**3. Conductiion system and its surgical significance**

#### **3.1. The development**

The coarseness of the apical trabeculation is the most constant feature of the right ventricle. The other differences are the direct septal attachment of the tension apparatus of the atrio‐

The inlet component is limited by the mitral valve and its tension apparatus. The mitral valve has two leaflets, the aortic or the anterior leaflet which is in fibrous continuity with the aortic valve, which is short and square and the other leaflet which is connected to the wall of the left

The leaflets do not have direct septal attachment unlike the right ventricle but instead attach

The apical myocardium is thin like the RV. The septum is not completely muscular unlike RV,

The muscular septal surface is characteristically smooth and the left bundle lies below the membranous septum corresponding to the zone of apposition between the right coronary and

The semilunar valves of the aortic and pulmonary valves are similar, the distal portion forms the sinotubular junction and the proximal part takes origin from the ventricular structure. The

The aorta and pulmonary artery form the vascular pedicle. The aorta gives rise to the brachio‐ cephalic or innominate artery, the left common carotid artery and the left subclavian artery. The pulmonary artery arises anteriorly and courses posteriorly, and is a short vessel giving rise to the right and left pulmonary arteries. The left pulmonary artery lies superior to the left bronchi in front of the descending aorta. The right pulmonary artery is anterior to the left main bronchus and has a long mediastinal course beneath the aortic arch and behind the superior vena cava to reach the hilum of the right lung. Sometimes a early branching large upper lobar

The coronary arteries arise from the aortic sinuses. According to Leiden convention the position is described in terms of an observer from the non-coronary sinus, the right hand of the person is called the sinus 1 and gives rise to the right coronary artery and left hand facing sinus is called the sinus 2 and gives rise to left coronary artery. The coronary artery arises beneath the sinotubular junction, and when it is displaced more than 1 cm from the ST junction

The left coronary artery has a single orifice,while in 50% there are two orifices in the right sinus, one gives rise to the main RCA and the smaller orifice gives rise to the infundibular or sinus nodal artery. It is important while giving ostial cardioplegia for stopping the heart to perform

The epicardial course of the coronary arteries follows the atrioventricular and interventricular grooves. The RCA gives to the acute marginal branches, the sinus nodal artery (55%), and

cardiac surgeries to instill into the smaller orifices to protect the sinus node.

ventricular valve, which is usually tricuspid in nature.

atrioventricular junction is called the mural or the posterior leaflet.

and it has a small membranous part which forms the subaortic outflow tract.

overall arrangement is like the crown, rather than forming an annulus. [9]

through anterolateral and posteromedial papillary muscles.

branch can be mistaken for the right pulmonary artery.

it is considered abnormal which occurs in 3.5% of hearts.

**2.4. The morphologic left ventricle**

228 Principles and Practice of Cardiothoracic Surgery

non-coronary leaflets.

The heart develops from the mesoderm from fusion of vascular channels which forms the heart tube. The heart starts beating from the time the embryo is 22 days old. Even from the beginning there is a polarity and the peristaltic type of motion of the tube starts from the venous end and ends in the arterial end. This sequential contraction ensures that even in the absence of valves there is very little regurgitation of the blood, and an ECG similar to the adult ECG is recognized at the end of 1st month. It is believed that this primitive heart tube persists as the remnant of conduction tissue and the myocardium grows around this to form the atrium and the ventricle. The conduction system is one of the most primitive structures in the heart which forms even before the heart tube starts looping.

There is a circle of conduction tissue at the atrioventricular junction, which as the atrioven‐ tricular valves form and the great arteries are assigned to the respective ventricles gradually becomes restricted.The only area of electrical continuity between the atrium and the ventricles is the AV node and the penetrating bundle where the muscular septum comes in contact with the AV junction. This establishes connection with the Purkinje network in the ventricular myocardium, to ensure sequential contraction of atrium and ventricles. (figure 4)

This sequence of events occurs in the usual d-looping of the heart.If there is l-looping of the heart as in congenitally corrected transposition, where the right atrium joins the left ventricle, which then gives rise to the pulmonary artery and the left atrium joins the right ventricle which gives rise to aorta, the bundle can be extremely elongated bringing it under the pulmonary valve anteriorly. The conduction system is vulnerable to injury during surgery and otherwise Both congenital and spontaneous heart blocks can occur at the rate of 2% per annum in this condition. [11]

sometimes it may be necessary to cut across the cavoatrial junction longitudinally which

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**3.** Sennings procedure –the SA node is at risk during suturing the pulmonary venous baffle.

**4.** Superior septal approach to the mitral valve – which may put the artery supplying the SA node at risk. Injury is manifested by nodal rhythm during which the P wave is absent in the ECG. The distal portion of the conduction system gradually takes over or the SA node

The AV node lies in the apex of the triangle of Koch, the penetrating bundle pierces the apex of the triangle and reaches the crest of the trabecular septum immediately beneath the membranous septum which is below the junction formed by the *right and noncoronary cusp*. It is in this area that the bundle is most vulnerable during surgical closure of ventricular septal defect. This corresponds to the commissure between the anterior and septal leaflets of the tricuspid valve which is usually supported by the medial papillary muscle.Sometimes there

The penetrating bundle crosses from the atrial septum to the aortic outflow and then joins the muscular septum. In normal hearts with normal alignment the apex of the triangle is close to the crest of the interventricular septum.The length of the bundle is small in this setting and this length of the non-branching bundle can be excessive in the presence of VSD in the inlet

It is only when the ventricular septum reaches the crux of the heart can a regular AV node join the AV conduction axis. The node and bundle is formed at the place where the ventricular

**a.** In perimembranous defects, which is also the type of defect usually seen in tetralogy of Fallot, the VSD patch should be sutured about 5 mm away from the posteroinferior margin, and in perimembranous defects with outlet extension the muscle protects the bundle and makes it more left sided and this makes the posteroinferior angle safe in VSD with outlet extension. It the perimembranous defects with inlet extension where the bundle is superficial and close to the posteroinferior angle of the defect, and hence is exposed to maximum risk of damage. The risk of damage to the node is minimal in cases

**c.** The fibrous tissue surrounding the VSD can be used to anchor the patch and this has to be differentiated from aneurysm of membranous septum which may sometimes harbour

itself recovers, making the need for a permanent pacemaker rare in this setting.

makes the SA node or the artery supplying this at risk.

is a cleft in the septal leaflet which points to this area.

A few rules may help avoid heart block while closing VSD's

**b.** The base of the septal leaflet tissue is always safe to place sutures.

of muscular and subpulmonic VSD's.

*3.2.2. Atrioventricular (AV) node*

portion of the ventricular septum.

septum joins the AV junction.

the bundle.

**Figure 4.** Conduction system

#### **3.2. Surgical perspective**

#### *3.2.1. Sinoatrial (SA) node*

SA node which is located at the lateral cavoatrial junction at the upper end of crista terminalis is the pacemaker which initiates contraction. This can be identified as a small oval shaped structure which is slightly more yellowish with SA nodal artery forming small ramifications over it.

This area is vulnerable during –


sometimes it may be necessary to cut across the cavoatrial junction longitudinally which makes the SA node or the artery supplying this at risk.


#### *3.2.2. Atrioventricular (AV) node*

**Figure 4.** Conduction system

230 Principles and Practice of Cardiothoracic Surgery

**3.2. Surgical perspective**

*3.2.1. Sinoatrial (SA) node*

This area is vulnerable during –

dividing the SVC.

over it.

SA node which is located at the lateral cavoatrial junction at the upper end of crista terminalis is the pacemaker which initiates contraction. This can be identified as a small oval shaped structure which is slightly more yellowish with SA nodal artery forming small ramifications

**1.** Glenn surgery – where the SVC is divided and anastomosed to the pulmonary artery end to side – the cavopulmonary anastomosis. Care has to be taken while clamping and

**2.** Sinus venosus atrial septal defect with partial anomalous pulmonary venous connection – some of the pulmonary veins can drain high into the SVC and during correction The AV node lies in the apex of the triangle of Koch, the penetrating bundle pierces the apex of the triangle and reaches the crest of the trabecular septum immediately beneath the membranous septum which is below the junction formed by the *right and noncoronary cusp*. It is in this area that the bundle is most vulnerable during surgical closure of ventricular septal defect. This corresponds to the commissure between the anterior and septal leaflets of the tricuspid valve which is usually supported by the medial papillary muscle.Sometimes there is a cleft in the septal leaflet which points to this area.

The penetrating bundle crosses from the atrial septum to the aortic outflow and then joins the muscular septum. In normal hearts with normal alignment the apex of the triangle is close to the crest of the interventricular septum.The length of the bundle is small in this setting and this length of the non-branching bundle can be excessive in the presence of VSD in the inlet portion of the ventricular septum.

It is only when the ventricular septum reaches the crux of the heart can a regular AV node join the AV conduction axis. The node and bundle is formed at the place where the ventricular septum joins the AV junction.

A few rules may help avoid heart block while closing VSD's


**d.** In AV canal defects the AV node and the coronary sinus are displaced inferiorly, and the AV node is placed in between the coronary sinus and the crest of interventricular septum at the so called 'NODAL triangle' rather than at the usual apex of the triangle of Koch. [12]

**5. The transition from fetal to neonatal circulation**

to leave the vestigial ligamentum teres and the ligamentum venosum.

the stabilization of many sick neonates before subjecting them to surgery [13].

ASD, VSD and PDA are the main lesions which shunt from left to right.

**6. The pathophysiology of L->R shunt lesions**

with signs of congestive heart failure (CHF) at this time.

diastolic murmur across the mitral valve.

The first breath causes the lungs to expand and oxygen content in the blood to increase and this provides the impetus for the ductus to constrict and close. The right ventricular output goes to the lungs and reaches the left atrium, the increased pressure in the left atrium causing the flap valve to shut, closing the foramen ovale. The umbilical vein and ductus venosus regress

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Maintaining the patency of ductus is critical to many potential fatal neonatal conditions. These can be any of the conditions in which the output of the heart through either the aorta or the pulmonary artery is critically reduced and the patent ductus maintains the flow from one great artery to the other. These are hypoplastic left heart syndrome, critical aortic stenosis and pulmonary atresia. The presence of ductus is also useful in mixing lesions like TGA though the degree of mixing is much better in the presence of atrial level communication. Patency of ductus can be maintained by Prostaglandin E1 infusion, the availability of which has enabled

In Atrial septal defect, the size of the shunt is determined by the size of the defect and the degree of pulmonary vascular resistance. Small shunts cause no enlargement of cardiac chambers, while large shunt cause significant RA and RV dilatation, mid- diastolic flow murmur though the tricuspid valve and ejection systolic murmur at the left upper sternal border due to increased flow across the pulmonary valve. The left chambers do not increase

The pathophysiology of the shunt in VSD and PDA are similar. The magnitude of shunt is determined by the size of the defect and the degree of pulmonary vascular resistance (PVR); PVR is more important in the large defects where it determines the degree of shunt. Since PVR is elevated at birth and falls by 6-8 wks, children with large VSD typically become symptomatic

A small defect causes no enlargement of cardiac chambers, the ECG and X-ray are normal, there is ejection systolic murmur and P2 is normal. For moderate sized defects, there is LA and LV enlargement unlike ASD and as the RV is contracting at the time of left to right shunt, it undergoes no volume load. However the increased blood pumped by the RV causes mid-

Large defects and PDA cause CHF in infancy, especially if the PVR is low. This reflects in biventricular hypertrophy with increased saturations, pan systolic murmur and loud P2. As the PVR increases, the heart size becomes normal on Chest X-ray though the pulmonary

segment remains prominent, the murmur is reduced, and there is pure RVH in ECG

in size as the increased return to LA is decompressed into the RA through the defect.

Transient damage to the conduction system can occur as a result of myocardial protection during cardiopulmonary bypass, which should usually recover in less than 7 days. A perma‐ nent pacemaker is usually needed if sinus rhythm does not return in 9-10 days
