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

2. Mechanisms of Arrhythmias

3. 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

4. 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

5. Action Potentials of Normal Automatic Cells

6. Cardiac Conduction Anatomy

7. Embryology of Conduction Tissues The position of primodial sinus node is located in the sinoatrial groove between the sinus venosus and primitive atriun

8. Embryology of Conduction Tissues
Conduction tissue development in normal septation of heart

9. Anatomy of the Right Atrium

10. Boundaries of Triangle Koch

11. Boundaries of Triangle Koch

12. Posterior Septum & Coronary Sinus

13. Human Atrial Pacemaker Complex
A, B . Two different P-wave morphologies.
Activation sequence A ; Two competing sites of initiation are shown. The anterior site depolarizes 5 ms before the posterior site.
Activation sequence B ; The next cycle demonstrates dominance shifting to the posterior site with passive depolarization of the previously dominant anterior site.
These are typical examples of the exchange of dominance between competing sites, which results in changing P-wave configurations in sinus arrhythmia. Although the P-wave morphology reflects the differences in global atrial depolarization, these patterns are a result of different initiating conditions.

14. 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 ms.
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.

15. 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.

16. 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 ms, 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.

17. Anatomic Principles for Ablation This diagram demonstrates the boundaries of each of four anatomic areas where accessory pathways can occur in WPW syndrome

18. 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

19. Abnormalities of Cardiac Rhythm
Bradyarrhythmias
1. Abnormal impulse formation
2. Abnormal impulse transmission
Tachyarrhythmias
1. Automaticity
2. Reentry
3. Triggered activity

20. 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

21. 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

22. Types of Automaticity

23. 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

24. 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

25. 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

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

27. 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

28. Reentry in WPW Syndrome

29. 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, 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

30. Triggered Activity (2)

31. 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

32. Atrial Flutter

33. Atrial Fibrillation

34. Automatic Atrial Tachycardia

35. Intra-atrial Reentrant SVT

36. AV Nodal Reentry Tachycardia

37. Orthrodromic SV Tachycardia

38. Sustained Ventricular Tachycardia

39. Ventricular Fibrillation

40. Diagnosis & Treatment

41. 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

42. 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.

43. Therapy for Cardiac Arrhythmias
Pharmacologic therapy
Pacemakers
Catheter ablations
Implantable defibrillators
Surgical therapy

44. 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

45. 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.

46. 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.

47. 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

48. 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

49. 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)

50. Surgical Principles of Arrhythmia

51. 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

52. 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.

53. 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

54. Endocardial Technique Left Free-wall Accessory Pathways

55. Endocardial Technique Posterior Septal Accessory Pathways

56. Endocardial Technique Right Free-wall Accessory Pathways

57. Endocardial Technique Anterior Septal Accessory Pathways

58. 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.

59. Cryosurgical Ablation of AV Node AV Nodal Reentrant

60. Endocardial Interruption AV Nodal Reentry
Posterior Septal Space
Posterior Septal Space
Dissection for Type A AVNRT
Dissection for Type B AVNRT

61. 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.

62. Electroanatomy of Reentrant Rhythm
Spontaneous re-entrant impulse
Therapeutic paced beat

63. Therapeutic Algorithm of VTs

64. 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