Conduction system of heart
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CONDUCTION SYSTEM OF HEART
Presenter-Dr. Jyotindra SinghNIZAMS INSTITUTE OF MEDICAL SCIENCES,HYDERABAD
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SEMINAR PLANDEVELOPMENTAL ASPECT
INTRODUCTION / COMPONENTS
PHYSIOLOGICAL ASPECT
CONDUCTION DISTURBANCES
CONGENITAL ANOMALIES
SURGICAL IMPLICATIONS
RECENT UPDATES
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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
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DEVELOPMENT CONDUCTION SYSTEM
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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
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The Tube Bends
SV
AV
BV D
The tube, as it grows, cannot be accommodated within the pericardial cavity and undergoes bending.
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CONDUCTION SYSTEM OF HEART
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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.
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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
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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
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CONDUCTION SYSTEM OF THE HEART
1.SINO ATRIAL NODE
2. INTERNODAL ATRIAL PATHWAY
3.ATRIOVENTRICULAR NODE
4.BUNDLE OF HIS
5.PURKINJEE SYSTEM
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Bundle of HIS
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BUNDLE BRANCHES
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Impulse Conduction through the Heart
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ORIGIN AND SPREAD OF CARDIAC EXCITATION
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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
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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
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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
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SA Node Potentials
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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
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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
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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.
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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
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A V NODE
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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
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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
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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
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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.
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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
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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
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Conduction Defects
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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
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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
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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
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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
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CONDUCTION SYSTEM IN CONGENITAL ANOMALIES
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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.
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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
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ASDUnoperated ASD – Atrial fibrillation/flutter
AV NODE – DISPLACED/HYPOPLASTIC
Post operatively-
CHILD - Junctional escape rhythm/
Atrioventricular dissociation/
Sick sinus syndrome
Adults - FLUTTER/ RBBB
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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
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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
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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
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Shallow Stitching Close to the Rim of the Ventricular Septal Defect Eliminates Injury to the Right Bundle Branch
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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.
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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.
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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
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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
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Tricuspid Atresia
Complete absence of communication between the right atrium and right ventricle
About 3 % of congenital heart disease
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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.
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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.
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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.
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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
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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
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RECENT ADVANCES
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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
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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
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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
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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
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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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