This document provides an overview of the conduction system of the heart. It begins with the development of the primitive cardiac tube and differentiation of heart structures. It then describes the specialized conduction tissues including the sinoatrial node, atrioventricular node, bundle of His, bundle branches, and Purkinje fibers. It discusses impulse conduction through the heart and characteristics of cardiac conduction cells. Finally, it covers conduction defects, implications for congenital heart anomalies like ASD and VSD, and considerations for cardiac surgery.

1. CONDUCTION SYSTEM OF
HEART
Presenter-Dr.
Jyotindra Singh
NIZAMS INSTITUTE OF MEDICAL SCIENCES,HYDERABAD

2. SEMINAR PLAN
DEVELOPMENTAL ASPECT
INTRODUCTION / COMPONENTS
PHYSIOLOGICAL ASPECT
CONDUCTION DISTURBANCES
CONGENITAL ANOMALIES
SURGICAL IMPLICATIONS
RECENT UPDATES

3. The primitive cardiac tube has five zones:
the arterial trunk
the bulbus cordis )
the ventricle
the atrium
and the sinus venosus
The arterial trunk will divide to separate the pulmonary and systemic supply.
The bulbus and the ventricle will differentiate into the right and left ventricles

4. DEVELOPMENT CONDUCTION SYSTEM

5. The cardiac tube grows at a greater
longitudinal rate then the rest of the
embryo, causing it to fold. As it does this
it falls to the right. This is known as
d-looping. It may fall to the left in an
l-loop: this will lead to a malformed heart.
.
normal d-loop
l-loop

6. The Tube Bends
V
B
D
A
V
SV
The tube, as it grows, cannot be accommodated within the pericardial cavity and undergoes
bending.

7. CONDUCTION SYSTEM OF
HEART

8. The Conduction System
The heart is controlled by the ANS – it
increases/decreases contraction, but it
does NOT initiate it.
The heart has its own regulating system =
conduction system
The conduction system is composed of
specialized muscle tissue that generates
action potentials within cardiac tissue.

9. Conduction system
The specialized heart cells of the cardiac
conduction system generate and coordinate the
transmission of electrical impulses to myocardial
cells
The result is sequential atrioventricular
contraction which provides for the most effective
flow of blood , thereby optimizing cardiac out put

10. Characteristics of Cardiac
Conduction Cells
Automaticity: ability to initiate an electrical
impulse
Excitability: ability to respond to an electrical
impulse
Conductivity: ability to transmit an electrical
impulse from one cell to another

11. CONDUCTION SYSTEM OF THE HEART
1. SINO ATRIAL NODE
2. INTERNODAL ATRIAL
PATHWAY
3. ATRIOVENTRICULAR
NODE
4. BUNDLE OF HIS
5. PURKINJEE SYSTEM

15. Bundle of HIS

16. BUNDLE BRANCHES

18. Impulse Conduction through
the Heart

19. ORIGIN AND SPREAD OF CARDIAC EXCITATION

20. SA NODE of Keith & Flack
Pacemaker of the heart
Lies- Junction of right atrial appendage with SVC
- underlies uppermost part of Sulcus terminalis
Dimensions – 10 to 20 mm X 1 mm X 3mm wide
Composition – Specialised branching myocardial
fibres embedded in dense matrix of fibrous tissue.
Artery to SA node – 55% - Right coronary artery
- 45% - Circumflex branch of LCA

22. WHY SA NODE LEADS THE HEART?
TISSUE
RATE OF IMPULSE
GENERATION
SA NODE
70-80/MIN
AV NODE
40 – 60/MIN
BUNDLE OF HIS
40/MIN
PURKINJE SYSTEM
24/MIN

23. Depolarization of SA Node
SA node - no stable resting membrane potential
Pacemaker potential
– gradual depolarization from -60 mV, slow influx of Na+
Action potential
– at threshold -40 mV, fast Ca+2 channels open, (Ca+2 in)
– depolarizing phase to 0 mV, K+ channels open, (K+ out)
– repolarizing phase back to -60 mV, K+ channels close
Each depolarization creates one heartbeat
– SA node at rest fires at 0.8 sec, about 75 bpm

24. SA Node Potentials

27. INTERNODAL CONDUCTION
PATHS
Special pathways in atrial wall
Mixture of purkinje fiber and ordinary cardiac muscle
cells
Function to transmit impulses rapidly from SA node
to AV node
•ANTERIOR-------- BACHMAN
•MIDDLE-------------WENCKEBACH
•POSTERIOR-------THOREL

28. ANTERIOR INTERNODAL TRACT
Bachmann’s Bundle
BEGINNING -leaves the anterior end of the
sinuatrial node
COURSE -passes anterior to the superior vena
caval opening -descends on the atrial septum
TERMINATION - in the atrioventricular node.
Tract composed of both ordinary Myocardial &
Purkinje fibres

29. MIDDLE INTERNODAL
PATHWAY of Wenkebach
BEGINNING -leaves the posterior end of the
sinuatrial node
COURSE
passes posterior to the superior vena caval
opening descends on the atrial septum
TERMINATION - upper end of atrioventricular
node.

30. POSTERIOR INTERNODAL PATHWAY
of Thorel
BEGINNING -Leaves the posterior part of the
sinuatrial node
COURSE -descends through the crista terminalis
and the valve of the inferior vena cava
TERMINATION - Atrioventricular node.
Formed mainly of Purkinje type fibres

31. A V NODE

32. AV Node
Node of Tawara
Lies- Subendocardially in medial wall of Rt atrium
- 1cm above the opening of coronary sinus
- basal attachment of septal cusp of tricuspid valve
Histologically – “An entanglement ” – fine poorly striated
branching specialised myocardial fibres. No dense fibrous
matrix.
Artery to AV node – 90% - Right coronary artery
- 10 % - Circumflex branch of LCA
Delay of about 0.12 sec in conduction through AV node

35. AV bundle of His
No sharp demarcation
2-3 cm long- passes into the substance of
central fibrous body- to reach lower margin of
membranous part of the Ventricular septum.
Vulnerability – surgical repair of VSD.
Accessory conducting bundle- WPW Syndrome

37. RIGHT BUNDLE BRANCH
Considered continuation of AV bundle.
Compact bundle- 1 mm thick
Its intramyocardial course varies in length
before it reaches subendocardium on the right
side.
Principal branch of the right bundle passes into
the moderator band- septomarginal trabecula
Becomes continuous with fibers of Purkinje
fibers

39. LEFT BUNDLE BRANCH
Pierces the interventricular septum
Passes down on its left side beneath the
endocardium
Divides into two branches -Anterior /Posterior
Eventually become continuous with the fibers of
the purkinje plexus of the left ventricle.

40. TISSUE
CONDUCTION RATE
(m/s)
RELATIVE VALUE
SAN
0.05
SECOND LEAST
ATRIAL
PATHWAY
1
AVN
0.02 – 0.05
BUNDLE OF HIS
1
PURKINJE
SYSTEM
4
VENTRICULAR
MUSCLE
1
LEAST
HIGHEST

41. •ATRIAL DEPOLARIZATION COMPLETES
0.1 S
AV NODAL DELAY 0.1 SEC
SPREADING OF DEPOLARIZATION
PURKINJE FIBERS – VENTRICLE
0.08 – 0.1 S
DEPOLARIZATION WAVE MOVES
FROM LEFT TO RIGHT THROUGH SEPTUM
THE LAST PART OF THE HEART TO BE
DEPOLARIZED
POSTERO BASAL PORTION OF THE LV
PULMONARY CONUS
ARP
RRP
UPPER MOST PORTION OF THE SEPTUM

43. Conduction Defects

45. Conduction disturbances
First Degree AV block
Most commonly due to fibrosis of AV node or
toxicity of medications such as beta blockers or
calcium channel blockers
Other causes include edema of AV node region
after mitral and aortic valve replacement
Electrolyte disturbances

47. Conduction disturbances
Second-Degree AV block
Mobitz Type II & I blocks are common after
valve replacement surgery
Drug effect or toxicity should be excluded as
potential causes
Temporary pacing may be needed depending on
degree of AV block and HR

49. Conduction disturbances
Complete AV block
May be secondary to cardioplegia washout
during immediate postoperative period or as a
consequence of antiarrhythmic drug therapy
It may be seen after valve replacement
secondary to trauma of surgical manipulation in
the area of AV node or bundle of HIS

50. Conduction disturbances
Complete AV block
Factors which predict low likelihood of recovery
include -calcified Aortic valve
-delayed appearance of AV block
-significant preop conduction defect

53. CONDUCTION SYSTEM IN
CONGENITAL ANOMALIES

54. Atrial Septal Defect
There are 3 major types:
Secundum ASD – at the Fossa Ovalis, most
common.
• Primum ASD – lower in position & is a form of AVSD,
MV cleft.
• Sinus Venosus ASD – high in the atrial septum,
associated w/partial anomalous venous return & the
least common.

55. ASD
ECG can be helpful in differentiating a primum ASD from the other forms of
ASD.
Because the triangle of Koch where the AV node and bundle of His are
usually located is absent in the setting of a primum ASD, the bundle must
pass in a more inferior direction to gain access to the ventricular septum.
This is associated with left axis deviation and a counterclockwise loop.
It is extremely rare for there to be left axis deviation with a secundum ASD
where the axis is more likely to be rightward than leftward depending on the
degree of right ventricular hypertrophy.
It is not uncommon to see a partial right bundle branch block reflecting right
ventricular intraventricular conduction delay

56. ASD
Unoperated ASD – Atrial fibrillation/flutter
AV NODE – DISPLACED/HYPOPLASTIC
Post operativelyCHILD -
Adults -
Junctional escape rhythm/
Atrioventricular dissociation/
Sick sinus syndrome
FLUTTER/ RBBB

57. SURGICAL IMPLICATIONS
Surgery for sinus venosus ASD is a rather complex undertaking
to avoid atrial arrhythmias.
When the sinus venosus defect is associated with an
anomalous pulmonary vein low in the superior vena
cava, usually one atrial incision away from the sino-atrial node
can provide enough exposure to safely close the ASD and
avoid conduction problems.
If the anomalous pulmonary veins drain high in the superior
vena cava, then an alternative operation is necessary. The
operation is called a Warden operation

58. VSD
Isolated VSD comparable to TOF
Perimembranous defect- Non branching
bundle can be considerably long- directly
underneath the septal remnant
Posteroinferior area of the rim is most critical
area
Muscular outlet defects – away from
conduction bundle
Muscular inlet defects-conduction axis at
antero superior quadrant

59. VSD
The perimembranous VSD is intimately
associated with the bundle of His which in
a d-loop heart passes through the tricuspid
annulus at the posterior and inferior corner
of the VSD.
The bundle soon branches into the right
and left bundle branch

61. Shallow Stitching Close to the Rim of the Ventricular
Septal Defect Eliminates Injury to the Right Bundle Branch

62. CORRECTED TGA
Since the right atrium must connect with the left ventricle (i.e.
atrioventricular discordance), it is not surprising that the
conduction system is abnormal. Pioneering work in this area
was undertaken by Anderson and colleagues.
In corrected transposition (C-TGA), the functional
atrioventricular node arises anteriorly and superiorly and is
usually lodged between the annulus of the mitral valve .
This functional AV node is therefore superior to the usual
location of the AV node which may be present as an
accessory node.

63. CORRECTED TGA
Often there is a posterior atrioventricular node in its usual
position within the triangle of Koch, but it is usually
disconnected from the remainder of the conduction tissue.
The conduction system in C-TGA is more tenuous than that of
normal hearts. Fibrosis of the junction between the
atrioventricular node and the atrioventricular bundle has been
seen in older patients
Artrial switch operation- Post operative arrhythmia less
compared to Mustard and Senning operation.

64. Tetrolgy of Fallot
4 components
VSD – PERIMEMBRANOUS/ MUSCULAR
Post op- RBBB
- SA node dysfunction
- Ventricular arrhythmias
- Complete heart block
Sudden Death – Fatal ventricular arrhythmias
Surgical approach – Right atrial vs right
ventricular

65. UNIVENTRICULAR HEART
Categorised – Left or right – based on
morphological operative single ventricle
Single right ventricle- no conduction
disturbances.
Single left ventricle- AV node is hypoplastic
- Prolonged PR interval
culminating in complete heart block

66. Tricuspid Atresia
Complete absence
of communication
between the right
atrium and right
ventricle
About 3 % of
congenital heart
disease

67. Tricuspid atresia with / with out
transposition
SA node is normal.
Posterior small AV node originates in close
relation to Tendon of Todaro.
Occasionally, the branching bundle may
be in close proximity to the posteroinferior rim
of the foramen and the right bundle-branch may
lie subendocardially in the rim of the defect.

68. Surgical implication
It is important, therefore, to appreciate
that the atrioventricular node is in close relation
to the tendon of Todaro, which is a readily
identifiable landmark during surgical exposure.
Closure of the foramen should usually be
accomplished safely provided that
deep sutures are not placed in the
posteroinferior quadrant.

69. POST OP ARRHYTHMIAS
Usual type of arrythmias with Atrial surgery are
SVT of which AF, Atrial flutter and junctional
rhythms are most common.
In large ostium primum type defect because of
posteriorly displaced AV node , it is frequently
associated with prolonged AV conduction.
Small osteum secundum defect causes no
problem during repair.

70. Hypothermia, ischemic arrest , direct injury to
conduction system, haematoma, injury to SA
nodal artery , oedema , forign body reaction to
suture material all are responsible for
arrhythmias
The most common conduction disturbance that
occurs after ventricular surgery is RBB block .
RBBB can be due to direct injury to main RBB
or right ventriculotomy ( in fallots tetrology
surgery ) by disrupting the right ventricular
subendocardial purkinje network

71. Post cardiac surgery
arrhythmias
Potential causes and precipitating factors
•Myocardial ischemia or infarction
•Hemodynamic instability
•Electrolyte abnormalities
a) Hypokalemia, b) Hypomagnesemia
•Metabolic disturbances
a) Acidosis, b) Alkalosis, c) Hypoxemia
•Drugs
a) Sympathomimetics, b) Antiarrhythmics, c) Anesthetic
•Reperfusion effect
•Tissue trauma or inflammation, indwelling catheters
•Increase in catecholamines

72. RECENT ADVANCES

73. Optical mapping/calcium imaging of dococs226 mutants reveals disrupted cardiac
conduction.
Chi N C et al. PNAS 2010;107:14662-14667
©2010 by National Academy of Sciences

74. Cardiac conduction, independent of hemodynamic flow or cardiac contraction, is required for
cardiomyocyte morphogenesis.
Chi N C et al. PNAS 2010;107:14662-14667
©2010 by National Academy of Sciences

75. GENE MAPPING
.
Mutations of Nkx2.5 - lead not only to structural
cardiac abnormalities
But also to progressive atrioventricular block.
FAMILIAL
Atrial septal defects and cardiac conduction
abnormalities - shown to have mutations of Nkx2.5

76. Kearns-Sayre Syndrome
Kearns-Sayre Syndrome is disorder characterized by external
opthalmoplegia, pigmentary degeneration of the retina,
premature dementia, and a dilated cardiomyopathy, often with
progressive conduction defect.
Most cases represent new deletions but there are reports of
familial transmission of the disorder.
Depending on the exact size and location of the mitochondrial
DNA deletion, patients may also exhibit weakness of facial,
pharyngeal, trunk and extremity muscles, deafness, short
stature, and markedly increased cerebrospinal fluid proteins.

77. Progressive Cardiac Conduction Defect
Progressive cardiac conduction defect (PCCD), also called
Len`egre or Lev disease,
It is characterized by progressive slowing of conduction
through the His-Purkinje system leading to right or left bundle
branch block and, ultimately, to complete atrioventricular
block, syncope, and sudden death.
Several familial cases of PCCD have been described,
Gene responsible for the disorder has been localized to
chromosome 19q13.3

78. HELLO– ANY QUESTIONS

79. Thank you
Have A Great Day…