Mechanism of Arrhythmia
Fellow School Lecture Series
Mahmoud Houmsse, MD.
July 11th, 2014
Cardiac Action Potential
+30 mV
0 mV
-90 mV
Transmembrane Potential
Basic Catheter Positions
Protocol for RFA:
1. Catheters introduced
via the femoral vein
2. Try
to
induce
arrhythmia by pacing
– defined protocol
3. Confirm diagnosis of
type of arrhythmia
4. Map and RFA
5. Retest to assess if
RFA was successful
His and Right
Bundle Potentials
Surface ECG I
Surface ECG III
Right Atrium
His Bundle –
Junction betwn.
RA and RV
Right Ventricle
Mechanisms
 Disorder of Impulse Formation
◦ Automaticity
◦ Triggered activity
 Two major causes of Impulse initiation (used to indicate
an electrical impulse that can arise in a single cell or
closely coupled cells through depolarization of the cell
membrane and rest of myocardium)
 Each has own unique cellular mechanism
 Disorders of Impulse Conduction
◦ Reentry
65 y/o Female Presented with Severe Near
Syncope and Palpitations
Fast, Regular and Narrow: PSVT
Mechanisms of Arrhythmias
 Reentry
 Dog chasing his tail or a Race Track
Scar –
tissue that
does not
conduct
AV Node Re-Entrant Tachycardia
 1 AV node pathway conducts rapidly
 Known as the “fast pathway”
 takes a long time to recover to conduct again
 2nd AV node pathway conducts slowly
 Known as the “slow pathway”
 takes a short time to conduct another beat
AV Node Re-Entrant Tachycardia
Typically, PAC blocks in the “fast” pathway,
conducts down the “slow” pathway,
then back up the “fast” pathway
Fast pathway
Slow pathway
Compact AV
node
Timed PAC to initiate AVNRT
12
13
Retrograde P wave
Atrio-Ventricular Preexcitation
WPW
 Accessory pathway that conducts from atrium
to ventricle (and usually from V to A too)
 Simultaneous conduction creates fusion beat
with a delta wave
delta wave
Atrio-Ventricular Preexcitation
WPW
Atrio-Ventricular Preexcitation
WPW

May proceed up or down the accessory
pathway
 Down
= antidromic
 wide
complex
 not common
antidromic
Atrio-Ventricular Preexcitation
WPW

May proceed up or down the accessory
pathway
orthodromic
 Up
= orthodromic
 narrow
complex
 common
Atrio-Ventricular Re-Entry due to a
Concealed Bypass Tract
 Atrium and ventricle are needed to sustain the
tachycardia
 Lack of antegrade conduction “conceals” the
presence of this pathway on the ECG
 There is NO delta wave
X
Atrio-Ventricular Re-Entry
Concealed Accessory Pathway

Up the accessory pathway,
Down the AV node
orthodromic
Atrial Tachycardia
 Automatic Atrial Tachycardia
 Intra-Atrial Re-Entrant Tachycardia
 Triggered Automaticity
 Digitalis Toxicity
PSVT Types
Atrial Tachycardia
AVNRT
AVRT/WPW
Atrial Flutter
Circuit
Reentrant Circuit
Around Anatomical
Barriers
Isthmus
Slow
Conduction
Slow Conduction
between tricuspid
valve & inferior vena
cava
52 y/o M with H/O HTN and
Recurrent Palpitations
Atrial Flutter: Catheter Lying
Along Tricuspid Valve
Tri. Valve
Inf Vena
Cava
Typical AFL: Intracardiac ECG
Recording catheter along tricuspid valve
Reentrant VT
*The QRS of the VT
begins here
*
Catheter Ablation
Procedure:
1. Induce the VT
2. Map the VT circuit, ie, find the
zone of slow conduction squeezed
by scar
3. Deliver RF energy to destroy
the zone of slow conduction and
thus eliminate reentry and VT
s
c
a
r
s
c
a
r
“Squeezed by
Scar”
Step #1 of a VT Ablation Procedure
EP Study: Induce VT
V1
aVF
RA
*
RV
*
*
*
*
*
VT
Early Electrical Signal Recorded at Zone of
Slow Conduction………Squeezed by Scar
*The QRS of the
VT begins here
*
*
s
c
a
r
s
c
a
r
Successful
Ablation
Site
*
*
*
QRS from Pacing During VT = QRS of the VT
*QRS of the VT
begins here
* * * * * * ** *
*
s
c
a
r
*
s
c
a
r
Pace
here
Concealed entrainment
* * * * * * ** *
Spontaneous impulse
initiation is a process
whereby cardiac cells
undergo spontaneous
diastolic depolarization
(phase 4) and initiate
electrical impulse in the
absence of external
stimulation.
Enhanced Normal
Automaticity – refers to
accelerated generation of
Action Potential (AP) by normal
pacemaker tissue
Abnormal Automaticity
occurs in cardiac cells when
there are major abnormalities in
transmembrane potentials
 Drugs, (digoxin)
 Cardiac disease, CAD,
 Electrolytes
 Change in autonomic
nervous
Normal Cardiac Automaticity
Automaticity
 Normal Automatcity-Intrinsic Rate determined by
 Diastolic potential
 Threshold potential
 Slope of phase 4
 Change in any above will alter rate of impulse
formation
 Above factors influenced by sympathetic /
parasympathetic systems
Automaticity
 Parasympathetic
 Reduces spontaneous discharge of SN
 Sympathetic
 Increase slope of diastolic depolarization
 Enhances pacemaker activity
Tissues with Intrinsic Automaticity
 SA node
 60 to 100 bpm
 AV node
 40 to 60 bpm
 Ventricular specialized conduction tissue
 20-30 bpm
Automatcity & Overdrive
Suppression
Triggered activity
 After-depolarizations are depolarizing oscillations in membrane
potential that follow the upstroke of a preceding action potential.
◦ Can occur early during repolarization phase of
(Early afterdepolarization)
or
◦ After completion of repolarization phase
(Delayed afterdepolarization)
Triggered Activity
 Triggered activity is not a self-generating rhythm.
But occurs as a response to a preceding impulse
(the trigger)
 Automatic rhythms can arrive de novo in the
absence of prior electrical activity
DADs
 DADs usually occur when Calcium Overload develops in
the Myoplasm and Sarcoplasmic Reticulum
 Possible Therapeutic meds include CCB and BB
DADs
 During repolarization Calcium influx can rise to critical
level and cause secondary spontaneous release of
Calcium
 DADs of Low Amplitude, usually not significant
 However, during pathological conditions
 Ischemia, Acidosis, Low Mg, Digitalis toxicity,
Rapid Atrial Pacing, Increased Catecholamines 
Amplitude of oscillations is increased.
 If process continues, tachycardia will ensue
(RVOT)
 Other causes, geneteic (Ryanodine receptor aka
RYR2)
Calcium Influx Pathways
Earlier DADs with increasing
amplitude
DAD
earlier
DAD
even
earlier
DADs
 Duration of AP
 Decrease in Cycle Length
(sinus tachycardia or paced rhythm)
 Triggered activity is influenced markedly by
overdrive pacing (both rate and duration)
 Overdrive acceleration obsereved with triggered
rhythm
 Overdrive suppression observed with automatic
rhythms
EADs
 Occur at phase 2 and 3
 More likely to propagate when membrane
potential is more negative.
 Fundamental condition that underlies the
development of EADS is AP prolongation which
is manifested by polonged QT.
 Hypokalemia, Hypomagnesemia, Bradycardia and Drugs
predispose to formation of EADs (Antibiotics, Non-sedating
Antihistamines)
 EAD mediated triggered activity likely underlies initiation of
characteristic PMVT
DADs Vs. EADs
 DADs are dependent on a rise in intracellular Calcium.
 EADs are dependent on AP prolongation.
 Pacing induced increases in heart rate shorten the AP
duration and reduce EAD amplitude
 Initiation of single premature depolarization will reduces
the magnitude of EADs
 Exception is long compensatrory pause followed by
PVC.
Questions??