
• SVT
•The patient is not acutely ill; There is no chronic, often congenital heart disease (AVNRT, AVRT, SNRT, can
be acquired (e.g. surgery), short RP tachycardia.
• VT
•Circuitry often involves malignant diseases and is not congenital..
• Easy to study in EP laboratories due to initiation that can induce &termination with PES
• Started by premature pulse
•Acquired during life (e.g. MI scarring) (VT).
• A state in which an impulse that has come out of a conduction path
through a ring road / lop re-entered the original path.
Reentry criteria
• Two parallel conduction pathways are proximal and distal with the
delivery network thus forming a potential electrical circuit.
•Anatomically functionally separate
• Refractory Period of one > rp path to another
•Unidirectional block
• Paths with shorter refractory periods should have slower conduction speeds than
other paths.
•Electrically connected
Reentry initiation
Termination reentry
Reentrant Tachycardia
• Atrial (macro or micro reentry : Afib, AFL)
• The reentry circuit requires the originator: active
• AVN
• AVNRT (2 path (slow & fast) AVN)
• AVRT ( 2 path (AVN & AP) AVN
• Ventrikel
• VT due to MI
Reentry AVNRT criteria

Prematur beat
Slow Pathway : Fast Pathway :
•Slow conduction •Fast conduction
•Short refractory •Long refractory
time Proksimal time

Distal
Reentry (WPW)
Trigger Activity
• Trigerred activity (TA) It occurs after impulse initiation due to "afterdepolarization".
• Involves leaking positive ions into the cardiac cell at the time after depolarisasi
( AD)
• If AD causes a large enough magnitude it will open Na channel so that ap follow-
up.
• Triggered is not spontaneous or not completely automatic
• EAD ( early after depolarization )
•Phase 2 & 3 : torsade, LQTS
• DAD ( delayed after depolarization )
•Phase 4 : RVOT, VT

• Triggered activity must be triggered by premature beats

Trigger Activity
• It has automatic features
•Affects the final phase 3 and the beginning of phase 4 of the AP
• It has a reentry feature
•Can be provoked by PES
• It can be seen in the toxicity of the drug and long QT (LQT)
• Difficult to diagnose in EP lab.

•Has a warm-up and cool down period

Trigger Activity
• Mechanism
•EADs : prolonged action potential
•DADs : excess intracellular Ca
• Cause :
•EADs : Hypokalemia, drugs, Congenital long QT syndrome
•DADs : ischemia, ketocolamine, digoxin toxity
• Association of risk with heart rate
• EADs : Increased risk of a slower heart rate
• DADs : Increased risk of faster heart rate
Early after depolarizations (EAD) dan Delayed after
depolarizations (DAD)
Triggered Tachycardias
• Atrial
•Digitalis toxic SVT
•AF (DAD)
• Junctional
•Focal junctional tachycardia
• Ventricular
•Torsades de pointes (EAD)
•LTQS (EAD)
•RVOT (EAD / DAD)
 KESIMPULAN

• Arrhythmias occur due to various changes and disorders related to the cellular
electrophysiological properties of the heart.
• Development for the enforcement of diagnosis and management of arrhythmias needs
to pay attention to the underlying electrophysiological mechanisms..
• Evaluate and determine the mechanism of arhytmia through EP when necessary
(reentry)

• The mechanism of arrhythmias is grouped into impulse formation

disorders (automaticity, trigger activity) or impulse alignment
disorders (reentry).
 .
HATUR NUHUN
TERIMA KASIH
GRACIAS
SYUKRON
DANKE
ARIGATO
KANSA HAMNIDA

TERIMA KASIH
HATUR NUHUN