Ventricular fibrillationI49.0

Ludwig and Hoffa were the first to describe ventricular fibrillation in 1849 (Fröhlig 2006).

In 1888, Mac William suspected ventricular fibrillation to be the cause of sudden cardiac death and thus established the idea of defibrillation (Fröhlig 2006).

11 years later, Prevost and Batelli were able to interrupt ventricular fibrillation in an animal for the first time by applying a high electrical voltage. It was not until 1932 that Kouwenhoven gained his first clinical experience with external defibrillators. Defibrillation of a human heart was first successfully performed in 1947 by the surgeon Beck from Cleveland (Fröhlig 2006).

In the 1940s, Wiggers described 4 different phases of ventricular fibrillation (for more details see "Classification" [Fröhlig 2006]).

Ventricular fibrillation (VF) is a pulseless cardiac arrhythmia caused by uncoordinated ineffective chaotic activation of the ventricular myocardium, which leads to circulatory arrest (Herold 2023).

A distinction is made between primary and secondary ventricular fibrillation. (van Aken 2007):

• Primary ventricular fibrillation:

This is usually caused by myocardial ischemia and occurs most frequently in the context of CHD. It is found in about 20 % of all cases of myocardial infarction (Secchi 2009).

Primary ventricular fibrillation is the most common cause of death within the first 24 hours after a myocardial infarction. It is also the cause of sudden cardiac death in approx. 90 % of cases (Roskamm 2004).

• Secondary ventricular fibrillation:

Secondary ventricular fibrillation occurs less frequently and can occur, for example, after a shock or in the context of heart failure (Secchi 2009). It is also found in primary ventricular tachycardia caused by degeneration (Michels 2017).

Wiggers divided ventricular fibrillation into 4 phases:

1. undulatory phase

This represents the transition from sinus rhythm to ventricular fibrillation and can begin with one or more depolarizations

2. convulsive phase

In this phase, the action potential shortens and the conduction velocity decreases. This phase lasts approx. 30 - 40 s

3. tremulous phase

As ischaemia increases, conduction slows down more and more, small depolarizations begin to travel more slowly around the ventricle and initiate the stage lasting approx. 2 - 3 min.

4th atonic phase

In this phase, the metabolic consequences of ischemia develop and slow down the excitation more and more until they lead to a stage of absent electrical activity (Fröhlig 2006).

Ventricular fibrillation is caused by a disordered activation of the ventricular myocardium as a result of multiple reentry excitations (Paul 2018).

The following diseases can lead to a reduction in the fibrillation threshold:

• Heart diseases such as
  • CHD
  • myocardial infarction
  • myocarditis
  • Cardiomyopathy including genetic cardiomyopathy
  • Severe heart failure
• Electrolyte disturbances such as:
  • Hypokalemia
  • Hypomagnesemia
• In the context of an apoplexy or apoplexy (very rare)
• Electrical accident
• Primary electrical diseases of the heart such as ion channel diseases (Herold 2023)

Ventricular fibrillation arises pathophysiologically through two mechanisms:

• 1. arrhythmogenic substrate

This is an ischemic zone in the area of the myocardium or an infarct area. Various factors such as circulating catecholamines, hyper- or hypothermia, metabolic disorders, sympathoadrenergic imbalance or arrhythmogenic drugs can influence the fibrillation threshold (Larsen 2022).

• 2 Trigger

The trigger is ultimately an R to T extrasystole or - more rarely - a ventricular tachycardia or an idioventricular rhythm (Larsen 2022).

The uncoordinated, high-frequency electrical activity of the heart muscle cells in ventricular fibrillation does not cause any ejection of the heart, which in turn leads to an immediate failure of the pumping function and thus to an interruption of the blood supply to all vital organs. As a result, the oxygen undersupply with the resulting acidosis in the heart muscle cells constantly increases and ultimately electrical activity is no longer possible, the ventricular fibrillation turns into asystole (Ullrich 2005).

The diagnosis is usually made by an ECG (Herold 2023).

• ECG

The ECG shows arrhythmic high-frequency fibrillation waves with a frequency >. 300 / min. At the beginning, these fibrillation waves can appear coarse, later on as fine (Herold 2023).

QRS complexes cannot be visualized, the morphology is constantly changing (Fröhlig 2006).

• Ventricular flutter

Ventricular flutter is a regular tachycardia (Braun 2022) with a frequency between 200 - 300 / min (Haas 2011).

• Sudden cardiac death (Braun 2022)

If ventricular fibrillation occurs, there is an absolute indication for immediate cardioversion at 50 or 100 J. Cardiopulmonary resuscitation measures should be carried out until the defibrillator is available (van Aken 2007).

As hypokalemia and tachycardia promote ventricular fibrillation, high normal potassium levels should be aimed for and beta-blockers should be used at an early stage (Roskamm 2004).

Without rapid treatment, ventricular fibrillation ends in asystole within 12 - 15 minutes (Secchi 2009).

Primary ventricular fibrillation generally has a better prognosis (van Aken 2007). If defibrillation can be performed within the first minute after the onset of ventricular fibrillation, the survival rate is 90 - 95 % (Larsen 2022).

Secondary ventricular fibrillation is lethal in approx. 40 % of cases. The long-term prognosis is not good due to the severe myocardial damage (Roskamm 2004).

In ventricular fibrillation, the total amplitude correlates with the likelihood of successful defibrillation. With amplitudes < 1 mm, defibrillation is rarely successful (van Aken 2007).

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