Ventricular Fibrillation: Pathophysiology, Etiology, Epidemiology, Causes, Symptoms, Prognosis and Treatment

A heart rhythm that produces a rapid and inadequate heartbeat and endangers life.

Ventricular fibrillation (VF) is a life-threatening cardiac arrhythmia in which the coordinated contraction of the ventricular myocardium is replaced by a high-frequency disorganized excitation, which causes the heart not to pump blood.

VF is the most commonly identified arrhythmia in patients with cardiac arrest. In the prehospital setting, 65-85% of patients in cardiac arrest have VF identified as the initial rhythm by the emergency services personnel. Ventricular fibrillation usually ends in death in minutes unless immediate corrective measures are established.

The survival rate in out-of-hospital cardiac arrest has increased with the expansion of community-based emergency rescue systems, the widespread use of automated external defibrillators (AEDs), and the number of laypeople trained in cardiopulmonary resuscitation (CPR).

Ventricular fibrillation is treated with advanced cardiac life support (ACLS) protocols in hospital settings. Long-term treatment can be achieved with medical therapy or an implantable cardioverter-defibrillator (ICD) placement.

Surgical correction of underlying disorders (e.g., percutaneous coronary intervention, coronary artery bypass surgery) may also be indicated.


Ventricular fibrillation occurs in various clinical situations, but it is often associated with coronary artery disease (CAD). Ventricular fibrillation can result from an acute myocardial infarction (MI), ischemia, or myocardial scarring of an old infarct.


Ventricular tachycardia (VT) can degenerate into VF. The accumulation of intracellular calcium, the action of free radicals, metabolic alterations, and autonomous modulation are important influences in the development of VF during ischemia.

The onset of VF can occur in several ways.

For example, if a premature ventricular complex stimulates the myocardium during the ascending extremity of the T wave, the impulse can propagate erratically through the variable refractory myocardial cells and establish reentry patterns that result in chaotic ventricular depolarization. Consequently, the coordinated myocardial contraction is interrupted.

The reentry patterns are divided into multiple more petite wavelets, and the level of disorganization increases with reentry circuits that produce high-frequency activation of cardiac muscle fibers. As the heart loses its ability to pump blood, myocardial ischemia worsens, and a vicious self-perpetuating cycle occurs that leads to death if not corrected.

In the electrocardiogram (ECG), ventricular fibrillation manifests as a chaotically irregular pattern. This pattern is initially thick but becomes thinner as ventricular disorganization increases. As the ECG waveform flattens, the probability of successful defibrillation decreases.


Coronary artery disease (CAD) is the most common etiologic factor predisposing patients to ventricular fibrillation. In survivors of cardiac arrest, CAD is observed with stenosis greater than 75% in 40-86% of patients, according to the age and sex of the population studied. In post-mortem studies of people who have died from VF, extensive atherosclerosis is the most common pathological finding.

In an autopsy study of 169 cases of coronary death, approximately 61% of patients had died suddenly of presumed VF, and another 15% of subjects showed more than 75% stenosis in 3 or 4 vessels and similarly severe injuries in At least two glasses No coronary artery injury is associated with an increased risk of ventricular fibrillation.

However, only approximately 20% of autopsies related to VF have shown evidence of a recent MI. A higher proportion of autopsies (40-70%) show evidence of a healed myocardial infarction. Many of these hearts also reveal evidence of plaque fissures, hemorrhage, and thrombosis.

The Coronary Artery Surgery Study (CAC) showed that improving surgically or restoring blood flow to the ischemic myocardium decreased the risk of VF, especially in patients with the 3-vessel disease and heart failure, compared with medical treatment.

This finding suggests that transient acute ischemia is one of the main events triggering sudden arrhythmic death. It is believed that the effectiveness of beta-blockers in decreasing premature death rates.

This is especially true when administered to patients with myocardial infarction with ventricular fibrillation, VT, and high frequency premature ventricular contractions (VLP). This is due in part to the ability of beta-blockers to decrease ischemia. Beta-blockers also increase the threshold of Ventricular fibrillation in ischemic animals and reduce the rate of ventricular ectopia in patients with MI.

Reperfusion of the ischemic myocardium with thrombolysis or angioplasty may induce transient electrical instability by several different mechanisms. One of these, the spasm of the coronary artery, exposes the myocardium to ischemia and insults of reperfusion.

Possible mechanisms of coronary vasospasm include:

  • Factors of the autonomic nervous system, especially alpha-adrenergic activity.
  • Vagal activity.
  • Susceptibility of the recipient.
  • Humoral factors, particularly those associated with the activation and aggregation of platelets.

Non-atherosclerotic coronary artery abnormalities are also associated with a higher incidence of sudden death. Such exceptions include congenital lesions, embolism, arteritis, and mechanical abnormalities, such as coronary artery aneurysms.

When documentation of antecedent rhythm is available, it often shows that rapid TV precedes ventricular fibrillation. In patients with chronic ischemic heart disease, monomorphic VT derived from a reentrant focus is the most common precursor of VF.

Other factors associated with an increased risk of VF include frequent CVP, particularly complex forms (such as CVP multiform), and others with short coupling intervals (RTT phenomenon).

Although many individuals have anatomical and functional cardiac substrates that predispose them to ventricular arrhythmias, only a tiny percentage develop VF. The interaction between regional ischemia left ventricular (LV) dysfunction and transient inciting events (e.g., aggravated ischemia, acidosis, hypoxemia, wall tension, drugs, metabolic alterations) has been proposed as the precipitator of the FV.

It is estimated that 3-9% of cases of VT and VF occur in the absence of myocardial ischemia. Up to 1% of patients with out-of-hospital cardiac arrest have idiopathic ventricular fibrillation without discernible structural heart disease.

Up to 15% of patients under 40 years of age who experience ventricular fibrillation do not have underlying structural heart disease. In a 1993 study, Belhassen and Viskin noted that 4 of 11 patients with a history of VF and without structural heart disease had histological abnormalities on the endomyocardial biopsy.


Many episodes of ventricular fibrillation are not seen, so it isn’t easy to assess an exact incidence. Of the approximately 300,000 cases of MSC that occur each year in the United States, up to a third are attributed to FV. This represents 0.08-0.16% per year in the adult population, representing more deaths than lung cancer, breast cancer, or acquired immunodeficiency syndrome (AIDS).

VF occurs in the pediatric and adolescent age groups, with an annual incidence of 1.3-8.5 cases per 100,000 people, representing approximately 5% of all deaths in this group. VF is usually the first expression of EAC and is responsible for about 50% of deaths from CAD. VF often occurs within the first hour after the onset of acute MI or acute coronary syndrome.

In several population studies, the incidence of out-of-hospital cardiac arrest in the United States has been observed a decrease in the last two decades. Still, the proportion of sudden deaths due to VF in patients with CAD has not changed.

There is a high incidence of VF among specific subgroups of the population (e.g., patients with chronic heart failure with ejection fraction <30%, patients in convalescent phase after myocardial infarction, and patients who survived a cardiac arrest); however, only a tiny percentage of the total number of VF events occur in these patients.

Survivors of a significant cardiovascular event have an increased risk of ventricular fibrillation in the first 6-24 months after the event. Up to 30% of cardiac arrest survivors may experience recurrent VF during the first year after.

The frequency of FV in other western industrialized nations is similar to that of the United States. The incidence of VF in different countries varies due to the prevalence of CAD in these populations. It is believed that the trend towards a higher frequency of VF events in developing countries reflects a change in dietary and lifestyle habits.

Cardiovascular events, including PVF ECF (but not asystole), occur more frequently in the morning and may be related to an increase in platelet aggregation. There also appears to be an increase in sudden cardiac deaths (MCS) during the winter months.


When the human heartbeats, the electrical impulses that trigger a contraction must follow a specific path to the heart. If there is something wrong with the passage of these impulses, arrhythmias or irregular heartbeats can occur.

When the muscles of the heart’s four chambers become tense, a heartbeat occurs. During a heartbeat, a camera closes and pushes the blood.

The muscle atria or smaller upper chambers contract and fill the relaxed ventricles with blood during a heartbeat.

The contraction begins when the sinus node, a small group of cells in the right atrium, emits an electrical impulse that causes the right and left atria to contract.

The electrical impulse continues to the heart’s center, to the atrioventricular node. This node is located in the pathway between the atria and the ventricles. The urge travels through the ventricles from the atrioventricular node, causing them to contract.

As a result, blood is pumped from the heart to the body.


The most common signs of ventricular fibrillation are a sudden collapse or fainting because the muscles and brain have stopped receiving blood from the heart.

Approximately one hour before ventricular fibrillation, some people experience:

  • Dizziness.
  • Nausea.
  • Chest pain.
  • Tachycardia or accelerated heartbeat and palpitations.


The chances of survival of an index event of VF depend on the spectator’s cardiopulmonary resuscitation (CPR), the availability or rapid arrival of personnel and devices for defibrillation and advanced life support, and transportation to a hospital.

Although patients with non-traumatic cardiac arrest are more likely to renew from ventricular fibrillation than from any other arrhythmia successfully, success depends a lot on time. The probability of success usually decreases at 2-10% per minute.

Early defibrillation often makes the difference between long-term disability and functional recovery. The placement of automated external defibrillators (AEDs) in all communities and public training on their use has the potential to improve the outcomes of sudden cardiac death (SCD).

In patients who come to an emergency department (ED) after an episode of ventricular fibrillation, the prognosis of morbidity and mortality can be determined by calculating the cardiac arrest score developed by Thompson and McCullough.

This score is based on systolic blood pressure, the time from the loss of consciousness to the return of spontaneous circulation, and the capacity for neurological response.

However, even under ideal circumstances, only 20% of people who suffer cardiac arrest outside the hospital survive until discharge from the hospital.

In a survival study of out-of-hospital cardiac arrest in New York City, only 1.4% of patients survived hospital discharge. On the other hand, studies in suburban and rural areas have indicated survival rates of up to 35%.

Routine coronary angiography, with percutaneous coronary intervention (PCI), if indicated, together with mild therapeutic hypothermia (central temperature of 32-34 ° C for 24 hours), may favorably alter the prognosis of patients resuscitated with stable hemodynamics after cardiac arrest in the hospital.

In a retrospective study of cardiac arrest survivors, 65.6% of patients who underwent an early coronary angiography survived hospital discharge, compared to 48.6% of those who did not receive coronary angiography.

A crucial adverse result of episodes of ventricular fibrillation is anoxic encephalopathy, which occurs in 30-80% of patients. A Minnesota study of all adult cardiac arrest survivors related to out-of-hospital VF between 1990 and 2008 found that long-term survivors had long-term memory deficits.

Treatment and management

Acute ventricular fibrillation (VF) is treated according to the protocols of advanced cardiac life support (ACLS). Interest in improving the rates of public cardiopulmonary resuscitation (CPR) training, with particular emphasis on the use of early defibrillation with automatic external defibrillators (AEDs) by public service personnel (e.g., fire, airline), is widespread.

These measures can help achieve the most significant public health benefits in the fight against sudden death. The prevention of ventricular fibrillation is directed to the underlying cause. Drug therapy or surgical treatment (e.g., operable coronary artery disease) may be appropriate in some cases, while radiofrequency ablation is effective in various disorders.

Implantable cardioverter defibrillators (ICDs), which provide early defibrillation effectively, are used in patients at high risk of recurrent ventricular fibrillation. Studies indicate that patients with PV arrest who receive ICD have better long-term survival rates than patients who receive only medication.


In acute ventricular fibrillation (VF), medications (e.g., vasopressin, epinephrine, amiodarone) are used after three defibrillation attempts to restore normal rhythm. Amiodarone can also be used long-term in patients who reject an implantable cardioverter-defibrillator (ICD) or are not candidates for an ICD.

However, amiodarone is not helpful for the primary prevention of ventricular fibrillation in patients with a depressed left ventricular ejection fraction (LV).

Antiarrhythmic agents Ia

Anti-arrhythmics of class Ia increases the refractory periods of the atria and ventricles. Myocardial excitability is reduced by increasing the excitation threshold and inhibiting ectopic pacemaker activity.

Procainamide (Procanbid, Pronestyl, Pronestyl [SR])

Procainamide is a third-line drug of choice for ventricular fibrillation. This medication is generally not recommended for patients with VF. Still, due to its long loading time, it can be used to prevent recurrences of VF or treat sustained ventricular tachycardia (VT).

Antiarrhythmic agents Ib

Class Ib antiarrhythmics suppress the automaticity of conduction tissue by increasing the threshold of electrical stimulation of the ventricle and the His-Purkinje system and inhibiting the spontaneous depolarization of the ventricles during diastole by direct action on the tissues.

Class Ib antiarrhythmics block the initiation and conduction of nerve impulses by decreasing the permeability of the neuronal membrane to sodium ions, resulting in the inhibition of depolarization, with subsequent conduction blockage.

Lidocaína (Xylocaine, Nervocaine, LidoPen, Duo-Trach)

Lidocaine is a local anesthetic and a class Ib antiarrhythmic agent that increases the electrical stimulation threshold of the ventricle, suppressing the automaticity of conduction through the tissue. Class Ib agents particularly shorten the action potential. Lidocaine can be tested in patients with VT due to ischemia.

Antiarrhythmic agents III

Class III antiarrhythmics prolong the duration of the action potential. Some agents in this class inhibit adrenergic stimulation (alpha and beta-blockade properties); affect the sodium, potassium, and calcium channels; and prolong the action potential and the refractory period in the myocardial tissue. These effects produce a decrease in atrioventricular conduction (AV) and the function of the sinus node.

Amiodarone (Pacerone, Cordarone, Nexterone)

Amiodarone is a class III antiarrhythmic agent indicated to treat life-threatening recurrent VF.

Amiodarone can be administered intravenously or orally.

Recurrent ventricular fibrillation that is not due to a reversible cause can be treated with intravenous amiodarone (AI). Decreases AV conduction and sinus node function. It also prolongs the action potential and the refractory period in the myocardium and inhibits adrenergic stimulation.

Amiodarone can also be used orally in the long term in patients who reject ICDs, are not candidates for ICD, or have frequent ventricular arrhythmias.

Antiarrhythmic agents V

Class V antiarrhythmics have a mechanism of action different from that of agents of classes I-IV; In many cases, its mechanism of action is unknown.

Magnesium sulfate

Magnesium acts as an antiarrhythmic agent and decreases the frequency of premature ventricular contractions, particularly when secondary to acute ischemia. Clinical trials have not been conclusive in demonstrating their ability to improve mortality rates in the context of refractory VF.


These agents increase cerebral and coronary blood flow present during the low-flow state associated with the hemodynamic compromise of VF.

Epinephrine (Adrenaline)

Epinephrine is considered the most helpful drug in cardiac arrest, although it has never benefited long-term survival or functional recovery. Epinephrine stimulates the alpha, beta1, and beta2 receptors, resulting in smooth muscle relaxation, cardiac stimulation, and dilatation of the muscular vasculature.

Vasopresina (ADH, Pitressin)

Vasopressin is a peptide hormone that regulates the body’s water retention by increasing the absorption of water in the collecting duct of the renal nephron. It also increases blood pressure by affecting peripheral vascular resistance.

Vasopressin has an indication not indicated for ventricular fibrillation that is causing a pulseless arrest. This agent can improve the blood flow of vital organs, the supply of cerebral oxygen, the patient’s ability to be reanimated, and the neurological recovery of the patient.