Mechanism of ArrhythmiaFellow School Lecture Series

Mahmoud Houmsse, MD.July 11th, 2014

Cardiac Action Potential

Transmembrane Potential

-90 mV

+30 mV

0 mV

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

Basic Catheter Positions

His and RightBundle Potentials

Right Atrium

His Bundle –Junction betwn. RA and RV

Right Ventricle

Surface ECG I

Surface ECG III

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

Slow pathway

Fast pathway

Compact AV node

Timed PAC to initiate AVNRT

12

13

Retrograde P wave

Atrio-Ventricular PreexcitationWPW

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 PreexcitationWPW

May proceed up or down the accessory pathway Down = antidromic

wide complex not common

antidromic

Atrio-Ventricular PreexcitationWPW

May proceed up or down the accessory pathway Up = orthodromic

narrow complex common

orthodromic

Atrio-Ventricular PreexcitationWPW

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-EntryConcealed Accessory PathwayAtrio-Ventricular Re-EntryConcealed Accessory Pathway

Up the accessory pathway, Up the accessory pathway, Down the AV nodeDown 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

Slow Conduction between tricuspid

valve & inferior vena cava

Isthmus

Slow Conduction

52 y/o M with H/O HTN and Recurrent Palpitations

Atrial Flutter: Catheter LyingAlong Tricuspid Valve

Tri. Valve

Inf Vena Cava

Typical AFL: Intracardiac ECG Recording catheter along tricuspid valve

Reentrant VT

scar

scar

“Squeezed by Scar”

Catheter Ablation Procedure:

1. Induce the VT

*The QRS of the VT begins here

*

2. Map the VT circuit, ie, find the zone of slow conduction squeezed by scar3. Deliver RF energy to destroy the zone of slow conduction and thus eliminate reentry and VT

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

scar

scar

*The QRS of the VT begins here

*

* ***Successful

Ablation Site

QRS from Pacing During VT = QRS of the VT

scar

scar

*

*QRS of the VT begins here

** * * * * * * * * ** * * * * * * *

Concealed entrainment

Pace here

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 Automaticityoccurs in cardiac cells when there are major abnormalities in transmembrane potentials Drugs, (digoxin) Cardiac disease, CAD, Electrolytes Change in autonomic nervous

Normal Cardiac 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

Automaticity

SA node 60 to 100 bpm

AV node 40 to 60 bpm

Ventricular specialized conduction tissue 20-30 bpm

Tissues with Intrinsic Automaticity

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 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

Triggered 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??