Ventricular Fibrillation in Emergency Medicine

Updated: Jan 12, 2021
  • Author: Keith A Marill, MD; Chief Editor: Erik D Schraga, MD  more...
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Overview

Background

Ventricular fibrillation (VF) begins as a quasiperiodic reentrant pattern of excitation in the ventricles with resulting poorly synchronized and inadequate myocardial contractions. The heart consequently immediately loses its ability to function as a pump. As the initial reentrant pattern of excitation breaks up into multiple smaller wavelets, the level of disorganization increases. Sudden loss of cardiac output with subsequent tissue hypoperfusion creates global tissue ischemia; brain and myocardium are most susceptible. VF is the primary cause of sudden cardiac death (SCD).

Ventricular fibrillation is shown in the rhythm strip below.

Ventricular fibrillation. Rapidly recurrent despit Ventricular fibrillation. Rapidly recurrent despite electrical biphasic defibrillation. Notice that recurrence begins after completion of the T wave and is not due to an R-on-T phenomenon in this case. This episode of ventricular fibrillation (VF) occurred in the emergency department and was present for less than 30 seconds prior to defibrillation, hence the coarse morphology. Also an undulating amplitude suggestive of torsades de pointes was present; however, the QT interval during sinus rhythm was normal, and the only known predisposing factors for tachydysrhythmia were newly diagnosed coronary artery disease with acute right coronary artery occlusion and a history of rheumatoid pericarditis.

Essential Update: COVID-19

Coronavirus disease 2019 (COVID-19) is defined as illness caused by a novel coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); it is known to spread through aerosolized particles produced by an infected person. [1] Emergency care personnel are at an increased risk of exposure owing to proximity to and aerosol-generating procedures performed on patients, such as intubation and CPR. The American Heart Association, in collaboration with seven other medical societies, has issued interim guidance to help rescuers treat adult and pediatric patients with cardiac arrest with suspected or confirmed COVID-19. [2, 3]

The Interim Guidance for Basic and Advanced Life Support in Adults, Children, and Neonates With Suspected or Confirmed COVID-19 includes detailed recommendations on life-saving interventions in the context of the COVID-19 pandemic, including the following:

  • General principles for resuscitation in patients with suspected and confirmed COVID-19
  • Algorithms with key updates to basic and advanced cardiovascular life support procedures for patients with suspected and confirmed COVID-19

  • Situation- and setting-specific considerations, including out-of-hospital and in-hospital cardiac arrest as well as maternal and neonatal considerations for patients with suspected and confirmed COVID-19

See the guidelines for complete information.

Patient Education

For patient education information, see the Heart Health Center and Healthy Living Center, as well as Cardiopulmonary Resuscitation (CPR) and the National Library of Medicine's Ventricular Fibrillation.

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Pathophysiology

Sudden cardiac death can be viewed as a continuum of electromechanical states of the heart: ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electrical activity (PEA), and asystole. VF is the most common initial state encountered, 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 partial or complete repolarization. Areas that are activated again after partial repolarization may again exhibit abnormal slow propagation allowing sustained reentry and fibrillation.

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. This progression of electrocardiographic abnormalities reflects the electrical and energetic changes described above. The probability of successful defibrillation decreases as the VF waveform becomes smoother with time. [4]

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Etiology

Cardiac causes with structural heart disease include the following:

  • Myocardial ischemia or infarction due to coronary artery disease: Coronary atherosclerosis and its consequences are responsible for approximately 80% of sudden cardiac deaths in the United States.

  • Cardiomyopathy: Dilated and hypertrophic cardiomyopathies are the second most important cardiac causes of sudden death. The degree of functional and physiologic left ventricular impairment is correlated with the risk of sudden death: dilated, hypertrophic, or arrhythmogenic right ventricular cardiomyopathy or dysplasia.

  • Pericardial tamponade

  • Congenital heart disease

Cardiac causes in the absence of structural heart disease include the following

  • Catecholaminergic polymorphic ventricular tachycardia and right ventricular outflow tract tachycardia

  • Mechanical (commotio cordis) [5] or electrical accidents

  • Preexcitation (including Wolff-Parkinson-White syndrome)

  • Heart block

  • Drug-induced QT prolongation with torsades de pointes

  • Channelopathies: long QT syndrome, short QT syndrome, or Brugada syndrome [6]

Noncardiac respiratory causes include the following:

Metabolic or toxic causes include the following:

  • Electrolyte disturbances and acidosis

  • Medications or drug ingestion

  • Environmental poisoning

  • Sepsis

Neurologic causes include the following:

  • Seizure

  • Cerebrovascular accident - Intracranial hemorrhage or ischemic stroke

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Epidemiology

United States data

The incidence of sudden cardiac death in the United States is approximately 300,000 cases per year. The distribution of rhythms found in patients with cardiac arrest depends largely on the average duration of the arrest state and, thus, the emergency medical system (EMS) response times. In monitored settings, such as casinos, where average response times are less than 5 minutes, the initial rhythm is ventricular fibrillation (VF) in approximately 70% of patients. [7] A circadian pattern of sudden cardiac death has also been reported.

The incidence of VF seems to be decreasing based on multiple reports. This may, in part, be due to improved treatment of coronary artery disease and acute myocardial infarction, implantable cardioverter-defibrillator (ICD) placement in patients at high risk, [8] or other unknown factors.

International data

Ventricular fibrillation also is prevalent worldwide, with a reported predominance in the northern hemisphere. Among some European populations, the annual incidence of cardiac arrests exceeds 6 cases per 10,000 people.

Race-, sex-, and age-related demographics

Black males have the highest incidence of sudden cardiac death.

Sudden cardiac death is more common among males than females, although the rates become similar for patients older than 70 years.

Incidence of sudden cardiac death initially peaks during the first 6 months of life, then rapidly declines until a second peak in those aged 45-75 years.

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Prognosis

The prognosis for survivors of ventricular fibrillation (VF) strongly depends on the time elapsed between onset and medical intervention. Early defibrillation often makes the difference between long-term disability and functional recovery.

The likelihood of survival of cardiac arrest victims also depends on the duration of arrest prior to treatment. Improved outcomes occur in patients who have a witnessed arrest, receive bystander cardiopulmonary resuscitation (CPR), obtain defibrillation and advanced cardiac life support from EMS personnel within 10 minutes of onset, and present with an initial rhythm of VF. [6]

Cardiac arrests witnessed by bystanders have a better prognosis because the victim is more likely to receive early treatment. The rate of survival from VF in the community varies from 4-33%. The survival rate of all cardiac arrest victims regardless of presenting rhythm has been reported to be as high as 18% and as low as 2% in various EMS systems. Large urban centers tend to have lower rates of survival. These lower rates of survival have been attributed to lower rates of bystander CPR, longer response intervals, and fewer patients presenting with VF. [9]

Morbidity/mortality

Postresuscitation death and disability after successful resuscitation directly correlate with the degree of central nervous system (CNS) damage during the event. Without intervention, by 4-6 minutes after onset of VF, the prognosis is poor. Few survive when VF lasts more than 8 minutes without intervention. Prediction rules have been developed to predict favorable neurologic survival from cardiac arrest. [10, 11]

The reported rate of survival from VF in the community varies from 4-33%. Survival is worst in dense urban and sparse rural areas, principally due to prolonged EMS response times.

Cardioverter-defibrillator implantation is the primary treatment of survivors of VF. Antidysrhythmic and beta-adrenergic blocking medicines may also be helpful to prevent VF recurrence. While these interventions lower the risk of sudden dysrhythmic death, the implantable cardioverter-defibrillator (ICD) in particular does not prevent or retard the progressive congestive heart failure that is often present in these patients.

Complications

Complications of ventricular fibrillation include the following:

  • CNS ischemic injury

  • Myocardial injury

  • Postdefibrillation arrhythmias

  • Aspiration pneumonia

  • Defibrillation injury to self or others

  • Injuries from CPR and resuscitation

  • Skin burns

  • Damage to implanted electronics (eg, ICD, pacemaker)

  • Death

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