CONDUCTION SYSTEM OF HEART

Presenter-Dr. Jyotindra SinghNIZAMS INSTITUTE OF MEDICAL SCIENCES,HYDERABAD

SEMINAR PLANDEVELOPMENTAL ASPECT

INTRODUCTION / COMPONENTS

PHYSIOLOGICAL ASPECT

CONDUCTION DISTURBANCES

CONGENITAL ANOMALIES

SURGICAL IMPLICATIONS

RECENT UPDATES

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

The primitive cardiac tube has five zones:

the arterial trunk

the bulbus cordis ) the ventricle

the atrium

and the sinus venosus

DEVELOPMENT CONDUCTION SYSTEM

The cardiac tube grows at a greaterlongitudinal rate then the rest of theembryo, causing it to fold. As it does thisit falls to the right. This is known asd-looping. It may fall to the left in anl-loop: this will lead to a malformed heart.

.

normal d-loop l-loop

The Tube Bends

SV

AV

BV D

The tube, as it grows, cannot be accommodated within the pericardial cavity and undergoes bending.

CONDUCTION SYSTEM OF HEART

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.

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

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

CONDUCTION SYSTEM OF THE HEART

1.SINO ATRIAL NODE

2. INTERNODAL ATRIAL PATHWAY

3.ATRIOVENTRICULAR NODE

4.BUNDLE OF HIS

5.PURKINJEE SYSTEM

Bundle of HIS

BUNDLE BRANCHES

Impulse Conduction through the Heart

ORIGIN AND SPREAD OF CARDIAC EXCITATION

SA NODE of Keith & FlackPacemaker 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

WHY SA NODE LEADS THE HEART?

TISSUE RATE OF IMPULSEGENERATION

SA NODE 70-80/MIN

AV NODE 40 – 60/MIN

BUNDLE OF HIS 40/MIN

PURKINJE SYSTEM 24/MIN

Depolarization of SA NodeSA 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

SA Node Potentials

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

INTERNODAL CONDUCTION PATHS

ANTERIOR INTERNODAL TRACTBachmann’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

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.

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

A V NODE

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

AV bundle of HisNo 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

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

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.

TISSUE CONDUCTION RATE(m/s)

RELATIVE VALUE

SAN 0.05 SECOND LEAST

ATRIALPATHWAY

1

AVN 0.02 – 0.05 LEAST

BUNDLE OF HIS 1

PURKINJE SYSTEM

4 HIGHEST

VENTRICULAR MUSCLE

1

ARP RRP

• ATRIAL DEPOLARIZATION COMPLETES0.1 S

AV NODAL DELAY 0.1 SEC

SPREADING OF DEPOLARIZATIONPURKINJE FIBERS – VENTRICLE0.08 – 0.1 S

DEPOLARIZATION WAVE MOVESFROM LEFT TO RIGHT THROUGH SEPTUM

THE LAST PART OF THE HEART TO BEDEPOLARIZED

POSTERO BASAL PORTION OF THE LV

PULMONARY CONUS

UPPER MOST PORTION OF THE SEPTUM

Conduction Defects

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

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

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

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

CONDUCTION SYSTEM IN CONGENITAL ANOMALIES

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.

ASDECG 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

ASDUnoperated ASD – Atrial fibrillation/flutter

AV NODE – DISPLACED/HYPOPLASTIC

Post operatively-

CHILD - Junctional escape rhythm/

Atrioventricular dissociation/

Sick sinus syndrome

Adults - FLUTTER/ RBBB

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

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

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

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

CORRECTED TGASince 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.

CORRECTED TGAOften 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.

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

UNIVENTRICULAR HEARTCategorised – 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

Tricuspid Atresia

Complete absence of communication between the right atrium and right ventricle

About 3 % of congenital heart disease

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.

Surgical implicationIt 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.

POST OP ARRHYTHMIASUsual 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.

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

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

RECENT ADVANCES

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

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

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

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.

Kearns-Sayre Syndrome

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

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Progressive Cardiac Conduction Defect

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