Excitation of the sinus muscle in the heart is transmitted to the working muscles of the atria, but these are electrically insulated from the ventricles, so that transmission of excitation at this point can occur only through the conduction of excitation by the atrioventricular node. Transmission through the muscle cell-containing atrioventricular node is delayed, thus enabling the coordinated rhythmic contraction of atrial and ventricular muscles in the first place. When the transmission of excitation through the atrioventricular node is no longer rapid enough or fails, physicians refer to it as AV block, whereas accelerated transmission of excitation usually results in palpitations and an elevated pulse in Wolff-Parkinson-White syndrome.
What is the atrioventricular node?
The atrioventricular node is also called the atrioventricular node or the Aschoff-Tawara node. First described in 1906 by Ludwig Aschoff and his student Sunao Tawara, the junction is part of the conduction of excitation in the heart. Excitation from the sinus node is transmitted to the ventricles via the atrioventricular node with a delay. The delay in excitation transmission is represented on the ECG as PQ time and is what allows coordination of contractions of the atrial and ventricular muscles in the first place. The atrioventricular node is thus the single, electrical connection between the atria and the ventricles. With a power velocity of 0.04 to 0.1 m/s, this part of the heart has the lowest conduction velocity. If the sinus node fails, the atrioventricular node may also take over its function.
Anatomy and structure
The atrioventricular node is located on the wall between the right and left atria of the heart. Thus, the conduction of excitation sits close to the border between the atria and the ventricle. The area of the right atrium, and thus the sensation of the atrioventricular node, is also called Koch’s triangle and continues into the excitation conduction of the His bundle. This His bundle can be divided into two legs, which, like the atrioventricular node, can be traced back to the research of Sunao Tawara. The legs of the His bundle are therefore also known as Tawara legs. Like all other cardiac excitatory conduits, the atrioventricular node is composed of individual cardiac myocytes that make its transmission function possible.
Function and Tasks
The sinoatrial node plays the role of the beat generator in cardiac function. Thus, this part of the heart makes the heart beat in a specific rhythm, which is also known as the sinus beat. Excitation thus emanates from the sinus node and reaches the working muscles of the heart in the atria. The working muscles of the atria eventually transmit the received excitation from the sinus node. However, the working muscles of the atria are electrically insulated from the ventricles by connective tissue. Thus, the excitation of the sinus node cannot reach the muscles of the ventricles in this way. Therefore, the atrioventricular node is required for transmission of excitation to the ventricular muscles. Transmission through the node occurs with a significant delay. In order for the ventricles to fill as well as possible, the atria contract first. The ventricles finally contract due to the delayed transmission of excitation by the atrioventricular node only after a certain time, thus ensuring filling of the ventricles.
Diseases
Among the most common complaints associated with the atrioventricular node is AV block. This is a common cardiac arrhythmia that results from a delayed or interrupted atrioventricular node. Often, AV block goes unnoticed. Unnoticed block usually corresponds to first-degree block. However, severe AV block causes the heart to beat more slowly. Thus, the phenomenon triggers what is known as bradycardia, which in the worst scenario causes the chambers to temporarily stop beating. Severe AV block therefore usually requires a pacemaker to bring the disturbed transmission back to normal. Such a severe disturbance of the node is also referred to as third-degree AV block. Any AV block can be diagnosed by ECG, where it can be seen as a prolonged PQ time, depending on its severity. Congenital AV block is extremely rare, but may occur in the context of a congenital heart defect. In most cases, however, AV block is acquired.They thus usually result from degenerative changes in the heart. Myocardial inflammation or infections, for example, can pave the way for an AV block. Normally, a patient with this clinical picture is initially treated with medication to bridge the gap. After a certain time, however, patients with AV block of severity two and three usually receive a pacemaker, since drug therapy is considered unreliable for this symptomatology. The opposite of AV block is accelerated conduction between the ventricles and the atrium. This phenomenon can occur, for example, in Wolff-Parkinson-White syndrome. This is also a cardiac arrhythmia that is usually triggered by an additional conduction pathway between the ventricles and atria. The accelerated conduction usually manifests itself in a strongly increased pulse and usually causes palpitations, i.e. tachycardia. In most cases, tachycardia can be self-regulated by the patient. For example, the pulse and heart rhythm settle down again by pressing hard or holding one’s breath. In addition, the physician usually provides tachycardia patients with medications such as Ajmalin. Unlike slowed transmission of sinus node excitation, surgical intervention is not indicated in most cases of accelerated conduction of excitation in the form of tachycardia.
Typical and common heart diseases
- Heart attack
- Pericarditis
- Heart failure
- Atrial fibrillation
- Heart muscle inflammation
