Corpus: Conduction system of the heart

The cardiac conduction system is an autonomous system of specialised cardiac muscle cells (pacemaker cells) that generate electrical signals through spontaneous depolarisation and transmit them to the working myocardium. It forms the basis for the coordinated contraction sequence of the heart (systole/diastole).

From a physiological point of view, a distinction can be made between excitation conduction and excitation generation. This is why the term excitation generation system is also used, which is then occasionally equated with the sinus node. However, this distinction is rather academic, as both systems form a unit and each part of the excitation conduction system can also take over excitation formation, e.g. if a higher pacemaker centre fails (secondary excitation formation).

The autonomic nervous system exerts a modulating influence on the excitation conduction system. The vagus nerve (parasympathetic nervous system) has an inhibitory effect via its rami cardiaci, while the nervi and rami cardiaci of the sympathetic nervous system have an accelerating effect. Fibres from both systems radiate into the cardiac plexus close to the heart, which controls the excitation conduction system. The parasympathetic fibres are connected in the ganglia cardiaca.

See also: Dromotropy

The cells of the conduction system are cardiac muscle cells with a modified structure. They have fewer myofibrils and therefore a less pronounced cross striation. They are rich in fluid and contain more glycogen than normal cardiac muscle cells.

The following structures can be distinguished in the cardiac conduction system:

• Sinus node, located near the mouth of the superior vena cava on the right atrium
• Atrioventricular node (AV node), at the transition from the right atrium to the right ventricle
• His bundle, in the membranous section of the ventricular septum
• Tawara bundle, running as right and left bundle in the muscular section of the ventricular septum
• Purkinje fibres, as terminal branching of the Tawara legs in the ventricular musculature

Starting from the sinus node, the excitation spreads via the atria, which contract shortly before the start of systole. To prevent premature contraction of the ventricles, conduction is delayed in the AV node. This is followed by rapid propagation in all ventricular areas in order to make them beat powerfully and synchronously. The contraction is coordinated from the apex of the heart in the direction of the valve plane. At the same time, the valve plane is pulled towards the apex of the heart. This causes suction on the atria and enables the atria to fill during systole.

In addition to the aforementioned structures of the conduction system, some people have so-called accessory pathways (AP) between the atrium and ventricle (e.g. Kent, Mahaim, James bundle). These accessory pathways are congenital and develop due to a lack of resorption of cardiomyocytes during embryogenesis. In principle, they can occur anywhere along the valve plane or the septum; they occur most frequently on the left posterior wall (50 %), septal (30 %), right paraseptal (10 %) and right anterior (10 %).

Accessory pathways enable antegrade conduction of the atrial excitation with premature activation of part of the ventricular myocardium (pre-excitation) bypassing the AV node, the His bundle and the Tawara bundle branch. In some cases, they additionally or exclusively cause retrograde atrial excitation from the ventricle. Pre-excitation syndromes include Wolff-Parkinson-White syndrome and Lown-Ganong-Levine syndrome.

An accessory pathway can lead to AV reentry tachycardia (AVRT). A distinction is made between:

• orthodromic AVRT
• antidromic AVRT
• permanent junctional reciprocal tachycardia (PJRT)

As the APs have a significantly lower conduction delay, there is a risk of inducing ventricular fibrillation if atrial fibrillation or flutter is present at the same time.

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