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Approaches for Arrhythmias Seoul National University Hospital Department of Thoracic & Cardiovascular Surgery

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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 - PowerPoint PPT Presentation

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Page 1: Approaches for Arrhythmias

Approaches for Arrhythmias

Seoul National University Hospital

Department of Thoracic & Cardiovascular Surgery

Page 2: Approaches for Arrhythmias

Mechanisms of Arrhythmias

Page 3: Approaches for 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

Page 4: Approaches for Arrhythmias

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

Page 5: Approaches for Arrhythmias

Action Potentials of Normal Automatic Cells

Page 6: Approaches for Arrhythmias

Cardiac Conduction Anatomy

Page 7: Approaches for Arrhythmias

Embryology of Conduction Tissues

The position of primodial sinus node is located in the sinoatrial groove between the sinus venosus and primitive atriun

Page 8: Approaches for Arrhythmias

Embryology of Conduction Tissues

• Conduction tissue development in normal septation of heart

Page 9: Approaches for Arrhythmias

Anatomy of the Right Atrium

Page 10: Approaches for Arrhythmias

Boundaries of Triangle Koch

Page 11: Approaches for Arrhythmias

Boundaries of Triangle Koch

Page 12: Approaches for Arrhythmias

Posterior Septum & Coronary Sinus

Page 13: Approaches for Arrhythmias

Human Atrial Pacemaker Complex

Page 14: Approaches for Arrhythmias

Normal Sinus Node & Atrium• Heart beat from cells of 5x15mm teardrop-shaped , ability t

o 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.

Page 15: Approaches for Arrhythmias

Normal Atrio-ventricular Node• Special cells transmit impulses very slowly, requiring 60 t

o 130ms to traverse about 1 cm of node.• Slowing of impulse facilitates optimal filling of ventricles af

forded 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.

Page 16: Approaches for Arrhythmias

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.

Page 17: Approaches for Arrhythmias

Anatomic Principles for Ablation

This diagram demonstrates the boundaries of each of four anatomic

areas where accessory pathways can occur in WPW syndrome

Page 18: Approaches for Arrhythmias

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

Page 19: Approaches for Arrhythmias

Abnormalities of Cardiac Rhythm

Bradyarrhythmias 1. Abnormal impulse formation 2. Abnormal impulse transmission Tachyarrhythmias 1. Automaticity 2. Reentry 3. Triggered activity

Page 20: Approaches for Arrhythmias

Mechanisms of Bradyarrhythmias

• Abnormal impulse formationSinus 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

Page 21: Approaches for Arrhythmias

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

Page 22: Approaches for Arrhythmias

Types of Automaticity

Page 23: Approaches for Arrhythmias

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 pre

parations of diseased human myocardium• Abnormal automatic arrhythmias usually have rates < 20

0 bpm

Page 24: Approaches for Arrhythmias

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

Page 25: Approaches for Arrhythmias

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

Page 26: Approaches for Arrhythmias

Reentry Once reentry is established, it continues in the same path and direction until one or more required conditions is no longer satisfied.

Page 27: Approaches for Arrhythmias

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

Page 28: Approaches for Arrhythmias

Reentry in WPW Syndrome

Page 29: Approaches for Arrhythmias

Triggered Activity (1)• Depolarization occurs after normal depolarization • "Triggered" by preceding impulses • Early afterdepolarization (EAD)

– 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, torsad

e de Pointes

• Delayed afterdepolarization (DAD) – At phase 4 of action potential – Due to transient inward current from Calcium overloa

d, ? Na+ current – Frequently show overdrive acceleration – Classically in digitalis intoxication

Page 30: Approaches for Arrhythmias

Triggered Activity (2)

Page 31: Approaches for Arrhythmias

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

Page 32: Approaches for Arrhythmias

Atrial Flutter

Page 33: Approaches for Arrhythmias

Atrial Fibrillation

Page 34: Approaches for Arrhythmias

Automatic Atrial Tachycardia

Page 35: Approaches for Arrhythmias

Intra-atrial Reentrant SVT

Page 36: Approaches for Arrhythmias

AV Nodal Reentry Tachycardia

Page 37: Approaches for Arrhythmias

Orthrodromic SV Tachycardia

Page 38: Approaches for Arrhythmias

Sustained Ventricular Tachycardia

Page 39: Approaches for Arrhythmias

Ventricular Fibrillation

Page 40: Approaches for Arrhythmias

Diagnosis & Treatment

Page 41: Approaches for Arrhythmias

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

Page 42: Approaches for Arrhythmias

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.

Page 43: Approaches for Arrhythmias

Therapy for Cardiac Arrhythmias

• Pharmacologic therapy

• Pacemakers

• Catheter ablations

• Implantable defibrillators

• Surgical therapy

Page 44: Approaches for Arrhythmias

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

Page 45: Approaches for Arrhythmias

Class I Antiarrhythmic Agents• Mechanism ; depression of fast sodium current as a c

ommon 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.

Page 46: Approaches for 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.

Page 47: Approaches for Arrhythmias

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

Page 48: Approaches for Arrhythmias

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

Page 49: Approaches for Arrhythmias

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)

Page 50: Approaches for Arrhythmias

Surgical Principles of Arrhythmia

Page 51: Approaches for Arrhythmias

Surgery for Arrhythmias

Excision or isolation of the tissues responsible for initiation or continuation of arrhythmias encircling endocardial ventriculotomy, cryoablation, subendocardial resection, corridor operation

• WPW syndrome & concealed bypass tracts• AV nodal reentry• Atrial fibrillation• Postinfarction uniform sustained VT• Ventricular fibrillation & rapid polymorphic VT

Page 52: Approaches for Arrhythmias

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.

Page 53: Approaches for Arrhythmias

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

Page 54: Approaches for Arrhythmias

Endocardial Technique Left Free-wall Accessory Pathways

Page 55: Approaches for Arrhythmias

Endocardial Technique Posterior Septal Accessory Pathways

Page 56: Approaches for Arrhythmias

Endocardial Technique Right Free-wall Accessory Pathways

Page 57: Approaches for Arrhythmias

Endocardial Technique Anterior Septal Accessory Pathways

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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.

Page 59: Approaches for Arrhythmias

Cryosurgical Ablation of AV NodeAV Nodal Reentrant

Page 60: Approaches for Arrhythmias

Endocardial Interruption AV Nodal Reentry

Dissection for Type A AVNRT

Dissection for Type B AVNRT

Posterior Septal Space Posterior Septal Space

Page 61: Approaches for Arrhythmias

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.

Page 62: Approaches for Arrhythmias

Electroanatomy of Reentrant Rhythm

Therapeutic paced beat

Spontaneous re-entrant impulse

Page 63: Approaches for Arrhythmias

Therapeutic Algorithm of VTs

Page 64: Approaches for Arrhythmias

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