Ventricular fibrillation: Wikis


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Ventricular fibrillation
Classification and external resources

ECG lead showing VF
ICD-10 I49.0
ICD-9 427.41
DiseasesDB failure.htm Heart failure
MeSH D014693

Ventricular fibrillation (V-fib or VF) is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver rather than contract properly. While there is activity, perhaps best described as "writhing like a can filled with worms" it is undetectable by palpation (feeling) at major pulse points of the carotid and femoral arteries especially by the lay person. Such an arrhythmia is only confirmed by ECG/EKG. Ventricular fibrillation is a medical emergency that requires prompt BLS/ACLS interventions because should the arrhythmia continue for more than a few seconds, blood circulation will cease, and sudden cardiac death (SCD) may occur in a matter of minutes.


Signs and symptoms

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly, rather than contracting in a coordinated fashion (from the apex of the heart to the outflow of the ventricles), 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.



Abnormal automaticity

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. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias.

It is interesting to note that most cardiac zain 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 potassium ions K+, a decreased intracellular concentration of sodium ions 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[1].


The role of re-entry or circus motion was demonstrated separately by Mines and Garrey[2]. 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 was 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.


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, disorganized electrical activity of the heart in such a way that the recorded electrocardiographic deflections continuously change in shape, magnitude and direction"[3].

Ventricular fibrillation most commonly occurs within diseased hearts, and, in the vast majority of cases, is a manifestation of underlying ischemic heart disease. Ventricular fibrillation is also seen in those with cardiomyopathy, myocarditis, and other heart pathologies. In addition, it is 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[4]. 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[5].

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 that 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[6].

Familial conditions that predispose individuals to developing ventricular fibrillation and sudden cardiac death are often the result of gene mutations that affect cellular transmembrane ion channels. For example, in Brugada Syndrome, sodium channels are affected. In certain forms of long QT syndrome, the potassium inward rectifier channel is affected.

Triggered activity

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[7]. Analysis of the fibrillation waveform is performed using a mathematical technique known as Fourier analysis.

Power spectrum

Ventricular firilation as seen in lead II

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[8][9].



Electric defibrillator

The condition can often be reversed by the electric discharge of direct current from a defibrillator. Although a defibrillator is designed to correct the problem, and its effects can be dramatic, it is not always successful.

Implantable electric defibrillator

In patients at high risk of ventricular fibrillation, the use of an implantable cardioverter defibrillator has been shown to be beneficial.

Precordial thump

If no defibrillator is available, a precordial thump can be delivered at the onset of VF to regain cardiac function. However, research has shown that the precordial thump releases no more than 30 joules of energy. This is far less than the 300–360 J typically used to bring about normal sinus rhythm. Consequently, in the hospital setting, this treatment is not used.

Antiarrhythmic agents

Antiarrhythmic agents like amiodarone or lidocaine can help, but, unlike atrial fibrillation, ventricular fibrillation rarely reverses spontaneously in large adult mammals.


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%[10]. The majority of these deaths are due to ventricular fibrillation secondary to myocardial infarction, or "heart attack"[11]. During ventricular fibrillation, cardiac output drops to zero, and, unless remedied promptly, death usually ensues within minutes.

History of Knowledge 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.[12] 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" (electrical) current to the heart.[13]

In 1874, Edmé Félix Alfred Vulpian coined the term mouvement fibrillaire, a term that he seems to have used to describe both atrial and ventricular fibrillation[14]. 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[15].

The first electrocardiogram recording of ventricular fibrillation was by August Hoffman in a paper published in 1912 [16]. 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[17]. 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[18]. The concept of "R on T ectopics" was further brought out by Katz in 1928[19]. 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"[20].

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 is discussed in detail in the relevant article.


  1. ^ Ho K 1993
  2. ^ Mines GR 1913, Garrey WE 1914
  3. ^ Robles de Medina EO, Bernard R, Coumel P, et al. (1978). "Definition of terms related to cardiac rhythm. WHO/ISFC Task Force". Eur J Cardiol 8 (2): 127–44. PMID 699945.  
  4. ^ Viskin S, Belhassen B (1990). "Idiopathic ventricular fibrillation". Am. Heart J. 120 (3): 661–71. doi:10.1016/0002-8703(90)90025-S. PMID 2202193.  
  5. ^ Brugada P, Brugada J (1992). "Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report". J. Am. Coll. Cardiol. 20 (6): 1391–6. PMID 1309182.  
  6. ^ Saumarez RC, Heald S, Gill J, et al. (1995). "Primary ventricular fibrillation is associated with increased paced right ventricular electrogram fractionation". Circulation 92 (9): 2565–71. PMID 7586358.  
  7. ^ Jalife J, Gray RA, Morley GE, Davidenko JM (1998). "Self-organization and the dynamical nature of ventricular fibrillation". Chaos 8 (1): 79–93. doi:10.1063/1.166289. PMID 12779712.  
  8. ^ Shusterman V, Beigel A, Shah SI, et al. (1999). "Changes in autonomic activity and ventricular repolarization". J Electrocardiol 32 Suppl: 185–92. doi:10.1016/S0022-0736(99)90078-X. PMID 10688324.  
  9. ^ Kaplan SR, Bashein G, Sheehan FH, et al. (2000). "Three-dimensional echocardiographic assessment of annular shape changes in the normal and regurgitant mitral valve". Am. Heart J. 139 (3): 378–87. doi:10.1016/S0002-8703(00)90077-2. PMID 10689248.  
  10. ^ National Institute for Health and Clinical Excellence Guidelines 2000
  11. ^ Myerburg RJ et al. 1995
  12. ^ Brewer LA (1983). "Sphygmology through the centuries. Historical notes". Am. J. Surg. 145 (6): 696–702. doi:10.1016/0002-9610(83)90124-1. PMID 6344674.  
  13. ^ Hoffa M et al. 1850
  14. ^ Vulpian A 1874
  15. ^ MacWilliam JA 1887
  16. ^ Hoffman A 1912
  17. ^ Kerr, WJ et al. 1922
  18. ^ De Boer S 1923
  19. ^ Katz LN 1928
  20. ^ Wiggers, CJ et al. 1940

See also

External links

Study guide

Up to date as of January 14, 2010

From Wikiversity

Rhythm Strip : Ventricular Fibrilation

Ventricular Fibrilation (VF) is a heart rhythm found in cardiac arrest. VF is characterised by chaotic electrical impulses, which originate in the ventricles. These chaotic impulses fail to create Systole, causing inadequate perfusion.

Defibrillation is the largest part of treatment, depolarizing the heart and allowing a normal sinus rhythm to be reestablished. After several attempts at defibrillation, (usually three) CPR and intubation can be initiated to facilitate better management.

Antiarrythmics, such as amiodarone are widely used in conjunction with a defibrillator, but have little value on their own. The causes of cardiac arrest can vary greatly, (i.e following trauma, to shock and drugs) or can be entirely spontaneous. Recovery can (rarely) also be spontaneous, known as ROSC (return of spontaneous circulation)

Prognosis, as with all forms of cardiac arrest is decidedly poor.



Sudden cardiac death can be viewed as a continuum of electromechanical states of the heart: ventricular tachycardia (VT), VF, pulseless electrical activity (PEA), and asystole. VF is the most common initial state, and, because of insufficient perfusion of vital cardiac tissues, it degenerates to asystole if left untreated.

The etiology of VF remains incompletely understood. It often occurs in the setting of acute cardiac ischemia or infarction, and acute myocardial infarction (MI) is diagnosed in up to half of sudden-death survivors. The incidence of sudden death is also relatively high in the postinfarction period for months after an MI. Abnormal rapid stimulation of the ventricles can lead to fibrillation. This can occur during VT or in conditions, such as Wolff-Parkinson-White syndrome, when atrial fibrillation or flutter waves pass rapidly through a bypass tract to the ventricular musculature. Severe left ventricular dysfunction, a variety of cardiomyopathies, and acquired or idiopathic long QT syndrome also increase the risk of fibrillation.

Multiple events may lead to the initiation of VF. One etiology is mechanical or electrical stimulation of the myocardium during the early phase of repolarization (termed R-on-T phenomenon). When an impulse is delivered to the heart during the time period that corresponds to the upslope of the T wave, the ventricular myocardium is in a variable state of excitability because some of the muscle is still partly or completely refractory. The impulse may propagate electrically through the tissue but at a decreased rate through a tortuous pathway. Slowed abnormal conduction may allow the wave of depolarization to circle around and reexcite areas that have had sufficient time for repolarization.

Sustained VF may be due to a relatively small number of macroreentrant circuits or rotors, which are relatively stationary or drift through the 3-dimensional volume of the ventricular myocardium. These rotors may activate the cardiac muscle fibers at a high frequency, with secondary wavefronts emanating, traveling, and breaking up at variable distances from the source.

All fibrillation is not the same. VF begins as a coarse, irregular deflection on the ECG, then degenerates to a fine, irregular pattern, and eventually becomes asystole. These electrocardiographic changes reflect the electrical changes described above. The probability of successful defibrillation decreases as the VF waveform becomes smoother with time.



Because of the critical importance of early defibrillation, prehospital care is vital for arrests due to VF that occur outside the hospital. Interventions that impact survival and outcome of resuscitation include the following:

  • Witnessed or early recognition of an arrest
  • Early activation of emergency medical services (EMS) system
  • Bystander CPR slows the degeneration of VF and improves survival.

Traditionally, CPR consists of artificial respirations and chest compressions. Mounting evidence demonstrates that chest compressions are the critical action to provide some cardiac perfusion during CPR, and artificial respirations are less important. Interruption of chest compressions to perform artificial respirations by a single resuscitator causes a loss of cardiac perfusion pressure, and even after restarting compressions, it may take some time before the previously obtained perfusion pressure is restored. Current guidelines recommend both artificial respirations and chest compressions for all patients as described in the algorithm below. Future guidelines may reflect developments in this ongoing area of research.

  • Automated external defibrillator (AED) application and defibrillation by trained personnel in the field

AEDs have revolutionized prehospital VF management because they decrease the time to defibrillation. This is accomplished by having the units prepositioned in the field where cardiac arrests are likely to occur (eg, airports, casinos, jails, malls, stadiums, industrial parks), eliminating the need for rhythm-recognition training and increasing the number of trained personnel and laypeople that can defibrillate at the scene.

AEDs are programmed to recognize 3 shockable rhythms: coarse ventricular fibrillation, fine ventricular fibrillation, and rapid ventricular tachycardia. Modern units have a sensitivity greater than 95% and specificity approaching 100% for the 3 shockable rhythms. The greatest difficulty is in distinguishing fine ventricular fibrillation from asystole.

AEDs can also be used for children. A pediatric dose-attenuating system should be used, if available, for children up to the age of 8 years, and a conventional AED can be used for children at or older than 8 years or with a corresponding weight of at least 25 kg (55 lb).

  • Early access to trained EMS personnel capable of performing CPR, defibrillation, and advanced cardiac life support (ACLS)

Emergency Department / In-Hospital Arrests


Electrical external defibrillation remains the most successful treatment of VF. A shock is delivered to the heart to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objective is to interfere with all reentrant arrhythmia and to allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker.

Successful defibrillation largely depends on the following 2 key factors: duration between onset of VF and defibrillation, and metabolic condition of the myocardium. VF begins with a coarse waveform and decays to a fine tracing and eventual asystole. These electrical changes that occur over minutes are associated with a depletion of the heart's energy reserves. CPR slows the progression of these events, but defibrillation is the primary treatment to interrupt the process and return the heart to a perfusing rhythm. Defibrillation success rates decrease 5-10% for each minute after onset of VF. The likelihood of defibrillation success can also be predicted based on the smoothness of the VF tracing. In strictly monitored settings where defibrillation was most rapid, 85% success rates have been reported.

Factors that affect the energy required for successful defibrillation include the following:

  • Paddle size: Larger paddles result in lower impedance, which allows the use of lower energy shocks. Approximate optimal sizes are 8-12.5 cm for an adult, 8-10 cm for a child, and 4.5-5 cm for an infant.
  • Paddle-to-myocardium distance (eg, obesity, mechanical ventilation): Position one paddle below the outer half of the right clavicle and one over the apex (V4-V5). Artificial pacemakers or implantable defibrillators mandate use of anterior-posterior paddle placement.
  • Use of conduction fluid (eg, disposable pads, electrode paste/jelly)
  • Contact pressure
  • Elimination of stray conductive pathways (eg, electrode jelly bridges on skin)
  • Previous shocks may lower the chest wall impedance and decrease the defibrillation threshold.

Biphasic defibrillation has a number of advantages over monophasic defibrillation including increased likelihood of defibrillation success for a given shocking energy. While this has not translated into a proven survival benefit thus far, if less shocks are required, there may be less interruption of CPR. Lower energy shocks associated with biphasic defibrillation may lead to less myocardial stunning after repeated defibrillation attempts. Furthermore, smaller and lighter defibrillation units are required to produce a biphasic waveform, and this is an important advantage for portable AED units.

Patients with VF for 4-5 minutes or more at the time defibrillation becomes available may benefit from a 1- to 3-minute period of CPR prior to initial defibrillation. The theoretical benefit of this intervention is "to prime the pump" by restoring some oxygen and other critical substrates to the myocardium to allow successful contraction post defibrillation. The benefit of this intervention has been demonstrated in a prospective clinical trial, and it has now been included as an optional protocol for Emergency Medical Services (EMS) in the ACLS guidelines.{Ref1}

The theoretical benefit of vasopressor medicines, such as epinephrine and vasopressin, is that they increase coronary perfusion pressure. Coronary perfusion pressure is the difference between aortic and right atrial pressure during the relaxation phase of CPR, and it determines myocardial blood flow. Higher levels of coronary perfusion pressure are associated with increased survival in animal models of VF arrest.

Vasopressors, such as epinephrine, increase coronary perfusion pressure; however, no vasopressors have been proven to increase survival in humans. Nevertheless, they are recommended due to possible benefit. Epinephrine, 1 mg, is recommended every 3-5 minutes once IV or IO access is established, and vasopressin, 40 units, may be administered once instead of the first or second epinephrine dose. Higher doses of epinephrine, 0.1-0.2 mg/kg, have been studied, but they are not clearly beneficial compared with the standard 1-mg dose. Recent data suggest no synergistic effect of administering vasopressin in addition to epinephrine.

Medication Therapy

Antidysrhythmic agents are recommended when initial defibrillation and vasopressor medicines fail or after successful defibrillation to prevent recurrence. Potential benefits of antidysrhythmic therapy include lowering the threshold for defibrillation and preventing immediate or delayed VF recurrence. Potential risks of antidysrhythmic therapy include hypotension due to decreased myocardial contractility or vascular tone, bradycardia, or asystole. No antidysrhythmic agent has been proven to improve survival to hospital discharge from VF arrest, but amiodarone may increase the likelihood of at least temporarily regaining a perfusing rhythm.

The mechanism of action of most antidysrhythmic agents is to alter the conductance of ions, such as sodium and potassium, across myocardial cell membrane ion conducting channels. Amiodarone and other Vaughn-Williams class III agents decrease the repolarizing flow of potassium across the cell membrane and cause a prolongation of the depolarized period. The cell is refractory to further excitation during this period and may not be able to conduct the VF waveform, thus breaking the reentrant cycle of excitation. Other class III agents that have been studied in cardiac arrest include bretylium and sotalol, but they have not been consistently shown to provide benefit.

Lidocaine is a Vaughn-Williams class IB agent that alters the depolarizing flow of sodium across the cell membrane and may be particularly effective in an ischemic or acidotic environment. Procainamide is a Vaughn-Williams class IA agent that affects both sodium and potassium flow across the cell membrane and may also rarely be used for refractory or recurrent VF.

Simple English


Ventricular fibrillation (often shortened to VF or V-Fib) is a cardiac arrhythmia in which there is an uncoordinated contraction of the cardiac muscle of the ventricles in the heart. The heart is unable to pump blood around the body properly, and ventricular fibrillation can cause tachycardia and hypoxia. Ventricular fibrillation is a medical emergency. If it is allowed to continue for more than a few seconds, the blood will stop circulating, which is what causes the loss of a pulse and respiration, and the person will die.

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly when it should contract in unison, and the ventricles cannot pump blood into the arteries and into the systemic circulation.


Ventricular fibrillation 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, but they are not always effective. Antiarrhythmic agents such as amiodarone or lidocaine can help, but, unlike atrial fibrillation, ventricular fibrillation rarely reverses spontaneously in large adult mammals. Although a defibrillator is designed to correct the problem, it is not always successful.

In patients at high risk of ventricular fibrillation the use of an implantable cardioverter-defibrillator has been shown to help.


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