AV node, atrial ventricular node, Aschoff-Tawara nodeThe AV node is part of the excitation conduction system of the heart. It also consists of the sinus node, the His bundle and the tawara legs. After the sinus node, the AV node forms the secondary pacemaker center in this system and transmits the excitation to the His bundle, which is subsequently divided into the two tawara legs. The regulation of the heart rate is the primary function of the excitation conduction system.
Anatomy
The AV node is located in the so-called Koch triangle, which is located in the right atrium near the atrial septum. Macroscopically (i.e. “with the naked eye”) it is difficult to distinguish it from the surrounding structures. Nerve tracts coming from the sympathetic nervous system as well as nerve tracts coming from the parasympathetic nervous system draw to the AV node and thus regulate its function. The AV node usually receives its blood supply from the arteria coronaria dextra.
Histology
Cardiomyocytes are specific heart muscle cells that form the AV node. These are poor in myofibrils and mitochondria compared to the cells of the working muscle (myocardium) of the heart.
Function
The function of the AV node is to transmit excitation from the sinus node to the His bundle. Since the excitation of the heart muscle cells does not simply pass through the connective tissue of the heart skeleton to excite the cells of the chamber muscles, the AV node is required. This is the only electrical connection between the atria and ventricles that transmits the excitation.
It induces a delay, which is important for heart function. This delay is also called the atrioventricular transfer time (AV time) and is important for the contraction of the atria and the chambers of the heart to take place in a coordinated manner. In the ECG this delay can be read off as a PQ interval.
Pathophysiology
If the sinus node can no longer fulfil its function, the AV node can take over the task of primary rhythm generator. However, the heart rate is then only 40-60 beats per minute. The time delay can also be too long or even fail completely, resulting in the clinical picture of the so-called AV block.
A distinction is made here between three degrees. In 1st degree AV block, the transition time between atrium and ventricle is longer. In the ECG this is visible as a longer PQ stretch (> 200 ms).
Usually the patients have no symptoms and no treatment is required. In 2nd degree AV block, the excitation transfer fails partially. There are two forms: With Mobitz type I (Wenckebach block) the transfer time (=PQ interval in the ECG) becomes longer with each heart action until a transfer fails completely at some point.
After the failure of the transfer, the PQ interval is extended in strokes from the beginning (Wenckebach period). This form of AV block generally has a good prognosis. With the 2nd degree AV block of the Mobitz II type, the transition time is not extended in principle (no increased PQ interval in the ECG), but every second, third or fourth atrial contraction is not passed on to the chamber.
The prognosis is less favourable than that of 2nd degree AV block, as the probability of developing a 3rd degree AV block is greater. In 3rd degree AV block, also called total AV block, the conduction between the atrium and the ventricles of the heart is completely absent. The atrium and ventricle beat completely uncoordinated and independently of each other.
The ventricle can develop a substitute rhythm, which then runs independently of the sinus rhythm. However, this is usually not sufficient to supply the body with oxygen-rich blood. The ECG does not show any connection between the P-wave (atrial fibrillation) and the QRS complexes (chamber excitation).
The opposite case, an accelerated transition between atrium and ventricle, is present in Wolff-Parkinson-White syndrome. This is caused by an additional (=accessory) conduction path between the atrium and the ventricle. Via this additional pathway, the excitation from the ventricle can be conducted back into the atrium and thus induce a new excitation in the ventricles via the AV node.
This results in the image of a circular movement and a seizure-like tachycardia (the heart beats much too fast). Typical here is the sudden appearance of a very high pulse (often 150 to 230 beats per minute), which ends just as abruptly.
