Introduction
In atrial fibrillation, our heart gets “out of sync” for various reasons and beats irregularly. About 1-2% of the total population suffer from this disease, making atrial fibrillation the most common persistent cardiac arrhythmia. Untreated, the risk of serious consequences, such as a stroke, increases enormously.
The ECG is the most important tool for making a diagnosis, as characteristic changes in atrial fibrillation are very common. The earlier therapeutic measures such as electrical cardioversion (“electroshock”) are taken, the more likely it is that our heart will return to the desired rhythm. In almost all cases, those affected must also take medication to “thin the blood“.
Normally, all sections of our heart work together as a well-rehearsed team. This creates a regular rhythm of the heartbeat. The “main clock generator” for this is a small nerve node in the wall of the right atrium – the sinus node.
From there, the electrical excitation is transmitted to other nerve points and fibers (e.g. AV nodes) within the heart muscle. This creates a directed excitation wave, so that atria and ventricles contract one after the other and pump blood into our circulation. In atrial fibrillation, on the other hand, the heart “gets out of rhythm”.
For various reasons, uncoordinated or undirected electrical excitation “circles” in the atria. As a result, the atria work independently of the ventricles and can no longer support them in their pumping function. Due to the chaotic circular excitations, the atria degenerate into rapidly successive twitches and “flicker”.
Fortunately, not all of these faulty electrical impulses are transmitted to the ventricles, otherwise life-threatening ventricular fibrillation would be the result! The responsible nerve point is the AV node in the cardiac septum, which serves as a kind of “filter” and ideally transmits only a few of the disturbing excitations to the ventricles. As the duration of atrial fibrillation increases, a change in the heart muscle cells and their electrical properties can be observed. Experts then speak of “cardiac remodelling”, which makes therapy considerably more difficult.
