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Ventricular fibrillation (V-fib or VF) is a cardiac condition that consists of a lack of coordination of the contraction of the muscle tissue of the large chambers of the heart that eventually leads to the heart stopping altogether.
Ventricular fibrillation is a medical emergency. If the arrhythmia continues for more than a few seconds, blood circulation will cease, as evidenced by lack of pulse, blood pressure and respiration, and death will occur.
Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly, rather than contracting in unison, and so the ventricles fail to pump blood into the arteries and into systemic circulation. Ventricular fibrillation is a sudden lethal arrhythmia responsible for many deaths in the Western world, mostly brought on by ischaemic heart disease. Despite much work, the underlying nature of fibrillation is not completely understood. Most episodes of fibrillation occur in diseased hearts, but others occur in so-called normal hearts. Much work still has to be done to elucidate the mechanisms of ventricular fibrillation.
Lyman Brewer suggests that the first recorded account of ventricular fibrillation dates as far back as 1500 BC, and can be found in the Ebers papyrus of ancient Egypt. The extract recorded 3500 years ago may even date from as far back as 3500 BC. It states: "When the heart is diseased, its work is imperfectly performed: the vessels proceeding from the heart become inactive, so that you cannot feel them … if the heart trembles, has little power and sinks, the disease is advanced and death is near." Whether this is a description of ventricular fibrillation is debatable [Brewer LA 1983]. The next recorded description occurs 3000 years later and is recorded by Vesalius who described the appearance of "worm-like" movements of the heart in animals prior to death.
The significance and clinical importance of these observations and descriptions possibly of ventricular fibrillation were not recognised until John Erichsen in 1842 described ventricular fibrillation following the ligation of a coronary artery [Erichsen JE 1842]. Subsequent to this in 1850, fibrillation was described by Ludwig and Hoffa when they demonstrated the provocation of Ventricular fibrillation in an animal by applying a "faradic" current to the heart [Hoffa M et al. 1850].
In 1874, Edmé Félix Alfred Vulpian coined the term mouvement fibrillaire, a term, which he seems to have used to describe both atrial and ventricular fibrillation [Vulpian A 1874]. John A. MacWilliam, a physiologist who had trained under Ludwig and who subsequently became Professor of Physiology at the University of Aberdeen, gave an accurate description of the arrhythmia in 1887. This definition still holds today, and is interesting in the fact that his studies and description predate the use of electrocardiography. His description is as follows - "The ventricular muscle is thrown into a state of irregular arrhythmic contraction, whilst there is a great fall in the arterial blood pressure, the ventricles become dilated with blood as the rapid quivering movement of their walls is insufficient to expel their contents; the muscular action partakes of the nature of a rapid incoordinate twitching of the muscular tissue…The cardiac pump is thrown out of gear, and the last of its vital energy is dissipated in the violent and the prolonged turmoil of fruitless activity in the ventricular walls." MacWilliam spent many years working on ventricular fibrillation and was one of the first to show that ventricular fibrillation could be terminated by a series of induction shocks through the heart [MacWilliam JA 1887].
The first electrocardiogram recording of ventricular fibrillation was by August Hoffman in a paper published in 1912 [Hoffman A 1912]. At this time, two other researchers, Mines and Garrey, working separately, produced work demonstrating the phenomenon of circus movement and re-entry as possible substrates for the generation of arrhythmias. This work was also accompanied by Lewis who performed further outstanding work into the concept of "circus movement."
Later milestones include the work by Kerr and Bender in 1922 who produced an electrocardiogram showing ventricular tachycardia evolving into ventricular fibrillation [Kerr WJ et al. 1922]. The re-entry mechanism was also advocated by DeBoer who showed that ventricular fibrillation could be induced in late systole with a single shock to a frog heart [De Boer S 1923]. The concept of "R on T ectopics" was further brought out by Katz in 1928 [Katz LN 1928]. This was called the “vulnerable period” by Wiggers and Wegria in 1940 who brought to attention the concept of the danger of premature ventricular beats occurring on a T wave.
Another definition of VF was produced by Wiggers in 1940. He described ventricular fibrillation as - "an incoordinate type of contraction which, despite a high metabolic rate of the myocardium, produces no useful beats. As a result, the arterial pressure falls abruptly to very low levels, and death results within six to eight minutes from anemia of the brain and spinal cord." [Wiggers CJ et al. 1940].
Spontaneous conversion of ventricular fibrillation to a more benign rhythm is rare in all but small animals. Defibrillation is the process that converts ventricular fibrillation to a more benign rhythm. This is usually by application of an electric shock to the myocardium and will be discussed later.
Mechanisms of ventricular fibrillation
Zipes divides the mechanisms of arrhythmia genesis into disorders of impulse formation and disorders of impulse conduction or both [Zipes DP 1994]. Zipes reminds us of the caveat that the present diagnostic tools do not permit unequivocal determination of the electrophysiological mechanisms responsible for most clinically occurring arrhythmias or their ionic basis. This he states is especially true for ventricular arrhythmias. In general terms, it is almost impossible to separate re-entry and automaticity. In most circumstances, we are able only to suggest that such an arrhythmia is consistent with a particular underlying mechanism.
For many years, due to the practical problems involved with mapping large areas of the heart simultaneously, ventricular fibrillation has been hard to study. Most observers have confined their interest and work to the induction and termination of ventricular fibrillation. Much of the current data on the dynamic electrophysiological changes during cardiac arrhythmias comes either from computer modeling, electrode studies or the use of high-resolution optical mapping and mathematical models.
Ventricular fibrillation has been described as "chaotic asynchronous fractionated activity of the heart" [Moe et al. 1964]. A more complete definition is that ventricular fibrillation is a "turbulent, disorganised electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction" [Robles de Medina 1978].
Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority, it is a manifestation of underlying ischaemic heart disease. Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis and other heart pathologies. It is also seen with electrolyte disturbances and overdoses of cardiotoxic drugs. It is also notable that ventricular fibrillation occurs where there is no discernible heart pathology or other evident cause, the so-called idiopathic ventricular fibrillation.
Idiopathic ventricular fibrillation occurs with a reputed incidence of approximately 1% of all cases of out-of-hospital arrest, as well as 3%-9% of the cases of ventricular fibrillation unrelated to myocardial infarction, and 14% of all ventricular fibrillation resuscitations in patients under the age of 40 [Viskin S et al 1990]. It follows then that, on the basis of the fact that ventricular fibrillation itself is common, idiopathic ventricular fibrillation accounts for an appreciable mortality. Recently-described syndromes such as the Brugada Syndrome may give clues to the underlying mechanism of ventricular arrhythmias. In the Brugada syndrome, changes may be found in the resting ECG with evidence of right bundle-branch block (RBBB) and ST elevation in the chest leads V1-V3, with an underlying propensity to sudden cardiac death [Brugada P et al. 1992].
The relevance of this is that theories of the underlying pathophysiology and electrophysiology must account for the occurrence of fibrillation in the apparent "healthy" heart. It is evident that there are mechanisms at work, which we do not fully appreciate and understand. Investigators are exploring new techniques of detecting and understanding the underlying mechanisms of sudden cardiac death in these patients without pathological evidence of underlying heart disease [Saumarez RC et al 1995].
Sudden cardiac arrest is the leading cause of death in the industrialised world. It exacts a significant mortality with approximately 70,000 to 90,000 sudden cardiac deaths each year in the United Kingdom, and survival rates are only 2% (National Institute for Health and Clinical Excellence Guidelines 2000). The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction ("heart attack") [Myerburg RJ et al. 1995]. During ventricular fibrillation, cardiac output drops to nil, and, unless terminated promptly, death usually ensues within minutes.
The condition can often be reversed by the electric discharge of direct current from a defibrillator. If no defibrillator is available, a precordial thump can be delivered at the onset of VF to regain cardiac function. Antiarrhythmic agents like amiodarone or lidocaine can help, but, unlike atrial fibrillation, VF rarely reverses spontaneously in large adult mammals. Although a defibrillator is designed to correct the problem, and its effects can be dramatic, it is not always successful.
In patients at high risk of ventricular fibrillation the use of an implantable cardioverter defibrillator has been shown to be beneficial.
The role of re-entry or circus motion was demonstrated separately by Mines and Garrey [Mines GR 1913, Garrey WE 1914]. Mines created a ring of excitable tissue by cutting the atria out of the ray fish. Garrey cut out a similar ring from the turtle ventricle. They were both able to show that, if a ring of excitable tissue were stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a refractory period that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of ischaemic or infarcted myocardium, or underlying scar tissue.
It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance - the propagation velocity - will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the wavefront.
In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through hypertrophy or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.
Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a hypoxic myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one pacemaker. This may well lead to the generation of a circus-entry arrhythmia. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may be the trigger to generate re-entry arrhythmias.
It is interesting to note that most cardiac pathologies with an associated increased propensity to arrhythmia development have an associated loss of membrane potential. That is, the maximum diastolic potential is less negative and therefore exists closer to the threshold potential. Cellular depolarisation can be due to a raised external concentration of K+, a decreased intracellular concentration of Na+, increased permeability to Na+, or a decreased permeability to K+. The ionic basis of automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to –50 to –60 mV. Myocardial cells are exposed to different environments. Normal cells may be exposed to hyperkalaemia; abnormal cells may be perfused by normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia. In conditions such as myocardial ischaemia, possible mechanism of arrhythmia generation include the resulting decreased internal K+ concentration, the increased external K+ concentration, norepinephrine release and acidosis [Ho K 1993].
Triggered activity can occur due to the presence of afterdepolarisations. These are depolarising oscillations in the membrane voltage induced by preceding action potentials. These can occur before or after full repolarisation of the fiber and as such are termed either early (EADs) or delayed afterdepolarisations (DADs). All afterdepolarisations may not reach threshold potential, but, if they do, they can trigger another afterdepolarisation, and thus self-perpetuate.
Characteristics of the ventricular fibrillation waveform
Ventricular fibrillation can be described in terms of its electrocardiographic waveform appearance. All waveforms can be described in terms of certain features, such as amplitude and frequency. Researchers have looked at the frequency of the ventricular fibrillation waveform to see if it helps to elucidate the underlying mechanism of the arrhythmia or holds any clinically useful information. More recently, Gray has suggested an underlying mechanism for the frequency of the waveform that has puzzled investigators as possibly being a manifestation of the Doppler effect of rotors of fibrillation [Gray RA et al. 1998]. Analysis of the fibrillation waveform is performed using a mathematical technique known as Fourier analysis
The distribution of frequency and power of a waveform can be expressed as a power spectrum in which the contribution of different waveform frequencies to the waveform under analysis is measured. This can be expressed as either the dominant or peak frequency, i.e., the frequency with the greatest power or the median frequency, which divides the spectrum in two halves.
Frequency analysis has many other uses in medicine and in cardiology, including analysis of heart rate variability and assessment of cardiac function, as well as in imaging and acoustics [Shusterman V et al. 1999, Kaplan SR et al. 2000].
- Atrial fibrillation
- Cardiac arrest
- Electric shock