Chamber replacement rhythm

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A ventricular escape rhythm (syn. Ventricular escape rhythm , chamber automaticity , English Ventricular escape beat ) is a cardiac arrhythmia , which as impulse formation disorder to failure or blockage of the parent energization forming centers (here: the sinus node and atrioventricular node ) occurs.

root cause

Spread of excitation in a healthy heart with a graphic representation of an ECG curve

The pathogenesis of a ventricular replacement rhythm is based on the unique ability of the heart muscle cells to "excite themselves", this is known as self-depolarization . In a healthy heart, normal excitation always runs from the sinus node (approx. 60-80 beats per minute) via AV nodes (approx. 40-60 beats per minute), bundles of His , Tawara thighs and Purkinje fibers to the working muscles ( → excitation conduction system ). This works because the sinus node has the shortest repolarization time (recovery of the cell after excitation) and can therefore trigger a new excitation in the heart before another cell does this.

If the sinus node, which normally depolarizes at approx. 60–80 bpm , does not generate any excitation due to a pathological disorder, this is taken over by subordinate cells, in this case the AV node first. The heart then only beats at a rate of approx. 40–60 bpm. If this mechanism does not work either, for example due to damage to the AV node or due to an AV block (type III), the first depolarization or excitation comes directly from cells that are in the ventricular plane (His- Bundle, tawara limbs, Purkinje fibers, single myocardial cell).

The ventricles and atria are thus excited independently of one another and no longer contract synchronously. The contraction of the heart chambers then only takes place at around 20–40 bpm.


Due to the greatly slowed heartbeat and the associated reduced ejection capacity ( cardiac output ), the affected person primarily feels symptoms of a circulatory disorder:

Typical symptoms of reduced blood flow to the heart can also occur ( angina pectoris ):


In addition to the symptoms described above, a noticeably slower and occasionally irregular pulse can be determined in the patient . An obligatory electrocardiography usually shows widened ventricular complexes ( QRS complex ), but occasionally also narrow ventricular complexes, as well as incoherent atrial and ventricular excitation.


A chamber replacement rhythm is the result of a serious disorder in the heart. The administration of β-mimetic catecholamines (e.g. orciprenaline ) can attempt to accelerate ventricular excitation . In the preclinical emergency situation it is indicated to increase the heart rate with an external pacemaker ( transcutaneous pacemaker ) in order to achieve a more stable blood supply to the organs.

Clinically, the search for the cause of the occurrence of the ventricular replacement rhythm and its control is crucial. Nevertheless, in the majority of cases it is necessary to implant a pacemaker in order to maintain a regular and adequate heart rate in the future.

Individual evidence

  1. Pschyrembel - Clinical Dictionary . 259th edition. de Gruyter, 2002, p. 828 .
  2. R. Huch, C. Bauer: Man - Body - Illness . 4th edition. Urban & Fischer, 2003, p. 279 .
  3. C.-S. So: Practical EKG interpretation . 3. Edition. Thieme, 2004, p. 146 ff .
  4. H.-P. Hündorf, P. Rupp: Textbook for preclinical emergency medicine . 2nd Edition. Stumpf and Kossendey, 2000, p. 109 ff .