Download Cryoablation Lesion with Atrial Arrhythmia after Fontan Operation

Approaches for Arrhythmias
Seoul National University Hospital
Department of Thoracic & Cardiovascular Surgery
Mechanisms of Arrhythmias
Cellular Physiology of Conduction
• Cardiac electrical activity is determined by transmembrane
potentials
• Normally intracellular compartment has more negative than
positive ions
• Each membrane channel is selective for its particular ions
(Na,K,Ca)
• Resting membrane potential for most cells is determined by
potassium current
• Following depolarization, resting potential is resorted by an
energy-dependent Na-K exchange pump
• The cell regains full capacity to depolarize once refractory
period is over
Normal Cardiac Electrical Activity
• Transmembrane potential ; Voltage difference
(polarized, 70-85mV); more negative in intracellular, more
positive in extracellular
• Changes of membrane potential ; Flow of positively
charged ion from ECF (Na, K, Ca) into intracellular through
membrane channel, or gap junction between the cardiac
cells
• Action potential
Phase 0 ; rapid upstroke by Na current at beginning of AP
Phase 1 ; top of action potential (depolarized)
Phase 2 ; Ca influx slightly later& last longer, plateau of AP
Phase 3 ; K efflux from cell, leading to repolarization
Phase 4 ; back to membrane potential
Action Potentials of Normal
Automatic Cells
Cardiac Conduction Anatomy
Embryology of Conduction Tissues
The position of primodial sinus node is located in the sinoatrial
groove between the sinus venosus and primitive atriun
Embryology of Conduction Tissues
• Conduction tissue development in normal septation of heart
Anatomy of the Right Atrium
Boundaries of Triangle Koch
Boundaries of Triangle Koch
Posterior Septum & Coronary Sinus
Human Atrial Pacemaker Complex
Normal Sinus Node & Atrium
• Heart beat from cells of 5x15mm teardrop-shaped , ability
to depolarize spontaneously (phase 4 depolarization).
• Impulses spread from SA node over atria, completing atrial
depolarization in about 80-100ms.
• Although bundles of atrial tissue with some enhanced
conduction properties ( Bachman’s bundle, Thorel’s tract ),
there are no specialized interatrial tract.
• The crista terminalis (particular arrangement of atrial cells)
facilitate impulse transmission along their long axis.
• Blood supply is from RCA in 55% & circumflex in 45%
• Richly innervated by both sympathetic & parasympathetic
fibers and responds depending on the balance.
Normal Atrio-ventricular Node
• Special cells transmit impulses very slowly, requiring 60 to
130ms to traverse about 1 cm of node.
• Slowing of impulse facilitates optimal filling of ventricles
afforded by atrial contraction & also protect from racing
in response to rapid atrial arrhythmias by not allowing all
impulse through.
• AV node has rich innervation from both autonomic nervous
system.
• Blood supply is from RCA in 90% and left circumflex in
10%.
• AV node cells have no capacity to depolarize spontaneously,
so-called nodal rhythms are in fact generated in the
infranodal portion of conduction.
His-Purkinje System & Ventricles
• Rapid impulse spread through ventricle is mediated by
cells of His-Purkinje system
• This network is situated just beneath the endocardial
surface
• Entire mass of ventricular myocardium is depolarized in
about 80-100ms, the same as in the atria.
• Blood supply to His and main bundles is from LAD ; the
very proximal His may have variable right coronary artery
supply.
• Cells within the HPS are capable of spontaneous
depolarization at rates of from 30 to 50 beats depending on
autonomic tone.
Anatomic Principles for Ablation
This diagram demonstrates the boundaries of each of four anatomic
areas where accessory pathways can occur in WPW syndrome
Ablation for Ventricular Arrhythmias
• Nonischemic ventricular tachycardia
Cardiomyopathy
Prior cardiac surgery for CHD
Cardiac tumor
Arrhythmogenic RV dysplasia
• Ischemic ventricular tachycardias
Fibrous scar
Presence of aneurysm
Abnormalities of Cardiac Rhythm
 Bradyarrhythmias
1. Abnormal impulse formation
2. Abnormal impulse transmission
 Tachyarrhythmias
1. Automaticity
2. Reentry
3. Triggered activity
Mechanisms of Bradyarrhythmias
• Abnormal impulse formation
Sinus node dysfunction
1. Inappropriate sinus bradycardia
2. Brady-tachy syndrome
• Abnormal impulse conduction
1. Atrioventricular block
2. Sinus nodal exit block
3. Bundle branch block
Mechanisms of Tachyarrhythmias
 Automaticity
1. Normal automaticity
2. Enhanced normal automaticity
3. Abnormal automaticity
 Reentry
1. Anatomic reentry
2. Functional reentry
3. Anisotropic reentry
4. Reflected reentry
 Triggered activity
1. Early afterdepolarization
2. Delayed afterdepolarization
Types of Automaticity
Abnormal Automaticity
• Rate of firing of SA node or His-Purkinje cells can be
increased by catecholamine or sympathetic stimuli
• Factors suppressing normal automaticity
1. Hyperkalemia
2. Hypoxemia
3. Acidosis
4. Some anti-arrhythmic drugs
• Abnormal automaticity has been observed in cellular
preparations of diseased human myocardium
• Abnormal automatic arrhythmias usually have rates
< 200 bpm
Reentry
 Most frequent mechanism of arrhythmias in
humans, supraventricular or ventricular
 Essential elements of reentrant arrhythmias
1. Presence of a closed loop of electrically
excitable tissue
2. Heterogeneity of electrophysiologic properties
(conduction velocity & refractoriness)
3. An initiator to begin the reentrant process
Types of Reentry
 Anatomic reentry ; in which the impulse circulates
around a fixed, anatomically determined path
 Functional reentry ; in which the impulse circulates
within a circuit whose size is determined by refractory
periods of the particular cells
 Anisotropic reentry ; in which both anatomic and
functional properties participate in determining the
path taken by the circulating wavefront
 Reflected reentry ; in which the impulse retraces its
steps along a linear path to return to or reflect on its
point of origin
Reentry
Once reentry is established, it continues in the same path
and direction until one or more required conditions is no
longer satisfied.
Arrhythmias due to Reentry

Supraventricular arrhythmias
Orthodromic tachycardia
Antidromic reentry in WPW
AV nodal reentry,
Some cases of atrial tachycardia,
Atrial flutter,
Atrial fibrillation

Ventricular arrhythmias
Uniform-morphology VT
Some cases of polymorphic VT
Ventricular fibrillation
Reentry in WPW Syndrome
Triggered Activity (1)
• Depolarization occurs after normal depolarization
• "Triggered" by preceding impulses
• Early afterdepolarization (EAD)
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At phase 2-3 of action potential
Due to increased inward current (hypoxia, injury)
Decreased repolarization outward current (K+)
Present in high catecholamine state, drugs, long QT,
torsade de Pointes
Delayed afterdepolarization (DAD)
– At phase 4 of action potential
– Due to transient inward current from Calcium overload, ?
Na+ current
– Frequently show overdrive acceleration
– Classically in digitalis intoxication
Triggered Activity (2)
Common Types of Arrhythmias
• SVT in patients with WPW syndrome
/concealed bypass tracts
• AV nodal reentry
• Atrial flutter
• Automatic atrial tachycardia
• Postinfarction uniform VT
• Bundle branch reentrant VT
Atrial Flutter
Atrial Fibrillation
Automatic Atrial Tachycardia
Intra-atrial Reentrant SVT
AV Nodal Reentry Tachycardia
Orthrodromic SV Tachycardia
Sustained Ventricular Tachycardia
Ventricular Fibrillation
Diagnosis & Treatment
Diagnosis of Cardiac Arrhythmias
• Clinical symptoms
• Noninvasive methods
1. Resting electrocardiography
2. Ambulatory electrocardiography
3. Event monitoring
4. Exercise testing
5. Signal-averaged electrocardiography
• Invasive methods
1. Electrophysiologic study
2. Endocardial mapping
Symptoms of Arrhythmias
• A wide variety of symptoms, ranging from
a complete absence of awareness of episode
to mild palpitation, light-headedness,
syncope, sudden cardiac death.
• Additional symptoms include chest pain,
throat tightness, or dyspnea, any of which
may occur alone or in combination with
others.
Therapy for Cardiac Arrhythmias
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Pharmacologic therapy
Pacemakers
Catheter ablations
Implantable defibrillators
Surgical therapy
Pharmacologic Treatment
• Perfect medication
Very high efficacy rate
Low rates of side effects
Low cost
Convenient dosing schedule
• Bradyarrhythmias
Rarely used (anticholinergic; scopolamine patches,
sympathetic stimulants; methylxanthines(theophylline),
withdrawl of medication
• Tachyarrhythmias
Complete suppression is ideal but, decrease in frequency
& reduction of severity, shortening of duration
Class I Antiarrhythmic Agents
• Mechanism ; depression of fast sodium current as a
common feature
• Class 1A ; procaine amide, quinidine, disopyramide cause
marked decrease in conduction velocity as well as an
independent prolongation of repolarization used in
preventing or slowing the heart rates.(VT, AF, Af, etc)
• Class 1B ; lidocaine, mexiletine cause moderate slowing
of conduction with minimal effect on repolarization.
• Class 1C ; flecainide, propafenone, cause marked decreases
in conduction velocity (more than class 1) but minimal effect
on repolarization, in treating almost all supraventricular &
ventricular arrhythmias.
Class II Antiarrhythmic Agents
• Mechanism ; act by antagonizing the effects of
epinephrine and norepinephrine at nerve
terminals in the heart and elsewhere
• These beta-adrenergic blocking drugs are most
useful in treating arrhythmias that depend on
AV node for perpetuation (SVT), also
adjunctively in ventricular arrhythmias
• Side effects include sinus bradycardia or AV
block, provocation of CHF, peripheral vascular
disease, reactive airway disease, and DM.
Class III Antiarrhythmic Agents
• Mechanism ; features of blocking intracellular currents
(mainly K ion) responsible for repolarization.
• Medications including amiodarone, bretylium, sotalol
prolong the QT interval, useful in treating almost all
types of supraventricular & ventricular arrhythmias,
but bretylium generally limited to use in ischemic
ventricular arrhythmia.
• Side effects ; aggrevation of sinus bradycardia & AV
conduction disturbance, heart failure, proarrhythmia.
• Amiodarone ; long tissue halh-life(months), & rare side
effect of pulmonary fibrosis occasionally can be fatal
Class IV Antiarrhythmic Agents
• Mechanism ; These agents, such as verapamil
& diltiazem , block the cardiac calcium
channels
• Used interchangeably with beta blockers in
supraventricular arrhythmias because of their
actions on the AV node (slowing ventricular
rates during atrial flutter or fibrillation,
preventing AV nodal reentry, or orthodromic
SVT etc.)
• Side effects ; heart failure, bradyarrhythmias
as is beta blockers or noncardiac side effects
Indications of Pacemakers
• Class I : Pacing definitely indicated
Complete heart block < 40 beats
Symptomatic type I, II heart block
Sinus bradycardia less than 40 beats
• Class II : Pacing potentially indicated
Asymptomatic complete AV block> 40 beats
Type II second-degree AV block
• Class III : Pacing not indicated
Prolonged PR interval & asymptomatic Type I
second degree AV block( Wenckebach)
Surgical Principles of Arrhythmia
Surgery for Arrhythmias
 Excision or isolation of the tissues responsible for
initiation or continuation of arrhythmias 
encircling endocardial ventriculotomy,
cryoablation, subendocardial resection,
corridor operation
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WPW syndrome & concealed bypass tracts
AV nodal reentry
Atrial fibrillation
Postinfarction uniform sustained VT
Ventricular fibrillation & rapid polymorphic VT
Surgery for Automatic Atrial
Tachycardia
• Surgery is reserved for symptomatic patients
who fail radiofrequency catheter ablation or
those with multiple foci
• Techniques for surgical treatment include ;
cryoablation of ectopic focus with or without
CPB, wide excision of foci , simple excision,
combination of excision & cryoablation in right
atrial lesions.
• Foci on the left atrium tend to be near the left
superior pulmonary vein ; localized isolation
procedure, but with limited success.
Surgery for Reentrant Tachycardia
• Surgical approaches
1. Endocardial technique
2. Epicardial technique
• Surgical locations
1. Left free-wall accessory pathways
2. Posterior septal accessory pathways
3. Right free-wall accessory pathways
4. Anterior septal accessory pathways
Endocardial Technique
Left Free-wall Accessory Pathways
Endocardial Technique
Posterior Septal Accessory Pathways
Endocardial Technique
Right Free-wall Accessory Pathways
Endocardial Technique
Anterior Septal Accessory Pathways
AV Nodal Reentrant Tachycardia
• Cryosurgical modification of AV node
1. The objective of surgery for AV nodal reentry
tachycardia is to interrupt one of the two conduction
pathways through the AV node.
2. The perinodal cryosurgical procedures ablates the
slow conduction pathway and preserve fast conduction
• Surgical dissection
1. Type A AV nodal reentry, superolateral connections
of AV node to the atrium via the coronary sinus are
left undisturbed
2. Type B AV nodal reentry, superior & medial connections
of AV node to the atrium are left undisturbed.
Cryosurgical Ablation of AV Node
AV Nodal Reentrant
Endocardial Interruption
AV Nodal Reentry
Posterior Septal Space
Dissection for Type A AVNRT
Posterior Septal Space
Dissection for Type B AVNRT
Surgical Indications for VTs
Endocardial Resection
• Inducible ventricular tachycardias are
reentrant, the patient may be candidate for
surgical resection of endocardial circuit,
whereas noninducible rhythm disorders are
perceived as automatic.
• If the rhythm is not inducible, placement of an
ICD may be appropriate.
• Inducible dysrrhythmia can be mapped or
anatomically localized and generous surgical
excision of this diseased tissue might cripple or
cure its arrhythmogenic potential.
Electroanatomy of Reentrant Rhythm
Spontaneous re-entrant impulse
Therapeutic paced beat
Therapeutic Algorithm of VTs
Arrhythmias from Cardiac Surgery
1. Bradyarrhythmias & conduction disturbances
a. Sinus node injury
b. Damage to AV conduction
c. Bundle branch block
2. Supraventricular tachyarrhythmias
a. Postoperative atrial fibrillation
b. Atrial flutter & intraatrial reentrant tachycardia
c. Accelerated junctional tachycardia
3. Ventricular tachyarrhythmias
a. Uniform sustained ventricular tachycardia
b. Ventricular fibrillation