Ventricular Fibrillation 

Updated: Jun 06, 2018
Author: Sandeep K Goyal, MD, FHRS; Chief Editor: Jeffrey N Rottman, MD 



Ventricular fibrillation (VF) is a life-threatening cardiac arrhythmia in which the coordinated contraction of the ventricular myocardium is replaced by high-frequency, disorganized excitation, resulting in [the effective] failure of the heart to pump blood. VF is the most commonly identified arrhythmia in cardiac arrest patients. In the prehospital setting, 65%-85% of patients in cardiac arrest have VF identified as the initial rhythm by emergency services personnel.[1, 2, 3] (See Presentation and Workup.)

VF usually ends in death within minutes unless prompt corrective measures are instituted. The rate of survival in out-of-hospital cardiac arrest has increased with the expansion of community-based emergency rescue systems, widespread use of automatic external defibrillators (AEDs), and increasing numbers of laypersons trained in bystander cardiopulmonary resuscitation (CPR), but it nonetheless remains low. (See Prognosis, Treatment and Medication.)

In hospital settings, VF is treated using Advanced Cardiac Life Support (ACLS) protocols. Long-term management may be accomplished with medical therapy or placement of an implantable cardioverter-defibrillator (ICD). Surgical correction of underlying disorders (eg, percutaneous coronary intervention, coronary artery bypass surgery) may also be indicated. (See Treatment and Medication.)

For related topics, see Ventricular Fibrillation in Emergency Medicine, Sudden Cardiac Death, Hypertrophic Cardiomyopathy, and Pediatric Ventricular Fibrillation.

Patient education

For patient education information, see the Heart Health Center, Cholesterol Center, and Healthy Living Center, as well as Atrial Fibrillation (A Fib), Chest Pain, Arrhythmias (Heart Rhythm Disorders), Heart Disease, Heart Attack, Cardiopulmonary Resuscitation (CPR), and Tetralogy of Fallot.


Ventricular fibrillation (VF) occurs in a variety of clinical situations but is most often associated with coronary artery disease (CAD). VF can result from acute myocardial infarction (MI) or ischemia, or from myocardial scarring from an old infarct.[4] Ventricular tachycardia (VT) may degenerate into VF. Intracellular calcium accumulation, the action of free radicals, metabolic alterations, and autonomic modulation are important influences on the development of VF during ischemia.

Initiation of VF can occur in several ways. For example, if the myocardium is stimulated by a ventricular premature complex (VPC) during the ascending limb of the T wave,[5] the impulse can propagate erratically through the variably refractory myocardial cells and establish reentrant patterns that result in chaotic ventricular depolarization. Consequently, coordinated myocardial contraction becomes disrupted.

The reentrant patterns break up into multiple smaller wavelets and the level of disorganization increases, with reentrant circuits producing high-frequency activation of cardiac muscle fibers. As the heart loses its ability to pump blood, myocardial ischemia worsens and a self-perpetuating vicious cycle ensues, leading to death if not corrected.

On the electrocardiogram (ECG), VF manifests as a chaotically irregular pattern. This pattern is coarse initially but becomes finer as ventricular disorganization increases. As the ECG waveform flattens, the likelihood of successful defibrillation decreases.[6]


Coronary artery disease (CAD) is the single most common etiologic factor predisposing patients to ventricular fibrillation (VF). In survivors of cardiac arrest, CAD with over 75% stenosis is observed in 40%-86% of patients, depending on the age and sex of the population studied. In postmortem studies of people who have died from VF, extensive atherosclerosis is the most common pathologic 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 cases showed more than 75% stenosis in three or four vessels as well as similar severe lesions in at least two vessels.[7] No single coronary artery lesion is associated with an increased risk for VF.

Nevertheless, only approximately 20% of VF-related autopsies have shown evidence of a recent myocardial infarction (MI). A greater proportion of autopsies (40%-70%) show evidence of a healed MI. Many of these hearts also reveal evidence of plaque fissuring, hemorrhage, and thrombosis.[8]

In young people, causes of autopsy-positive sudden cardiac death (SCD) include hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular dysplasia (ARVD), whereas inherited arrhythmogenic etiologies cause autopsy-negative SCD, including long QT syndrome (LQTS),  catecholaminergic polymorphic ventricular tachycardia (CPVT), Wolff- Parkinson-White (WPW) syndrome, idiopathic VF, and Brugada syndrome.[9]

The Coronary Artery Surgery Study (CASS) showed that surgically improving or restoring blood flow to the ischemic myocardium decreased the risk of VF, especially in patients with three-vessel disease and heart failure, compared with medical treatment.[10] This finding suggests that transient acute ischemia is one of the major triggering events for sudden arrhythmic death.

The efficacy of beta-blocking agents in reducing sudden death mortality rates, especially when administered to patients suffering from MI with VF, ventricular tachycardia (VT), and high-frequency premature ventricular contractions (PVCs), is thought to be partially caused by the ability of beta blockers to decrease ischemia. Beta blockers also increase the VF threshold in ischemic animals and reduce the rate of ventricular ectopy in patients with MI.

Reperfusion of ischemic myocardium with thrombolysis or angioplasty can induce transient electrical instability by several different mechanisms. One of these, coronary artery spasm, exposes the myocardium to both ischemia and reperfusion insults. Possible mechanisms of coronary vasospasm include autonomic nervous system factors, especially alpha-adrenergic activity; vagal activity; vessel susceptibility; and humoral factors, particularly those associated with platelet activation and aggregation.

Nonatherosclerotic coronary artery abnormalities are also associated with an increased incidence of sudden death. Such abnormalities include congenital lesions, embolism, arteritis, and mechanical abnormalities, such as coronary artery aneurysms.

When documentation of the antecedent rhythm is available, it often shows that rapid VT precedes VF. In patients with chronic ischemic heart disease, monomorphic VT arising from a reentrant focus is the most common precursor to VF. Other factors associated with an increased risk of VF include frequent PVCs, particularly complex forms (such as multiform PVCs) and ones with short coupling intervals (R-on-T phenomenon).[11]

Even though many individuals have anatomic and functional cardiac substrates that predispose them to ventricular arrhythmias, only a small percentage develop VF. The interplay among regional ischemia, left ventricular (LV) dysfunction, and transient inciting events (eg, worsened ischemia, acidosis, hypoxemia, wall tension, drugs, metabolic disturbances) has been proposed to be the precipitator of VF.

An estimated 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 VF with no discernable structural heart disease.[12] Up to 15% of patients younger than 40 years who experience VF have no underlying structural heart disease. Belhassen and Viskin noted that 4 of 11 patients in their study with a history of VF and no structural heart disease had histologic abnormalities on endomyocardial biopsy.[13]

Acute and chronic ischemic heart disease

Cardiac arrest attributable to ventricular arrhythmias may occur with acute ischemia or in the absence of an acute disturbance of coronary flow, due to scarring from a previous MI. An infarct scar can serve as the focus for reentrant ventricular tachyarrhythmias, which may occur shortly after the infarct or years later. Many studies support the relationship of symptomatic and asymptomatic ischemia as markers of myocardium at risk for arrhythmias.[14, 15]

Patients resuscitated from out-of-hospital cardiac arrest are at an increased risk for recurrent cardiac arrest and express an increased incidence of silent ST-segment depressions.[16] In animal models, experimentally induced myocardial ischemia has shown a strong relationship with the development of VF.

Nonischemic cardiomyopathies

Patients with nonischemic cardiomyopathies are the second largest group of patients who experience VF, accounting for approximately 10% of VF cases. Nonischemic myopathies, for the purposes of this article, can be divided into dilated, hypertrophic, and other, rarer, forms. These cardiomyopathies can predispose to both VT and VF. The VT can degenerate into VF, persist as a rhythm that is stable enough to allow detection and directed therapy, or terminate spontaneously, with or without associated symptoms.

Dilated cardiomyopathy

Dilated cardiomyopathy (DCM) is recognized more frequently, with a reported annual incidence of approximately 7.5 cases per 100,000 people. The prognosis after a VF event is very poor for these patients, with a 1-year mortality rate of 10%-50%, depending on the New York Heart Association functional class; VF causes approximately 30%-50% of these deaths.

DCM has varied etiologies, including idiopathic, viral, autoimmune, genetic, or environmental (eg, alcohol abuse). The predominant mechanism of sudden death in patients with DCM appears to be ventricular tachyarrhythmias, although bradyarrhythmias and electromechanical dissociation have also been observed, especially in patients with advanced LV dysfunction.[17] Extensive subendocardial fibrosis leading to ventricular dilatation and subsequent generation of reentrant tachyarrhythmias is a proposed substrate for VF.

Multiple factors contribute to an increased risk for VF in this population. The most important hemodynamic predictor is an increase in LV end-diastolic pressure and the resulting increased wall tension. Other important factors are an increased sympathetic tone, neurohumoral activation, and electrolyte abnormalities. Many drugs used in the treatment of heart failure, such as antiarrhythmics, inotropic agents, and diuretics, have proarrhythmic properties, which may provoke arrhythmias in some patients.

The genetic causes of DCM are myriad, with many genes, including those that encode actin, myosin, and troponin proteins, being implicated in its causation. Most familial DCMs are inherited in an autosomal dominant fashion, with mutations typically occurring in the proteins found in the cardiac sarcomere.

Interestingly, genes such as PSEN1 and PSEN2, which are responsible for early onset Alzheimer disease, have also been implicated in DCM. X-linked inheritance of DCM has been described in patients with mutations in the DMD (Duchenne muscular dystrophy) gene and the TAZ (Barth Syndrome) gene. Autosomal recessive inheritance has been described in mutations of the TNNI3 gene, which encodes the troponin I muscle protein.

Hypertrophic cardiomyopathy

HCM is usually an autosomal dominant, incompletely penetrant genetic disorder resulting from a mutation in one of the many (>45) genes that encode proteins of the cardiac muscle sarcomere.[18] Among the described genetic abnormalities are mutations in the genes encoding the beta-myosin heavy chains (MYH7), cardiac troponin T (TNNT2), myosin-binding protein C (MYBPC3), and cardiac troponin I.

Mutations in these four genes account for approximately 90% of HCM. The incidence of VF in this population is 2%-4% per year in adults and 4%-6% per year in children and adolescents. HCM is the most common cause of VF before age 30 years.

The mechanism of VF in HCM is not entirely understood. Ventricular arrhythmias in HCM are probably a result of a substrate of electrical instability and disorganized electrophysiologic (EP) transmission due to abnormal LV myocardial architecture. Intramural CAD leading to episodic myocardial ischemia and the resulting necrosis and fibrosis has also been implicated as a potential substrate for VT/VF.[19]

The vast majority of young people who die of HCM are previously asymptomatic. Many experience VT/VF while at rest or with mild exertional activity; however, in a significant portion of these patients, the VF event occurs after vigorous exertion. The postexertional drop in blood pressure and shunting of blood to extracardiac tissues is postulated to worsen the outflow tract gradient and may therefore induce cardiac ischemia and malignant arrhythmias.

This downward cycle does not revert spontaneously, and it responds poorly to resuscitative efforts. HCM is the single greatest cause of VF in athletes and is therefore the major entity to screen for during the physical examination of an athlete.[18, 20]

Arrhythmogenic right ventricular cardiomyopathy/dysplasia

Arrhythmogenic right ventricular (RV) cardiomyopathy/dysplasia (ARVC/D) is characterized by replacement of the RV wall with fibrofatty tissue. Involvement of the interventricular septum is unusual, and involvement of the left ventricle is associated with poorer outcomes.[21, 22]

The genetics of ARVC/D are extremely heterogeneous. At least 10 genes (TGFB3, RYR2, DSP, PKP2, DSG2, TMEM43, JUP, TTN, DES, DSC2)[23] and four additional loci (14q12-q22, 2q32.1-32.3, 10p14-p12, and 10q22) have been implicated in the pathogenesis of this disorder, which is inherited in an autosomal dominant fashion with incomplete penetrance. Eight of these genes are thought to be responsible for approximately 42.5% of the total cases of ARVC/D.[24]

The majority of the genetic mutations relate to desmosomal abnormalities. The desmosomes are proteins that are instrumental in cell-to-cell binding of myocytes.

Patients with ARVC/D, which is more prevalent in men than in women, may present with signs and symptoms of RV hypertrophy and dilatation, often with sustained monomorphic VT with left bundle-branch block morphology, with an axis usually between negative 90°-100°. Less commonly, patients present with polymorphic VT. Atrial arrhythmias may be present in up to 25% of patients. The annual incidence rate of VF in patients with ARVC/D is approximately 2%.

Syncope and sudden death in ARVC/D are often associated with exercise. In many patients, sudden death—the incidence of which is highest in persons aged 30-50 years—is the first manifestation of the disease. Symptoms are rare in preadolescent children.

The most common electrocardiographic (ECG) abnormality in ARVC/D is T-wave inversion in leads V1 -V3. Epsilon waves are seen in V1 or V2 as sharp spikes in the ST segment. In V1, a delayed-onset S wave (from nadir to baseline >60 msec) is a specific sign of ARVC/D (see the image below). In addition, PVCs with a left bundle-branch block pattern are common. Signal-averaged ECGs are abnormal in the majority of patients.

This image shows an epsilon wave on the electrocar This image shows an epsilon wave on the electrocardiogram of a patient with arrhythmogenic right ventricular dysplasia (ARVD).

ARVC/D differs from Uhl anomaly, a condition in which the RV wall is extremely thin because of apposition of the endocardial and epicardial layers. Uhl anomaly usually manifests in the pediatric population, whereas ARVC usually manifests in adults.

The diagnosis can be confirmed with echocardiography or, preferably, with cardiac magnetic resonance imaging (CMRI) studies. Voltage mapping of the RV can be performed using a three-dimensional (3-D) mapping system and can show the presence of low-voltage areas (surrogate for scar or fatty infiltration) in the so-called triangle of dysplasia.

Because there is no gold standard for the diagnosis of ARVC/D, clinicians resort to the use of a variety of clinical abnormalities known as major and minor criteria. The diagnosis of ARVC/D is thought to be definite if the patient has any of the following[25, 26] :

  • At least two (2) major criteria

  • One (1) major and two (2) minor criteria

  • Four (4) minor criteria

Valvular lesions

Aortic stenosis

Before the advent of surgical therapy for valvular heart disease, SCD was fairly common in patients with progressive aortic stenosis. Chizner et al followed 42 patients with isolated, unoperated aortic stenosis for over 5 years and found that symptomatic patients had a high mortality rate and that 56% of deaths occurred suddenly (within hours of the development of new symptoms). However, there were no deaths in asymptomatic patients.[27]

The mechanism of SCD in patients with uncorrected aortic stenosis is unclear, although malignant tachyarrhythmias and bradyarrhythmias have been documented. VF accounts for up to 20% of deaths after aortic valve replacement and remains the second most common cause of postoperative death in this population. The incidence of VF after aortic valve surgery is highest in the first 3 weeks after the procedure and then plateaus at 6-month follow-up.


Patients with chronic aortic insufficiency usually present with signs of chronic heart failure due to progressive LV dilatation and remodeling. As part of this process, reentrant or automatic ventricular foci may develop and cause symptomatic ventricular arrhythmias. After valve replacement, LV wall tension can be expected to lessen, and the risk of arrhythmia can be expected to decrease.

Mitral stenosis has become uncommon in the United States because of widespread use of antibiotics in primary streptococcal infections. SCD due to mitral stenosis is very rare.

The incidence of VF is low in patients with mitral valve prolapse (MVP). In clinically significant MVP, the risk of VF seems to rise along with the total mortality rate. The incidence of sudden death appears to vary with the presence of symptoms and the severity of mitral regurgitation. MVP has a 5%-7% occurrence rate in the general population.[28]

Congenital structural heart disease

The causes of SCD are much more diverse in children than in adults. In reviewing 13 studies, involving 61 children and adolescents with VF, Driscoll and Edwards found that 50% of cases were due to HCM and that 25% resulted from anomalous origin of the left coronary artery.[29]  The remaining cases were due to aortic stenosis, cystic medial necrosis, and sinus node artery obstruction.

Disease entities associated with VF in patients with known, previously recognized (including repaired) congenital heart disease include the following:

  • Tetralogy of Fallot[30]

  • Transposition of the great arteries

  • Physiologic single ventricle

  • Aortic stenosis

  • Marfan syndrome

  • Eisenmenger syndrome[31]

  • Congenital heart block

  • Ebstein anomaly

The predominant mechanism is ventricular arrhythmia. In patients with tetralogy of Fallot, up to 10% have VT after surgical correction of the anomaly, and the incidence of sudden death is 2%-3%. In the Fontan procedure to correct a physiologic single ventricle, even atrial arrhythmias can cause severe hemodynamic compromise and arrhythmic death.

Patients who develop secondary pulmonary hypertension (Eisenmenger syndrome) despite attempted correction of the anatomic defects have a very poor prognosis. The terminal event may be bradycardia or VT progressing to VF.

Acquired childhood diseases associated with VF include Kawasaki syndrome, DCM, and myocarditis. Causes of VF in patients with previously unrecognized structural heart disease include HCM, congenital coronary artery abnormalities, and ARVD.

Paroxysmal VF or short-coupled torsades

Paroxysmal familial VF can be caused by mutations in either the SCN5A or DPP6 gene. Mutations in the SCN5A gene are also associated with VF during MI.[32]

Idiopathic VF and VT

Idiopathic VF

Idiopathic VF is triggered by ventricular premature beats that may originate in the distal Purkinje conducting system, LV septum, anterior RV, or RV outflow tract (RVOT). Early repolarization, or J wave (elevation at the junction of between the QRS complex and ST-segment), has been identified in patients with idiopathic VF and has been associated with mutations in a variety of ion channel genes.[33] Catheter ablation that targets triggers of ventricular premature beats can provide long-term freedom from recurrence of idiopathic VF.[34]

Idiopathic VT

Although RVOT tachycardia is responsible for 70%-80% of idiopathic VTs, it is a rare cause of VF. Idiopathic VT is generally associated with a benign prognosis.

RVOT tachycardia has a left bundle-branch block/inferior or right-axis morphology on ECG. Idiopathic VTs that originate from the LV outflow tract (LVOT), aortic root, or LV septum are less common. However, with newer techniques of mapping and ablation, more PVC and VT foci are being mapped to the LVOT and aortic cusp area. Many patients with previous failed ablation for RVOT PVCs have undergone successful mapping and ablation in the LVOT or aortic cusp region.[35]

RVOT tachycardia is believed to be adrenergic-receptor mediated, because exogenous and endogenous adenosine can terminate the arrhythmia. Maneuvers that increase endogenous acetylcholine may also terminate the arrhythmia.

Symptoms typical of RVOT tachycardia include palpitations, presyncope, or syncope, often occurring during or after exercise or emotional stress, but VT can also occur at rest. VF has been reported in patients with RVOT who have PVCs with short coupling intervals (in contrast to the long coupling intervals seen in patients with benign forms of RVOT tachycardia).[36]

Treatment of RVOT is based on the symptomatic frequency and severity. Beta blockers are first-line therapy. Patients with symptoms not relieved by medical therapy are best treated with radiofrequency catheter ablation. Successful ablation is reported in 83%-100% of cases.

The next most common form of idiopathic VT arises from the fascicles of the LV, notably the left posterior fascicle. These patients present with an ECG pattern during VT showing a right bundle-branch block and superior axis. The initial drug of choice is a calcium channel blocker. Catheter ablation is very effective. Other, less common forms of idiopathic VT originate from the LV papillary muscles or from the crux of the heart (the region at the base of the ventricle nearest the atrioventricular [AV] node).[37]

Pulmonary embolism

Pulmonary embolism is a frequent cause of sudden death in at-risk people. Risk factors include a previous personal or family history of deep venous thromboembolism (DVT), malignancy, hypercoagulable states, and recent mechanical trauma such as hip or knee surgery. Patients with pulmonary embolism can develop fatal ventricular arrhythmias (eg, VF) due to hemodynamic collapse and/or severe hypoxia.

Aortic dissection

Aortic dissection or aneurysmal rupture is a rather uncommon, but significant, cause of out-of-hospital cardiac arrest. Predisposing factors for aortic dissection include genetic deficiencies of collagen such as Marfan syndrome, Ehlers-Danlos syndrome, and aortic cystic medial necrosis. VF may be an observed finding at the scene of an aortic aneurysmal rupture, or the sudden death from the hemodynamic collapse may be presumed to reflect associated VF without the presence of that rhythm.

Electronic control devices

Whether electronic control devices (eg, TASERs) can trigger VF has been studied in animal models, with contradictory results.[38] However, Zipes reported human cases in which TASER stimulation apparently caused cardiac electrical capture and provoked cardiac arrest from VT/VF.[39]

Nonstructural abnormalities

Nonstructural abnormalities generally are a group of abnormalities in which patients have no apparent structural heart disease but have a primary EP abnormality that predisposes them to VT or VF.[40] Some imaging techniques have detected abnormal sympathetic neural function in these patients. An ECG can provide clues to the diagnosis; consider a familial component to these conditions.

Causes of VF in patients with previously unrecognized, nonstructural heart disease include the following:

  • LQTS

  • CPVT

  • WPW syndrome

  • Primary VT and VF

  • Primary pulmonary hypertension

  • Commotio cordis (traumatic blow to the chest wall causing VT/VF)

  • Brugada syndrome: It is possible that some patients with what is thought to be primary VF may have Brugada syndrome; VF in these patients usually has no preceding symptoms; the prognosis is unfavorable, and the recurrence rate is as high as 33%.

Congenital long QT syndrome

Congenital LQTS results from abnormalities of channel proteins in the cardiac membrane. The most common forms involve loss of function of the potassium channel. Other forms may involve the sodium or calcium ion channels.

Prolongation of the QT interval is seen in the following genetic disorders:

  • Idiopathic LQTS

  • Romano-Ward syndrome

  • Jervell and Lange-Nielsen syndrome (JLNS)

  • Andersen-Tawil syndrome

  • Timothy syndrome

Current cardiologic practice, however, is moving away from eponyms and instead toward denoting LQTS by numbered type, based on identified underlying mutations. For example, long QT 1 is caused by mutations in the KCNQ1 gene; it is seen in Romano-Ward syndrome and JLNS.

The clinical course of LQTS is quite variable, with some patients remaining asymptomatic and others developing torsade de pointes with syncope and sudden death. In 30% of cases, the syndrome is identified during an evaluation for syncope or aborted sudden death.

Patients at high risk for VF include those with deafness and first-degree relatives of patients with VF. VF in these patients is associated with emotional extremes, auditory auras or stimulation, and vigorous physical activity. Symptoms usually begin in childhood or adolescence. Schwartz et al have suggested diagnostic criteria for LQTS in the absence of genetic testing (see Table 1, below).[41]

Table 1. Long QT syndrome diagnostic criteria (Open Table in a new window)




Electrocardiographic Findings

Corrected QT interval

≥480 ms


460-479 ms


450-459 ms (in males)


Torsade de pointes


T wave alternans


Notched T waves in three leads


Low heart rate for age (resting rate below second percentile


Clinical History


With stress


Without stress


Congenital deafness


Family History

Family members with definite long QT syndrome


Unexplained sudden cardiac death before age 30 years in immediate family members without definite long QT syndrome


Adapted from Schwartz PJ, Moss AJ, Vincent GM, Crampton RS. Diagnostic criteria for the long QT syndrome. An update. Circulation. 1993 Aug;88(2):782-4. PMID: 8339437[41]


  • ≤1 point = Low probability of long QT syndrome
  • >1 to 3 points = Intermediate probability of long QT syndrome
  • ≥3.5 points = High probability of long QT syndrome

The absence of a long QT interval on a single resting ECG does not exclude the diagnosis of LQTS. For example, it is possible that the patient may have incomplete penetrance that could be accentuated by drugs or metabolic conditions.

Treatment for LQTS includes beta blockers, high thoracic left sympathectomy, and ICDs.[42] For more information, see the Medscape Drugs and Diseases article Long QT Syndrome.

Idiopathic long QT syndrome

Idiopathic LQTS is characterized clinically by a propensity to develop malignant ventricular arrhythmias. It is a rare familial disorder.

Romano-Ward syndrome

Romano-Ward syndrome describes a family of nonsyndromic LQTS. It is characterized by prolongation of the QT interval, as well as T-wave abnormalities and polymorphic VT. Patients with this disease are predisposed to events of polymorphic VT, which can be self-limited, resulting in syncope. It can also transition into VF and can cause SCD.

Romano-Ward syndrome is inherited in an autosomal dominant fashion, with a penetrance of approximately 50%. Mutations in the KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes are known to be causative, and these five genes together are responsible for virtually 100% of cases of Romano-Ward syndrome.

Jervell and Lange-Nielsen syndrome

JLNS is characterized by congenital sensorineural deafness and a prolonged QT interval. Cardiac events tend to occur at a young age. JLNS is caused by mutations in the KCNQ1 or KCNE1 gene and has an autosomal recessive pattern of inheritance. Persons who are heterozygous for mutations in these genes may be asymptomatic or may manifest Romano-Ward syndrome, but they will have normal hearing.

Andersen-Tawil syndrome

Andersen-Tawil syndrome is chiefly characterized by the triad of periodic flaccid paralysis, prolonged QT interval, and dysmorphic facies. Patients with Andersen-Tawil syndrome have low-set ears, hypertelorism, micrognathia, syndactyly, and short stature.[31] They may also have mild learning disability.

This syndrome is caused by mutation in the KCNJ2 gene, which encodes the ik1 channel and is inherited in an autosomal dominant fashion. About half of affected patients have a de novo mutation.

Timothy syndrome

Timothy syndrome is characterized by the presence of a prolonged QT interval and cutaneous syndactyly. The syndactyly may be unilateral or bilateral and may be of variable severity. Other possible manifestations include cardiac defects, characteristic facial features, and neurologic problems.

Timothy syndrome is caused by mutation in the CACN1C gene, which encodes the α subunit of the calcium channel. It is usually the result of a de novo mutation but is transmitted in an autosomal dominant fashion.[43]

Acquired long QT syndrome

A number of antiarrhythmics (especially class Ia and class III) and other medications, electrolyte abnormalities, cerebrovascular diseases, and altered nutritional states cause QT prolongation and put patients at risk for torsade de pointes. This usually occurs when QT prolongation is associated with a slow heart rate and hypokalemia.

The QT interval is prolonged in up 32% of patients with intracranial hemorrhage (especially subarachnoid hemorrhage). Stroke or intracranial trauma can also result in QT interval prolongation. Lesions in the hypothalamus are thought to lead to this phenomenon. In rare cases, QT prolongation from subarachnoid hemorrhage results in torsades de pointes.

Electrolyte abnormalities that cause acquired LQTS include hypokalemia, hypomagnesemia, and hypocalcemia. Such abnormalities may result from nutritional deficiencies associated with modified starvation diets and severe weight-loss programs. Altered autonomic status (eg, diabetic neuropathy) can cause LQTS. Rarely, hypothyroidism may result in QT interval prolongation.

Class Ia antiarrhythmic drugs that cause acquired LQTS include quinidine, disopyramide, and procainamide. Class III antiarrhythmic drugs that cause acquired LQTS include the following:

  • Sotalol

  • Amiodarone

  • Dofetilide

  • Ibutilide

Other drugs that can cause acquired LQTS include the following:

  • Tricyclic and tetracyclic antidepressants

  • Phenothiazines

  • Haloperidol

  • Antibiotics (eg, intravenous erythromycin, sulfamethoxazole/trimethoprim)

  • Chemotherapeutics (eg, pentamidine, anthracycline)

  • Serotonin antagonists (eg, ketanserin, zimeldine)

  • Organophosphorus insecticides

A comprehensive list of drugs that can prolong the QT interval is available at

Catecholaminergic polymorphic VT

CPVT can be triggered by emotional stress or exercise and can also be induced by catecholamine administration. Patients may present with syncope, or SCD may occur if polymorphic VT degrades into VF. Results of physical examination or resting ECG are usually normal.

CPVT may be caused by mutations in the RYR2 gene (autosomal dominant) or the CASQ2 gene (autosomal recessive).[44] An additional locus has been mapped to chromosome 7p22-p14. Symptoms, including sudden death, usually appear in childhood or among young adults. Most cases of CPVT respond to beta-blocker therapy. Flecainide has also been found to be beneficial.[45] Invasive treatments include left cervical sympathectomy, ICD placement, or both.

Wolff-Parkinson-White syndrome

WPW syndrome is a rare cause of sudden death. The presence of multiple accessory pathways, posteroseptal accessory pathways, and a preexcited R-R interval of less than 220 msec during atrial fibrillation is associated with higher risk for VF.[46]

Most cases of VF in patients with WPW syndrome are induced by atrial fibrillation with a rapid ventricular response over the accessory pathway (see the image below). In a study by Klein et al of 31 patients with VF and WPW syndrome, a history of atrial fibrillation or reciprocating tachycardia was an important predisposing factor.[46]

Ventricular fibrillation appeared during rapid atr Ventricular fibrillation appeared during rapid atrial fibrillation in a patient with Wolff-Parkinson-White syndrome.

Mutation in the PRKAG2 gene can cause WPW. The syndrome is likely inherited in an autosomal dominant manner with reduced penetrance. It is not known what percentage of patients with WPW has a mutation in this gene.

Treatment of WPW should be individualized for each patient and is based in part on risk assessment. Risk assessment can be noninvasive, but symptomatic patients and those with sustained preexcitation during a treadmill exercise stress test require invasive risk stratification via an EP study (EPS.

In high-risk patients (ie, those with multiple pathways, a history of sustained reciprocating tachycardia, or short preexcited RR interval during atrial fibrillation [< 220 msec]), preventing the occurrence of arrhythmias is possible by interrupting the anomalous pathway with catheter ablation. Autonomic tone can alter conduction over a bypass tract, and complete assessment of the “shortest preexcited RR interval” includes assessment with the infusion of isoproterenol.[47]

Atrial fibrillation in patients with WPW can be associated with rapid ventricular rates due to rapid conduction over an accessory pathway with a short refractory period. Pure AV nodal blocking drugs (beta blockers, calcium channel blockers) should not be used alone, as they will block the AV node without affecting the accessory pathway; this can increase preferential conduction over the pathway, leading to faster ventricular rates.

Drugs such as ibutilide, procainamide, and amiodarone are useful, as they prolong the anterograde refractory period of the pathway and hence slow the conduction over the pathway. Electrical cardioversion is the preferred treatment for patients with hemodynamic instability.

Brugada syndrome

Brugada syndrome was first described in 1992 by Brugada and Brugada.[48] It is characterized by a specific ECG pattern of right bundle-branch block and ST-segment elevation in leads V1 and V2 without any structural abnormality of the heart.[49]

Brugada syndrome can be caused by mutations in many genes. The principal gene associated with the syndrome is SCN5A, over 400 mutations of which have been described.[50, 51] Other genes known to cause the syndrome include GPD1L, CACNA1C, CACNB2, SCN1B, KCNE3, SCN3B, and HCN4. Brugada syndrome is inherited in an autosomal dominant fashion.

Patients with this syndrome are at high risk for VF. In equivocal cases, intravenous (IV) procainamide will augment the Brugada ECG pattern.[52] In an early follow-up study of 63 patients with the syndrome, asymptomatic patients were found to have the same risk for arrhythmia as patients who had an episode of aborted sudden death.[53]  In this study, treatment with amiodarone, beta blockers, or both did not confer a lower risk of death, whereas the patients with ICDs had no deaths due to arrhythmia. Thus, placement of an ICD is considered the treatment of choice for Brugada syndrome.[53]

Larger, subsequent studies have emphasized a much lower risk for SCD in asymptomatic patients with an episodic Brugada pattern.[54] Other therapeutic options include IV isoproterenol for management of VF storm and oral quinidine as outpatient therapy for avoiding ICD shocks.[55] Other important aspects of therapy include prompt treatment of fever and avoidance of drugs that cause sodium channel blockade.


United States and international data

Many episodes of ventricular fibrillation (VF) are unwitnessed, making it difficult to assess an exact incidence. Of the approximately 300,000 cases of SCD that occur each year in the United States, up to one third are attributed to VF.[56] This represents an incidence of 0.08%-0.16% per year in the adult population, accounting for more deaths than from lung cancer, breast cancer, or acquired immunodeficiency syndrome (AIDS). In the pediatric and adolescent age groups, VF occurs with an annual incidence of 1.3-8.5 cases per 100,000 persons, accounting for approximately 5% of all deaths in this group.

VF is often the first expression of coronary artery disease (CAD) and is responsible for approximately 50% of deaths from CAD. VF often occurs within the first hour after the onset of an acute myocardial infarction (MI) or acute coronary syndrome (ACS).

In several population-based studies, although the incidence of out-of-hospital cardiac arrest in the United States has been noted as declining in the past 2 decades, the proportion of sudden deaths from VF in patients with CAD has not changed. A high incidence of VF occurs among certain population subgroups (eg, patients with chronic heart failure with ejection fraction < 30%, patients in the convalescent phase after MI, patients who survived cardiac arrest); however, only a small percentage of total VF events occur in these patients, because the population size is small relative to lower-risk groups.

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

The frequency of VF in other industrialized Western nations is similar to that in the United States.[57] The incidence of VF in other countries varies as a reflection of CAD prevalence in those populations. The trend toward an increasing frequency of VF events in developing nations is thought to reflect a change in dietary and lifestyle habits.

Cardiovascular events, including sudden cardiac death (SCD) from VF (but not asystole), most frequently occur in the morning and may be related to increased platelet aggregability. A spike in the number of SCDs also appears to occur during the winter months.

Race-, sex-, and age-related demographics

Most data are inconclusive regarding racial differences and the incidence of VF. Some studies suggest that a greater proportion of coronary deaths have been sudden in black individuals than in white individuals.[58] In a report by Gillum on SCD from 1980-1985 data, the percentage of CAD deaths occurring out of the hospital and in emergency departments was higher in black patients than in white patients.[59]

The incidence of VF is higher in men than in women (3:1).[60] This ratio generally reflects the higher incidence of CAD in men. Although the mechanism of MI tends to differ by sex—coronary plaque rupture in men and plaque erosion in women—it is unclear whether this difference accounts for the male predominance of VF.

The incidence of VF parallels the prevalence of CAD, with the peak rate of VF occurring in people aged 45-75 years. However, the proportion of sudden deaths from CAD decreases with age. In the Framingham Heart Study, the proportion of sudden CAD deaths was 62% in men aged 45-54 years, decreasing to 58% in men aged 55-64 years and to 42% in men aged 65-74 years.[61] According to Kuller, 31% of deaths are sudden in people aged 20-29 years.[62]


The chances of survival from an index ventricular fibrillation (VF) event depend on bystander cardiopulmonary resuscitation (CPR), rapid availability or arrival of personnel and apparatus for defibrillation and advanced life support, and transport to a hospital. Although patients with nontraumatic cardiac arrest are more likely to be successfully resuscitated from VF than from any other arrhythmia, success is highly time dependent. The probability of success generally declines at a rate of 2%-10% per minute.

Early defibrillation often makes the difference between long-term disability and functional recovery. Placement of automated external defibrillators (AEDs) throughout communities and training of the public in their use has the potential to improve outcomes from sudden cardiac death (SCD).[63]

In patients presenting to an emergency department (ED) after a witnessed episode of VF, the prognosis for morbidity and mortality can be determined by calculating the cardiac arrest score, developed by McCullough and Thompson.[64] This score is based on systolic blood pressure, time from loss of consciousness to return of spontaneous circulation, and neurologic responsiveness. (See Presentation for details.)

Even under ideal circumstances, however, only an estimated 20% of persons who have out-of-hospital cardiac arrest survive to hospital discharge. In a study of out-of-hospital cardiac arrest survival in New York City, only 1.4% of patients survived to hospital discharge.[65] However, studies in suburban and rural areas have indicated survival rates of up to 35%.[66]

Routine coronary angiography, with percutaneous coronary intervention (PCI), if indicated, along with mild therapeutic hypothermia (core temperature of 32°-34°C for 24 hours), may favorably alter the prognosis of resuscitated patients with stable hemodynamics after out-of-hospital cardiac arrest.[67] In a retrospective study of cardiac arrest survivors, 65.6% of patients who underwent early coronary angiography survived to hospital discharge, compared with 48.6% of those who did not receive coronary angiography.[68]

A major adverse outcome from VF episodes is anoxic encephalopathy, which occurs in 30%-80% of patients. A study conducted in Minnesota on all adult survivors of out-of-hospital VF-related cardiac arrest from 1990-2008 found that long-term survivors had long-term memory deficits.[69]  A 2017 report that evaluated 2009-2013 data from the Pan-Asian Resuscitation Outcomes Study (PAROS) registry to determine characteristics and outcomes of 3244 young adults (aged 16-35 years) who suffered out-of-hospital cardiac arrest found that factors associated with favorable neurologic outcomes included first arrest rhythms of VF/VT/unknown shockable rhythm, cardiac etiology, bystander-witnessed arrest, and bystander CPR.[70] However, traumatic out-of-hospital cardiac arrest had a poor prognosis.




Obtaining a thorough history from the patient, family members, or other witnesses is necessary to obtain insight into the events surrounding the episode of ventricular fibrillation (VF). Patients at risk for VF may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints, but many are asymptomatic. Up to 45% of persons who have VF have been noted to visit their physician in the 4 weeks before death, although in up to 75% of these patients, the complaints were not related to the cardiovascular system.

A history of left ventricular (LV) dysfunction (LV ejection fraction [LVEF] < 30%-35%) is the single greatest risk factor for sudden death from VF. Risk factors that relate to coronary artery disease (CAD) and to subsequent myocardial infarction (MI) and ischemic cardiomyopathy are also important and include a family history of premature CAD, smoking, dyslipidemia, hypertension, diabetes, obesity, and a sedentary lifestyle. Specific considerations include the following:

  • CAD

  • Previous cardiac arrest

  • Syncope or near-syncope

  • Prior MI, especially within 6 months

  • LVEF less than 30%-35%

  • History of frequent ventricular ectopy (>10 premature ventricular contractions [PVCs] per hour or nonsustained ventricular tachycardia [VT])

  • Drop in systolic blood pressure or ventricular ectopy upon stress testing, particularly when associated with acute myocardial ischemia

  • Dilated cardiomyopathy (DCM) from any cause (but most commonly ischemic or idiopathic)

  • Hypertrophic cardiomyopathy (HCM), obstructive or nonobstructive

  • Use of inotropic medications, particularly in patients with decompensated heart failure or acute myocardial ischemia

  • Valvular heart disease (severe uncorrected aortic or mitral stenosis or regurgitation; valve replacement within 6 months)

  • Myocarditis

Given the possibility of sustained or prolonged VT being the underlying cause, aggressively pursue a history of syncope.

Some forms of congenital heart disease increase the risk for VF. Long QT syndrome (LQTS) can result in VF, particularly in patients with a family history of sudden cardiac death (SCD) (the risk is also increased in acquired LQTS caused by medications that prolong the QT interval). In patients with Wolff-Parkinson-White (WPW) syndrome with extremely rapid conduction over an accessory pathway, degeneration to VF can occur. Other congenital heart diseases that increase VF risk include Brugada syndrome and arrhythmogenic right ventricular (RV) cardiomyopathy/dysplasia (ARVC/D).


VF can occur during any of the following conditions or situations[1] :

  • Antiarrhythmic drug administration

  • Hypoxia

  • Ischemia

  • Atrial fibrillation with very rapid ventricular rates in the presence of preexcitation

  • Electric shock administered during cardioversion

  • Electric shock caused by accidental contact with improperly grounded equipment

  • Competitive ventricular pacing to terminate VT (including that delivered by an implantable device)

Physical Examination

Risk stratification and prognosis determination are crucial in the emergency department (ED) evaluation and treatment of patients with ventricular fibrillation (VF). Patients who survive to ED presentation can be stratified by their cardiac arrest score, which has excellent prognostic value.

The cardiac arrest score, developed by McCullough and Thompson, can be used for patients with witnessed out-of-hospital cardiac arrest.[64] The score uses three criteria: ED systolic blood pressure (SBP), time to return of spontaneous circulation (ROSC) after loss of consciousness, and neurologic responsiveness. The score is calculated as follows[71] :

  • ED SBP: Above 90 mm Hg = 1 point; below 90 mm Hg = 0 points

  • Time to ROSC: Less than 25 minutes = 1 point; longer than 25 minutes = 0 points

  • Neurologically responsive = 1 point; comatose = 0 points

In-hospital mortality rates and neurologic recovery (defined as being discharged home and able to care for oneself), stratified by the initial cardiac arrest score, are shown in Table 2, below.

Table 2: Outcome according to initial cardiac arrest score (Open Table in a new window)

Cardiac Arrest Score

In-Hospital Mortality Rate (%)

Neurologic Recovery (%)













McCullough et al found that even in the setting of ST elevation and early invasive management with primary angioplasty and intraaortic balloon pump insertion, patients with low cardiac arrest scores are unlikely to survive.[72] Consequently, invasive management is rarely justified in patients with scores of 0, 1, or 2; instead, conservative management with empiric supportive and medical therapy may be more appropriate.



Diagnostic Considerations

In all adult cases, ischemic cardiomyopathy is at the top of the differential diagnosis of causes of ventricular fibrillation (VF). However, dilated cardiomyopathy (DCM) has become increasingly common. That is, the differential diagnosis typically relates to the underlying etiology rather than the rhythm per se. Occasionally, electrical artifact due to resuscitative efforts or repetitive muscular activity can superficially appear similarly to very coarse VF. However, it is often possible to see the underlying narrower electrocardiographic (ECG) complexes in the putative VF rhythm strip. Accordingly, whenever possible, the ECGs from the reported VF episode should be directly reviewed.

In children and adolescents, hypertrophic cardiomyopathy (HCM) is most common. VF in these patients often occurs at rest or with mild exertional activity, but vigorous exercise is the trigger in a significant portion of cases.

Differential Diagnoses



Approach Considerations

The presence of ventricular fibrillation (VF) can be confirmed only with electrocardiography (ECG). In addition, ECG is indicated in all patients who have experienced VF, as it may provide evidence of an underlying condition that led to the episode.

Signal-averaged ECG is of limited value.[73] In patients with dilated cardiomyopathy (DCM) (unlike those with ischemic cardiomyopathy), increased asymptomatic ventricular ectopy and nonsustained ventricular tachycardia (VT) are not predictive of VF. Approximately 80% of persons with DCM have these findings on Holter monitoring, hence the limited diagnostic value.

The evaluation of patients who have experienced VF should also include echocardiography, whereas nuclear imaging studies can help in the assessment of patients at risk for VF. In targeted patients, electrophysiologic (EP) studies (EPS) play diagnostic, prognostic, and therapeutic roles.

Appropriate laboratory studies may include the following:

  • Serum electrolyte levels, including calcium and magnesium

  • Cardiac enzymes (eg, creatine kinase, myoglobin, troponin)

  • Complete blood cell (CBC) count to detect contributing anemia

  • Arterial blood gases (ABGs) to assess degree of acidosis or hypoxemia

  • Quantitative drug levels (eg, quinidine, procainamide, tricyclic antidepressants, digoxin)

  • Toxicologic screens and levels, as clinically indicated

  • Thyroid-stimulating hormone: Hyperthyroidism can lead to tachycardia and tachyarrhythmias; over a time period, it can also lead to heart failure

  • B-type natriuretic peptide (BNP)

Elevations in levels of cardiac enzymes may indicate myocardial ischemia or infarction, with the extent of myocardial damage usually correlating with the degree of elevation in the enzyme levels. Patients with myocardial infarction (MI) are at increased risk for arrhythmia in the peri-infarct period.

Measurement of drug serum levels is indicated in patients taking agents that may have a proarrhythmic effect. With some medications, serum levels exceeding the therapeutic index can promote arrhythmia. Subtherapeutic levels of drugs for specific cardiac conditions can also increase the risk for arrhythmia. Most of the antiarrhythmic drugs also have proarrhythmic effects. A toxicology screen for drugs that can lead to vasospasm-induced ischemia (eg, cocaine) is warranted if suspicion exists.

BNP measurement may be useful in the diagnosis of decompensated heart failure as the cause of VF. BNP is highly specific and sensitive for this diagnosis when elevated left ventricular (LV) end-diastolic pressure is causing increased myocardial oxygen consumption and decreased cardiac output, leading to the abnormal myocardial substrate conditions conducive to the development of VF. For more information, see Natriuretic Peptides in Congestive Heart Failure.

Chest radiography may reveal whether a patient is experiencing congestive heart failure. Radiographs can also show signs of left or right ventricular hypertrophy. Signs of pulmonary hypertension may be evident.

First-degree relatives of patients who are diagnosed with DCM, hypertrophic cardiomyopathy (HCM), or arrhythmogenic right ventricular dysplasia (ARVD) should be screened. Screening consists of a history and physical examination, an ECG, and an echocardiogram. The value of genetic testing in conditions such as congenital long QT and HCM is still being evaluated. Some studies have recommended the testing of siblings and close relatives of people with VF caused by these conditions.


An electrocardiogram can identify conditions that place patients at risk for ventricular fibrillation, such as the following[74] :

  • Myocardial infarction

  • Prolonged or short QT interval

  • Epsilon sign (arrhythmogenic right ventricular cardiomyopathy/dysplasia [ARVC/D])

  • Brugada sign

  • Short PR interval

  • Wolff-Parkinson-White (WPW) pattern

  • Digitalis toxicity


Two-dimensional (2-D) echocardiography with Doppler is essential in the evaluation of ventricular fibrillation (VF). In patients who have had an myocardial infarction (MI), the use of 2-D echocardiograms to evaluate left wall ̶ motion abnormalities (using the left ventricular [LV] wall ̶ motion score index) can help to predict outcome and the risk for major cardiac events, including sudden death. A decrease in the ejection fraction and worsening wall-motion abnormalities with exercise may confer increased risk for the development of VF.

In the course of resuscitative attempts, VF may deteriorate or be succeeded by electromechanical dissociation or pulseless electrical activity; when this occurs, consideration of possible cardiac tamponade arises and may prompt desperate attempts at pericardiocentesis. In such situations, having echocardiographic information regarding not only LV function but also the presence or absence of pericardial fluid is advantageous.

Nuclear Imaging

Resting thallium-201 (201Tl) or technetium-99m (99mTc) scintigraphy is helpful in assessing myocardial damage after a myocardial infarction (MI).[75] In addition, resting scintigraphy tests can be very helpful in patients with low functional capacity (eg, because of chronic obstructive pulmonary disease, peripheral vascular disease, or orthopedic problems).

A larger myocardial defect on scintigraphy has been associated with greater risk for future cardiac events. However, the Multicenter Post-Infarction Research Group provided evidence that resting ejection fraction was the most important noninvasive predictor of sudden cardiac death (SCD), most commonly from ventricular fibrillation (VF), and other cardiac events in patients with MI.[76]

Exercise nuclear scintigraphy is very sensitive for detecting the presence, extent, and location of myocardial ischemia. Gibson et al found that pharmacologic-stress nuclear (dipyridamole or adenosine) scintigraphy was better than submaximal exercise ECG and coronary angiography in predicting cardiac death and other cardiac events.[75]

Coronary Angiography

Perform cardiac catheterization in patients with probable coronary artery disease (CAD) who survive ventricular fibrillation (VF), to assess the severity and extent of the coronary artery disease. The number of vessels with severe obstruction and the degree of left ventricular (LV) dysfunction are important variables in predicting cardiac events, with LV ejection fraction (LVEF) being the best predictor of significant cardiac events and survival. Coronary angiography can also help to identify coronary anomalies and other forms of congenital heart disease.

Coronary angiography is typically the initial step in the acute revascularization, indicated when VF is the presenting manifestation of acute myocardial infarction.

Angiography is performed with the goal of identifying patients who may benefit from revascularization. Revascularization is potentially the treatment for ischemic myocardium, which is the most common underlying substrate of ventricular tachycardia and VF, but it has been shown to have less utility when the underlying myocardial substrate primarily involves scar rather than ischemic myocardium.

Electrophysiologic Studies

Electrophysiologic (EP) studies (EPS) are usually performed after ischemic and structural heart disease has been diagnosed and addressed as best as it can be. These studies are generally not indicated for the subset of patients in whom ventricular fibrillation (VF) occurred within the first 24-48 hours of an acute myocardial infarction (MI), unless the patient had previous VF events. In all other patients with VF, however, consider EPS for diagnostic and therapeutic guidance.

EPS have been used to distinguish patients with inducible ventricular tachycardia (VT)/VF from those with no inducible sustained ventricular arrhythmias. The presence of inducible sustained VT or VF, at baseline or when the patient is on antiarrhythmic medications, confers a higher risk for sudden death.[77]  Significantly lower ventricular function has also been observed in patients with inducible sustained VT or VF.

Sustained monomorphic VT induced with up to triple extrastimuli confers increased risk of sudden cardiac death. However, polymorphic VT or VF induced by the use of triple extrastimuli is less specific and may not represent clinically significant arrhythmia.[78, 79]

EPS can also risk-stratify patients with borderline severe depression of ejection fraction (< 40% but >30%). These patients are candidates for primary prevention with an implantable cardioverter defibrillator (ICD) if a sustained monomorphic ventricular arrhythmia is induced during an EPS.[80]

Inducible bundle-branch reentrant VT can be observed in patients with dilated cardiomyopathy and in the postoperative period after valvular replacement. Up to 20% of patients with hypertrophic cardiomyopathy have inducible sustained monomorphic VT. Identification of accessory pathways is possible with EPS.



Approach Considerations

Acute ventricular fibrillation (VF) is treated according to Advanced Cardiac Life Support (ACLS) protocols.[81, 82] ) Interest in improving rates of public cardiopulmonary resuscitation (CPR) training—with a special emphasis on the use of early defibrillation with automated external defibrillators (AEDs) by public service personnel (eg, police, fire, airline)—is widespread.[2] These measures can help to achieve the greatest public health benefits in the fight against sudden death.

Prevention of VF is directed at the underlying cause (see Etiology). Pharmacotherapy or surgical treatment (eg, operable coronary artery disease [CAD]) may be appropriate in some cases, whereas radiofrequency ablation is effective in a variety of disorders.

Antiarrhythmic drugs appear to be beneficial for individuals with unsuccessful initial early CPR and defibrillation attempts when these agents are administered early.[83]  When defibrillation and antiarrhythmic medications are ineffective, potential additional survival benefit may be seen with other interventions, such as percutaneous coronary intervention (PCI) and extracorporeal CPR.[83]

Implantable cardioverter-defibrillators (ICDs), which effectively provide early defibrillation, are used for patients at high risk for recurrent VF. Studies indicate that patients with VF arrest who receive ICDs have better long-term survival rates than do patients who receive only medication.[84, 85, 86, 87]


External electrical defibrillation remains the most successful treatment for ventricular fibrillation (VF). A shock is delivered to the heart to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objectives are 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 two key factors: the duration of the VF and the metabolic condition of the myocardium. The VF waveform usually begins with a relatively high amplitude and frequency; it then degenerates to a smaller and smaller amplitude until, after approximately 15 minutes, asystole is reached, possibly because of depletion of the heart's energy reserves. Unfortunately, VF waveform measures do not appear to be useful for differentiating ischemic from nonischemic cardiac arrest etiology.[88]

Consequently, early defibrillation is vital; emergency medical services (EMS) personnel can perform defibrillation at the scene, long before the patient could be seen at the emergency department (ED). In addition, the placement of automated external defibrillators (AEDs) in public places such as airports, casinos, and restaurants allows prompt use of these devices by trained laypersons.

Defibrillation success rates decrease about 5%-10% for each minute after the onset of VF. In strictly monitored settings where defibrillation was performed most promptly, success rates of 85% have been reported.

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

  • Time from onset of VF to defibrillation

  • Paddle size

  • Paddle-to-myocardium distance: This is affected, for example, by obesity or mechanical ventilation

  • Use of conduction fluid (eg, disposable pads, electrode paste/jelly)

  • Contact pressure

  • Stray conductive pathways (eg, electrode jelly bridges on skin)

  • Previous shocks, which decrease the defibrillation threshold

The goal is to use the minimum amount of energy required to overcome the threshold of defibrillation. Excessive energy can cause myocardial injury and arrhythmias.

Larger paddles result in lower impedance, which allows the use of lower-energy shocks. Approximate optimal sizes are 8-12.5 cm (3.15-4.92 inches) for an adult, 8-10 cm (3.15-3.94 inches) for a child, and 4.5-5 cm (1.77-1.97 inches) for an infant. Position one paddle below the outer half of the right clavicle and one over the cardiac apex (V4 -V5) (see the following image).

Position of the paddle electrodes during defibrill Position of the paddle electrodes during defibrillation/cardioversion, position of the heart, and flow of intrathoracic energy during delivery of the electric shock are shown.

Before initiating any defibrillation, remove all patches and ointments from the chest wall because they create a risk of fire or explosion. The patient must be dry and not in contact with metallic objects. Rescuers must remember to ensure the safety of everyone around the patient before each shock is applied.

If defibrillation reestablishes coordinated myocardial contraction, a period of low cardiac output (ie, postcountershock myocardial depression) may ensue. Recovery of cardiac output may take minutes to hours.

Defibrillation causes serum creatine phosphokinase (CPK) levels to increase in proportion to the amount of electric energy delivered. If customary voltage is used to defibrillate a patient, the proportion of myocardial fraction (CK-MB) should remain within reference ranges unless an infarction has caused myocardial injury.

Although the precordial thump is less appropriate for VF than for VT, it is actually not appropriate in both. Use it only for witnessed, monitored arrests in which no defibrillator is immediately available.

ACLS Algorithm

Cardiopulmonary resuscitation

For an adult who is unresponsive, pulseless, and not breathing (or has only agonal respirations), activate the emergency response system, dial 911 or the emergency number, and retrieve an automated external defibrillator (AED). Initiate cardiopulmonary resuscitation (CPR) by giving 30 chest compressions; then, open the airway and deliver 2 breaths. Continue CPR in this compression-to-ventilation ratio (30:2) until the AED/defibrillator arrives and is set up. Chest compressions should be hard and fast—2 inches or more, at a rate of at least 100-120 per minute—with complete recoil in between.

In a secondary analysis of data from the Circulation Improving Resuscitation Care trial to evaluate preshock pause and termination of ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT) 5s postshock (TOF) and return of organized rhythm (ROOR) with mechanical load-distributing band (LDB)-CPR and manual (M)-CPR, Olsen et al found that for first shocks with LDB-CPR, preshock pause duration was associated with TOF but that there was no association for the rate of ROOR.[89] For M-CPR, in which no shocks were given during continuous chest compressions, there were no significant associations between preshock pause duration and TOF or ROOR.[89]

Note that a growing body of research has found no benefit from ventilation in CPR for out-of-hospital cardiac arrest.[90, 91] Indeed, the adoption of chest-compression–only CPR (also known as cardiocerebral resuscitation) has been shown to substantially increase neurologically intact survival of patients with out-of-hospital cardiac arrest from VF.[92] The American Heart Association (AHA) currently recommends the use of chest compression-only CPR ("hands-only CPR") by laypeople in the out-of-hospital setting, in response to witnessed sudden collapse of a teen or adult.


Connect the AED/defibrillator and check for a shockable rhythm. If a shockable rhythm is present, continue CPR while the defibrillator is charging. Deliver one (1) defibrillation shock to the patient (monophasic, 200 J for an adult, 2 J/kg for a child; or equivalent biphasic energy). Resume CPR immediately. Give three (3) cycles of CPR, and then check the rhythm.

Additional actions

While minimizing interruption of chest compression, do the following[81] :

  • Consider placement of an advanced airway (continuous chest compressions can be given after an advanced airway is in place)

  • Consider waveform capnography

  • Obtain intravenous (IV) or intraosseous (IO) access

  • Consider administering vasopressors and antiarrhythmics

  • Correct reversible causes

Vasopressors (epinephrine or vasopressin) are given per the asystole/pulseless electrical activity (PEA) advanced cardiac life support (ACLS) algorithm:

  • Epinephrine 1 mg IV/IO, repeat every 3-5 minutes, or

  • Vasopressin (1-time dose), 40 U IV/IO, to replace the first or second dose of epinephrine.

Antiarrhythmic agents can be given before or after the shock. Amiodarone is given as 300 mg IV/IO once (then, consider an additional 150 mg IV/IO, once). Alternatively, lidocaine is given in a first dose of 1-1.5 mg/kg IV/IO, followed by 0.5-0.75 mg/kg IV/IO, for a maximum of three (3) doses or 3 mg/kg. If torsade de pointes is present, consider administering magnesium sulfate, loading dose 1-2 g IV/IO.

Treat the following underlying provocative abnormalities, if present:

  • Myocardial infarction

  • Hypovolemia

  • Hemorrhagic shock

  • Anoxia/hypoxia

  • Pneumothorax/hemothorax

  • Hypercalcemia

  • Drug overdose (eg, narcotic, tricyclic antidepressant, cocaine, barbiturate)

  • Carbon monoxide poisoning

  • Hyperkalemia

Refractory VF

Lack of response to the standard defibrillation protocol is challenging, and the addition of magnesium and/or procainamide is often ineffective.[93] If amiodarone was not used earlier, consider giving 15 mg/min for 10 minutes, followed by 1 mg/min for 6 hours, and then 0.5 mg/min for 18 hours. Reported defibrillation alternatives such as transesophageal and intracardiac defibrillation or thoracotomy with internal defibrillation are generally impractical because of limited experience and availability of equipment and trained personnel.

Postresuscitative Care

Careful postresuscitative care is essential to survival, because studies have shown a 50% repeat in-hospital arrest rate for people admitted after a ventricular fibrillation (VF) event. Multiple randomized trials have confirmed the benefit of treating myocardial ischemia, heart failure, and electrolyte disturbances.

Important considerations

Resuscitated patients must be admitted to an intensive care unit (ICU) and closely monitored because of the high rate of early recurrence. Antiarrhythmics successfully used during resuscitation are usually continued. Maintenance infusions of lidocaine (1-4 mg/min) or amiodarone (0.5-1 mg/min) are the most commonly used therapies. Control any hemodynamic instability. Administer vasopressors as indicated.

Postdefibrillation arrhythmias (mainly atrioventricular [AV] blocks) have been reported in up to 24% of patients. The incidence is related to the amount of energy used for defibrillation.

Assess for complications (eg, aspiration pneumonia, cardiopulmonary resuscitation [CPR]-related injuries), and establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).

Mild therapeutic hypothermia has been shown to improve neurologic outcomes and survival after out-of-hospital cardiac arrest and should be considered in appropriate patients.[20, 94] Traditionally, a target temperature of 32°-34°C (89.6°-93°F) has been recommended. A study has shown, however, that in unconscious survivors of out-of-hospital cardiac arrest of presumed cardiac cause, hypothermia at a targeted temperature of 33°C (91.4°F) did not confer a benefit as compared with a targeted temperature of 36°C (96.8°F).[95]  During therapeutic hypothermia in patients with aborted arrhythmic sudden cardiac death (SCD), a prolonged T-wave peak to T-wave end (Tpeak-Tend) interval and QTc interval may predict the development of VF in the follow-up period.[96]

Patients require stabilization and monitoring for the possibility of a coexistent emergency or complication. Empiric beta blockers are reasonable in many circumstances because of favorable properties discussed in Etiology. However, empiric antiarrhythmics, including amiodarone, should not supersede implantable cardioverter-defibrillator (ICD) placement unless control of recurrent VT is needed while the patient is hospitalized.

Evaluation of ischemic injury to the central nervous system, myocardium, and other organs is essential. Survivors should undergo thorough diagnostic testing to establish the underlying etiology of the VF episode. If available, perform indicated interventions to improve long-term prognosis.

An analysis of data from the Israeli ICD Registry suggests that the presence of anemia in patients with ICDs is an independent factor that increases the risk for ventricular arrhythmias over the long term.[97]  Clinically at-risk patients with anemia were older, had more advanced heart failure symptoms, and/or had atrial fibrillation. At 2.5 years of follow-up, patients with lower hemoglobin levels had significantly greater rates of appropriate shocks than those with higher hemoglobin levels, and the presence of anemia was associated not only with a significant 56% increased risk for first appropriate ICD shock but also with a greater risk for all-cause mortality and hospitalizations for, or deaths from, heart failure.[97]

Radiofrequency Ablation

Radiofrequency ablation (RFA) is indicated for prevention of ventricular fibrillation (VF) in patients with the following:

  • Atrioventricular (AV) bypass tracts

  • Bundle-branch block ventricular tachycardia (VT)

  • Right ventricular outflow tract (RVOT) tachycardia

  • Idiopathic left ventricular (LV) tachycardia

  • Idiopathic VF[34]

  • Rare forms of automatic focal VT (however, these almost never cause VF)

  • Scar-related VT due to ischemic or nonischemic myopathy

Unfortunately, most cases of VF are not amenable to radiofrequency ablation, with such patients requiring placement of an implantable cardioverter-defibrillator (ICD).

In patients with Wolff-Parkinson-White (WPW) syndrome, VF may be due to preexcited atrial tachycardias; patients with WPW and VF should undergo catheter ablation of the accessory pathway.

Implantable Cardioverter-Defibrillators

Survivors of ventricular fibrillation (VF) that does not have a clear and readily reversible cause should undergo placement with an implantable cardioverter-defibrillator (ICD). Transvenous ICDs can be placed with minimal morbidity and mortality. Several multicenter trials have demonstrated the prophylactic value of ICD therapy in patients at high risk for VF.

In a comparative effectiveness study of ICD therapy in survivors of in-hospital cardiac arrest, investigators linked data from a national inpatient cardiac arrest registry with Medicare files and identified 1200 adults who were discharged after surviving an in-hospital cardiac arrest due to VF or pulseless ventricular tachycardia (VT) and who otherwise met traditional inclusion and exclusion criteria for secondary prevention ICD trials.[98] Using an optimal match propensity-score analysis, the investigators evaluated the association between ICD treatment and long-term mortality and found that ICD therapy in survivors of in-hospital cardiac arrest due to a pulseless ventricular rhythm is associated with lower long-term mortality.[98]

In several studies that compared ICD placement with antiarrhythmic therapy in patients with VT/VF and/or prior cardiac arrest, ICD placement was shown to be associated with a significantly decreased mortality rate.[84, 99, 100] However, ICD placement may also be appropriate in conjunction with antiarrhythmic therapy. Matsue et al demonstrated the benefit of ICD placement and medication in patients with vasospastic angina who had been resuscitated from lethal ventricular arrhythmia.[101]

The use of ICDs as primary prevention for VF has also been demonstrated in patients with LV dysfunction. Newer ICDs have pacing capabilities and have addressed bradyarrhythmias that either cause or complicate VT or VF. ICDs are indicated for the secondary prevention of VF and for the primary prevention of VF in patients with an LV ejection fraction (LVEF) of less than 35%, whether due to ischemic or nonischemic cardiomyopathy.[102, 103]

Findings from a study of subcutaneous ICD (S-ICD) in 60 patients following its introduction in Japan as an alternative to conventional transvenous ICD (TV-ICD) in February 2016 show it is safe and effective in those at high risk of sudden cardiac death.[104] Of 56 patients who underwent a postprocedure defibrillation test, VF was induced in 55 patients (98%), with 100% termination by a single 65-J shock. No complications related to the procedure or infection were noted. During a median follow-up period of 275 days, one patient (1.7%) received an appropriate shock for VF with termination, but five patients (8.3%) received an inappropriate shock from myopotential (n = 3) or T-wave (n = 1) oversensing or for detection of a supraventricular tachycardia (n = 1).[104] These preliminary findings for S-ICD require more studies.

Cardiac Surgery

Cardiac surgery can be a primary treatment for VF via a variety of strategies. Surgical treatment in patients with ventricular arrhythmias and ischemic heart disease includes coronary artery bypass grafting (CABG). The Coronary Artery Surgery Study (CASS) illustrated that patients with significant coronary artery disease (CAD) and operable vessels who underwent CABG had a decrease in the incidence of VT/VF arrest compared with patients on conventional medical treatment. The reduction was most evident in patients who had three-vessel disease and chronic heart failure.[10]

By itself, CABG prevents recurrent VF only if the ejection fraction is normal and ischemia was the cause of the arrest.

Surgical treatment of ventricular arrhythmias in patients with nonischemic heart disease includes excision of VT foci after endocardial mapping and excision of LV aneurysms. This is practiced very infrequently due to significant morbidity and limited efficacy.

Aortic valve replacement is associated with improved outcome in patients with hemodynamically significant valvular stenosis and well-preserved ventricular function. Mitral valve replacement is indicated for patients with mitral valve prolapse who have malignant tachyarrhythmias such as VT and VF associated with significant valvular regurgitation and LV dysfunction.

Orthotopic heart transplantation is indicated in patients with refractory heart failure and/or ventricular arrhythmias, in whom significant improvement in actuarial survival is expected. Given a limited donor supply, this form of treatment is expected to be beneficial for very few people who survive VF.

Screening for Hypertrophic Cardiomyopathy

To prevent ventricular fibrillation (VF), screen for hypertrophic cardiomyopathy (HCM) in young patients who are at high suspicion for HCM, particularly those who are prospective candidates for competitive-level athletics.[30]

Coventional risk factors for sudden cardiac death (SCD) in HCM include the following:

  • Syncope

  • Abnormal blood pressure response (ie, hypotension) to exercise

  • Nonsustained or sustained ventricular tachycardia (VT)

  • Paroxysmal supraventricular tachycardia (PSVT)

  • Paroxysmal atrial fibrillation (PAF)

  • Family history of sudden cardiac death (SCD) from suspected or diagnosed HCM

Nonconventional risk factors for an increased risk of SCD in HCM include the following:

  • Magnetic resonance imaging (MRI)-based scar: Extensive late gadolinium enhancement (LGE) by contrast cardiac MRI has been introduced as an independent marker of sudden death (SD) in HCM.[105]  The risk increases linearly with respect to the percentage (%) LGE of the left ventricular (LV) myocardium: 15% LGE conveys a two-fold increase in risk. Extensive LGE acts as a risk factor even in the absence of conventional markers, identifying patients at SD risk who otherwise would not be considered candidates for implantable cardioverter-defibriIlators (ICDs).[105]  Absent or focal LGE is associated with low risk and is a source of reassurance.[105]

  • LV apical aneurysms: LV apical aneurysms are relatively uncommon in HCM. However, they are associated with an increased risk of SCD due to monomorphic VT, and placement of an ICD may be justified.[106]

When HCM is identified in a young patient, treatment should be initiated as quickly as possible.


A cardiologist must be involved in the care of patients who have had a ventricular tachycardia/ventricular fibrillation (VT/VF) cardiac arrest or who have symptoms of ischemic heart disease, valvular disorders, or presentations with complex arrhythmias. Cardiac electrophysiologists should also be involved in the care of these patients, which generally involves placement of an implantable cardioverter-defibrillator (ICD).

Other consultants include an interventional cardiologist and a cardiac surgeon. Such consultations are made on a case-by-case basis. Patients should be cared for at centers where intensive cardiac monitoring and appropriate invasive and noninvasive studies can be performed. In general, a cardiovascular service, including interventional cardiology, electrophysiology, and cardiac surgery, is needed.



Guidelines Summary

Advanced cardiac life support (ACLS) guidelines

Updated cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) guidelines were issued in 2015, 2017, and/or 2018 by the following organizations:

  • American Heart Association (AHA) [81, 107, 108]
  • European Resuscitation Council (ERC) [109]
  • The International Liaison Committee on Resuscitation (ILCOR) [82, 110]

The following summarizes the AHA adult cardiac arrest algorithm for ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT)[81, 107, 108] :

  • Activate the emergency response system.
  • Initiate CPR and give oxygen when available.
  • Rescuers trained in CPR using chest compressions and ventilation (rescue breaths) should provide a compression-to-ventilation ratio of 30:2 for adults in cardiac arrest (class IIa).
  • Verify the patient is in VF as soon as possible (ie, automated external defibrillator [AED] and quick look with paddles).
  • Defibrillate once: Use device-specific recommendations (ie, 120-200 J for biphasic waveform; if unknown, use the maximum available. Use 360 J for monophasic waveform).
  • Resume CPR immediately without pulse check and continue for five (5) cycles. One (1) cycle of CPR equals 30 compressions and 2 breaths; 5 cycles of CPR should take roughly 2 minutes (compression rate of 100-120 per minute). Do not check for rhythm/pulse until 5 cycles of CPR are completed.
  • During CPR, minimize interruptions while securing intravenous (IV)/intraosseous (IO) access and performing endotracheal intubation. Once the patient is intubated, continue CPR at 100-120 compressions per minute without pauses for respirations, and administer respirations at 10 breaths per minute.
  • Check the cardiac rhythm after 2 minutes of CPR.
  • Repeat a single defibrillation if  VF/pVT persists at the rhythm check. The selection of fixed versus escalating energy for subsequent shocks is based on the specific manufacturer’s instructions. [81] For a manual defibrillator capable of escalating energies, using higher energy for the second and subsequent shocks may be considered.
  • Resume CPR for 2 minutes immediately after defibrillation.
  • Continuously repeat the cycle of (1) rhythm check, (2) defibrillation, and (3) 2 minutes of CPR.
  • Administer a vasopressor: Give a vasopressor during CPR before or after the shock when IV/IO access is available. Administer epinephrine 1 mg every 3-5 minutes.
  • Administer antidysrhythmics: Give an antidysrhythmic during CPR before or after the shock. Administer amiodarone 300 mg IV/IO once; then, consider administering an additional 150 mg, once.

In addition, correct the following causes if necessary and/or possible[81] :

  • Hypovolemia
  • Hypoxia
  • Hydrogen ion (acidosis): Consider bicarbonate therapy.
  • Hyperkalemia/hypokalemia and other metabolic derangements
  • Hypoglycemia (Check fingerstick or administer glucose.)
  • Hypothermia (Check the core rectal temperature.)
  • Toxins
  • Tamponade, cardiac (Assess with ultrasonography.)
  • Tension pneumothorax (Consider needle thoracostomy.)
  • Thrombosis, coronary or pulmonary: Consider thrombolytic therapy, if suspected.

The AHA indicates that If all the following conditions are present, termination of resuscitation in out-of-hospital cardiac arrest (OHCA) may be considered[111] :

  • Arrest was not witnessed by emergency medical services (EMS) personnel
  • No return of spontaneous circulation (ROSC) prior to transport
  • No AED shock delivered prior to transport

In addition, in intubated patients, failure to achieve an end-tidal carbon dioxide (ETCO2) level above 10 mm Hg by waveform capnography after 20 minutes of CPR may be considered as one component of a multimodal approach to decide when to end resuscitative efforts.[111, 112] However, no studies of nonintubated patients have been reviewed, thus, ETCO2 should not be used as an indication to end resuscitative efforts.[111, 112]


AHA recommendations for defibrillation include the following[81] :

  • Defibrillators (using biphasic truncated exponential [BTE], rectilinear biphasic [RLB], or monophasic waveforms) to treat atrial and ventricular arrhythmias (class I)
  • Defibrillators using biphasic waveforms (BTE or RLB) are preferred for atrial and ventricular arrhythmias (class IIa).
  • A single-shock strategy (as opposed to stacked shocks) for defibrillation (class IIa).
  • The benefit of using a multimodal defibrillator in manual instead of automatic mode is uncertain (class IIb).
  • The value of VF waveform analysis to guide management of defibrillation is uncertain (class IIb). [113]

Overall, the ERC and ILCOR guidelines concur with the AHA,[82, 109, 110] but the ERC includes an additional recommendation for self-adhesive defibrillation pads, which are preferred over manual paddles and should always be used when they are available.[109]

Adjuncts for airway control and ventilation

The AHA guidelines provide the following recommendations for airway control and ventilation[81, 108, 113] :

  • Advanced airway placement in cardiac arrest should not delay initial CPR and defibrillation for VF cardiac arrest (class I).
  • Use supplementary oxygen when it is available, at the maximal feasible inspired oxygen concentration, during CPR (class IIb).
  • Before placement of an advanced airway (supraglottic airway [SGA] or endotracheal tube [ETT]), it is reasonable for EMS providers to perform CPR with cycles of 30 compressions and 2 breaths (class IIa); before placement of an advanced airway, it may be reasonable for EMS providers to use a rate of 10 breaths per minute (1 breath every 6 seconds) to provide asynchronous ventilation during continuous chest compressions (class IIb).
  • If advanced airway placement will interrupt chest compressions, consider deferring insertion of the airway until the patient fails to respond to initial CPR and defibrillation attempts or demonstrates ROSC (class IIb).
  • The routine use of cricoid pressure in cardiac arrest is not recommended (class III).
  • Either a bag-mask device or an advanced airway may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital setting (class IIb). The choice of bag-mask device versus advanced airway insertion should be determined by the skill and experience of the provider (class I).
  • For healthcare providers trained in their use, either an SGA device or an ETT may be used as the initial advanced airway during CPR (class IIb).
  • Whenever an advanced airway (SGA or ETT) is inserted during CPR, it may be reasonable for providers to perform continuous compressions with positive-pressure ventilation delivered without pausing chest compressions (class IIb); it may be reasonable for the provider to deliver 1 breath every 6 seconds (10 breaths per minute) while continuous chest compressions are being performed (class IIb).
  • Providers who perform endotracheal intubation should undergo frequent retraining (class I).
  • To facilitate delivery of ventilations with a bag-mask device, oropharyngeal airways can be used in unconscious (unresponsive) patients with no cough or gag reflex and should be inserted only by trained personnel (class IIa).
  • In the presence of known or suspected basal skull fracture or severe coagulopathy, an oral airway is preferred (class IIa).
  • Continuous waveform capnography plus clinical assessment is the most reliable method of confirming and monitoring correct placement of an ETT (class I).
  • If continuous waveform capnometry is not available, a nonwaveform carbon dioxide (CO 2) detector, esophageal detector device, or ultrasound used by an experienced operator is a reasonable alternative (class IIa).
  • After placement of an advanced airway, it is reasonable for the provider to deliver one (1) breath every 6 seconds (10 breaths/min) while continuous chest compressions are performed (class IIb).
  • Automatic transport ventilators (ATVs) can be useful for ventilation of adult patients in noncardiac arrest who have an advanced airway in place in both out-of-hospital and in-hospital settings (class IIb).

There are no significant differences in the recommendations from the ERC or ILCOR.[82, 109, 110]

Medication management

The 2015 AHA guidelines offers the following recommendations for the administration of drugs during cardiac arrest[81] :

  • Amiodarone may be considered for VF or pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy; lidocaine may be considered as an alternative (both class IIb).
  • Routine use of magnesium for VF/pVT is not recommended in adult patients (class III).
  • Inadequate evidence exists to support the routine use of lidocaine after cardiac arrest. However, the initiation or continuation of lidocaine may be considered immediately after ROSC from cardiac arrest due to VF/pVT (class IIb).
  • Inadequate evidence exists to support the routine use of a β-blocker after cardiac arrest. However, the initiation or continuation of an oral or IV β-blocker may be considered early after hospitalization from cardiac arrest due to VF/pVT (class IIb).
  • Atropine during pulseless electrical activity (PEA) or asystole is unlikely to have a therapeutic benefit (class IIb).
  • Standard-dose epinephrine (1 mg every 3-5 minutes) may be reasonable for patients in cardiac arrest (class IIb); high-dose epinephrine is not recommended for routine use in cardiac arrest (class III).
  • Vasopressin has been removed from the Adult Cardiac Arrest Algorithm because it offers no advantage in combination with epinephrine or as a substitute for standard-dose epinephrine (both class IIb)
  • It may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest due to an initial nonshockable rhythm (class IIb).

ICD therapy

In their 2008 joint guidelines for device-based therapy, the American College of Cardiology /American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) provided recommendations that included those outlined below.[102]

Class I

ICD therapy is indicated for the following people:

  • Survivors of cardiac arrest due to VF or hemodynamically unstable sustained VT after evaluation to determine the etiology and to exclude any completely reversible causes (level of evidence [LOE]: A)

  • Patients with structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable (LOE: B)

  • Patients with syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT/VF induced at electrophysiological study (EPS) (LOE: B)

  • Patients with an LVEF up to 35% due to prior myocardial infarction (MI) who are at least 40 days post-MI and are in New York Heart Association (NYHA) functional class II or III (LOE: A)

  • Patients with nonischemic dilated cardiomyopathy (DCM) who have an LVEF up to 35% and who are in NYHA functional class II or III (LOE: B)

  • Patients with LV dysfunction due to prior MI who are at least 40 days post-MI, have an LVEF up to 30%, and are in NYHA functional class I (LOE: A)

  • patients with nonsustained VT due to prior MI, LVEF up to 40%, and inducible VF or sustained VT at EPS

Class IIa

ICD implantation is reasonable for patients with the following:

  • Sustained VT and normal or near-normal ventricular function (LOE: C)
  • Catecholaminergic polymorphic VT who have syncope and/or documented sustained VT while receiving beta blockers. (LOE: C)
  • Brugada syndrome who have had (1) syncope or (2) documented VT that has not resulted in cardiac arrest (LOE: C)
  • Unexplained syncope, significant LV dysfunction, and nonischemic DCM (LOE: C)
  • Hypertrophic cardiomyopathy (HCM) who have one or more major risk factors for sudden cardiac death (SCD) (LOE: C)
  • Cardiac sarcoidosis, giant cell myocarditis, or Chagas disease (LOE: C)

ICD implantation is also reasonable for (1) reduction of SCD in patients with long-QT syndrome who are experiencing syncope and/or VT while receiving beta blockers (LOE: B) or (2) prevention of SCD in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy) (ARVD/C) who have one or more risk factors for SCD (LOE: C).

Class III

ICD implantation is not indicated for the following patients:

  • Those who do not have a reasonable expectation of survival with an acceptable functional status for at least 1 year, even if they meet ICD implantation criteria specified above (LOE: C)

  • Those with incessant VT or VF (LOE: C)

  • Those with significant psychiatric illnesses that may be aggravated by device implantation or that may preclude systematic follow-up (LOE: C)

  • Those with syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart disease. (LOE: C)

  • When VF or VT is amenable to surgical or catheter ablation (eg, atrial arrhythmias associated with the Wolff-Parkinson-White syndrome, RV or LV outflow tract VT, idiopathic VT, or fascicular VT in the absence of structural heart disease) (LOE: C)

  • Those with ventricular tachyarrhythmias due to a completely reversible disorder in the absence of structural heart disease (eg, electrolyte imbalance, drugs, or trauma) (LOE: B)

In the 2012 ACC Foundation/AHA/HRS focused update, after a review of all published evidence since the publication of the 2008 guidelines, it was determined that no changes were warranted in the recommendations for ICD indications.[114]

Idiopathic VF 

In its 2013 expert consensus statement on inherited primary arrhythmia syndromes, the Heart Rhythm Society/European Heart Rhythm Association/Asia Pacific Heart Rhythm Society (HRS/EHRA/APHRS) recommended a diagnosis of idiopathic VF when a resuscitated cardiac arrest victim, preferably with documentation of VF, has known cardiac, respiratory, metabolic, and toxicologic etiologies excluded through clinical evaluation.[115]

Treatment recommendations include[115] :

  • ICD implantation (class I)
  • Consider antiarrhythmic therapy with quinidine, programmed electrical stimulation guided or empirical, in patients in conjunction with ICD implantation or when ICD implantation is contraindicated or refused (class IIb).
  • Consider ablation of Purkinje potentials in patients presenting with uniform morphology premature ventricular contractions in conjunction with ICD implantation or when ICD implantation is contraindicated or refused (class IIb)
  • If a first-degree relative presents with unexplained syncope and no identifiable phenotype, then after careful counseling an ICD implant may be considered (class IIb).

Guidelines released in 2015 by the European Society of Cardiology (ESC) for the management of ventricular arrhythmias and prevention of SCD, include the following recommendations for the treatment of idiopathic VF (all class I)[116] :

  • ICD implantation is recommended in all survivors of idiopathic VF.
  • When performed by experienced operators, catheter ablation can terminate premature ventricular complexes (PVCs) triggering recurrent VF that lead to ICD interventions, or of PVCs leading to electrical storm.


Medication Summary

In acute ventricular fibrillation (VF), drugs (eg, vasopressin, epinephrine, amiodarone) are used after three defibrillation attempts are performed to restore normal rhythm. Amiodarone can also be used on a long-term basis in patients who refuse placement of an implantable cardioverter-defibrillator (ICD) or who are not candidates for an ICD. However, amiodarone has not been shown to be of value for primary prevention of VF in patients with a depressed left ventricular (LV) ejection fraction (LVEF).

In an analysis of the association between rearrest and intraresuscitation antiarrhythmic drugs in relation to the Resuscitation Outcomes Consortium (ROC) amiodarone, lidocaine, and placebo (ALPS) trial, investigators did not find a difference in rearrest rates between those who received amiodarone or lidocaine and those who received placebo.[117]  However, the electrocardiographic waveform characteristics were associated with the treatment group and rearrest, and rearrest was associated with poor survival and neurologic outcomes.

A retrospective study (2007-2013), using the nationwide Japanese Diagnosis Procedure Combination inpatient database comprising 2961 patients who had cardiogenic out-of-hospital cardiac arrest and who had VF on hospital arrival to assess the association between nifekalant or amiodarone on hospital admission and in-hospital mortality in these patients, found no significant in-hospital mortality association in the two groups but did reveal improved admission rates with nifekalant.[118]  These findings require additional investigation to confirm and validate the results.

Antidysrhythmics, Ia

Class Summary

Class Ia antiarrhythmics increase the refractory periods of the atria and ventricles. Myocardial excitability is reduced by an increase in the threshold for excitation and inhibition of ectopic pacemaker activity.

Procainamide (Procanbid, Pronestyl, Pronestyl [SR])

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

Antidysrhythmics, Ib

Class Summary

Class Ib antidysrhythmics suppress automaticity of conduction tissue by increasing the electrical stimulation threshold of the ventricle and His-Purkinje system and by inhibiting spontaneous depolarization of the ventricles during diastole by a direct action on the tissues. Class Ib antidysrhythmics block the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions, resulting in inhibition of depolarization, with resultant blockade of conduction.

Lidocaine (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 may be tried in patients with VT due to ischemia.

Antidysrhythmics, III

Class Summary

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

Amiodarone (Pacerone, Cordarone, Nexterone)

Amiodarone is a class III antiarrhythmic agent indicated for the management of life-threatening recurrent VF.

Amiodarone may be administered intravenously or orally.

Recurrent VF that is not due to a reversible cause can be treated with intravenous (IV) amiodarone. It decreases AV conduction and sinus node function. It also prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Amiodarone can also be used orally on a long-term basis in patients who refuse ICDs, are not candidates for ICDs, or have frequent ventricular arrhythmias.

Antidysrhythmics, V

Class Summary

Class V antidysrhythmics have a mechanism of action different from those of agents in classes I-IV; in many cases their mechanism of action is unknown.

Magnesium sulfate

Magnesium acts as an anti-arrhythmic agent and diminishes the frequency of premature ventricular contractions, particularly when secondary to acute ischemia. Clinical trials have been inconclusive in demonstrating its ability to improve mortality rates in the setting of refractory VF.


Class Summary

These agents augment the coronary and cerebral blood flow that is present during the low-flow state associated with hemodynamic compromise from VF.

Epinephrine (Adrenalin)

Epinephrine is considered to be the single most useful drug in cardiac arrest, although it has never been shown to benefit long-term survival or functional recovery. Epinephrine stimulates alpha, beta1, and beta2 receptors, resulting in relaxation of smooth muscle, cardiac stimulation, and dilation of muscle vasculature.

Vasopressin (ADH, Pitressin)

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

Vasopressin has an off-label indication for VF that is causing pulseless arrest. This agent may improve vital organ blood flow, cerebral oxygen delivery, the patient's ability to be resuscitated, and the patient's neurologic recovery.


Questions & Answers


What is ventricular fibrillation (VF)?

Where can patient education resources about ventricular fibrillation (VF) be found?

What is the pathophysiology of ventricular fibrillation (VF)?

What is the role of Brugada syndrome in the etiology of ventricular fibrillation (VF)?

What is the role of coronary artery disease (CAD) in the etiology of ventricular fibrillation (VF)?

What is the role of ischemic heart disease in the etiology of ventricular fibrillation (VF)?

What is the role of nonischemic cardiomyopathies in the etiology of ventricular fibrillation (VF)?

What is the role of dilated cardiomyopathy (DCM) in the etiology of ventricular fibrillation (VF)?

What is the role of hypertrophic cardiomyopathy (HCM) in the etiology of ventricular fibrillation (VF)?

What is the role of arrhythmogenic right ventricular (RV) cardiomyopathy/dysplasia (ARVC/D) in the etiology of ventricular fibrillation (VF)?

What is the role of aortic stenosis in the etiology of ventricular fibrillation (VF)?

What is the role of chronic aortic insufficiency in the etiology of ventricular fibrillation (VF)?

What is the role of mitral stenosis in the etiology of ventricular fibrillation (VF)?

What is the role of mitral valve prolapse (MVP) in the etiology of ventricular fibrillation (VF)?

What is the role of congenital structural heart disease in the etiology of ventricular fibrillation (VF)?

What causes paroxysmal ventricular fibrillation (VF)?

What causes idiopathic ventricular fibrillation (VF)?

What is the role of idiopathic ventricular tachycardia (VT), in ventricular fibrillation (VF)?

What is the role of pulmonary embolism in the etiology of ventricular fibrillation (VF)?

What is the role of aortic dissection in the etiology of ventricular fibrillation (VF)?

What is the role of Tasers in the etiology of ventricular fibrillation (VF)?

What is the role of nonstructural abnormalities in the etiology of ventricular fibrillation (VF)?

What is the role of congenital long QT syndrome in the etiology of ventricular fibrillation (VF)?

What is the role of Romano-Ward syndrome in the etiology of ventricular fibrillation (VF)?

What is the role of Jervell and Lange-Nielsen syndrome in the etiology of ventricular fibrillation (VF)?

What is the role of Andersen-Tawil syndrome in the etiology of ventricular fibrillation (VF)?

What is the role of Timothy syndrome in the etiology of ventricular fibrillation (VF)?

What are is the role of acquired long QT syndrome in the etiology of ventricular fibrillation (VF)?

Which medications cause ventricular fibrillation (VF)?

What is the role of catecholaminergic polymorphic VT (CPVT in the etiology of ventricular fibrillation (VF)?

What is the role of Wolff-Parkinson-White (WPW) syndrome in the etiology of ventricular fibrillation (VF)?

What is the incidence of ventricular fibrillation (VF) in the US?

What is the global incidence of ventricular fibrillation (VF)?

Which patient groups have the highest incidence of ventricular fibrillation (VF)?

What is the prognosis of ventricular fibrillation (VF)?

What is the prevalence of anoxic encephalopathy in patients with ventricular fibrillation (VF), and how does it affect prognosis?


Which clinical history findings are characteristic of ventricular fibrillation (VF)?

What are risk factors for ventricular fibrillation (VF)?

Which conditions increase the risk of ventricular fibrillation (VF)?

What is the role of the cardiac arrest score in the initial evaluation of ventricular fibrillation (VF) and how is it calculated?


Which conditions should be included in the differential diagnoses of ventricular fibrillation (VF)?

What are the differential diagnoses for Ventricular Fibrillation?


How is ventricular fibrillation (VF) diagnosed?

Which lab tests are performed in the workup of ventricular fibrillation (VF)?

What is the role of chest radiography in the workup of ventricular fibrillation (VF)?

Who should be screened for ventricular fibrillation (VF)?

What is the role of electrocardiography in the evaluation of ventricular fibrillation (VF)?

What is the role of echocardiography in the workup of ventricular fibrillation (VF)?

What is the role of nuclear imaging in the workup of ventricular fibrillation (VF)?

What is the role of coronary angiography in the workup of ventricular fibrillation (VF)?

What is the role of electrophysiologic studies (EPS) in the workup of ventricular fibrillation (VF)?


How is ventricular fibrillation (VF) treated?

What is the role of defibrillation in the treatment of ventricular fibrillation (VF)?

How is defibrillation administered for ventricular fibrillation (VF)?

What is the advanced cardiac life support (ACLS) algorithm for cardiopulmonary resuscitation and defibrillation for ventricular fibrillation (VF)?

Which vasopressors are administered during advanced cardiac life support (ACLS) for ventricular fibrillation (VF)?

What is the role of antiarrhythmic agents in the advanced cardiac life support (ACLS) algorithm for ventricular fibrillation (VF)?

Which abnormalities should be treated during advanced cardiac life support (ACLS) for ventricular fibrillation (VF)?

What is included in advanced cardiac life support (ACLS) for refractory ventricular fibrillation (VF)?

What is included in postresuscitative care in patients with ventricular fibrillation (VF)?

What is the role of radiofrequency ablation (RFA) in the treatment of ventricular fibrillation (VF)?

What is the role of implantable cardioverter-defibrillators (ICD) in the treatment of ventricular fibrillation (VF)?

What is the role of cardiac surgery in the treatment of ventricular fibrillation (VF)?

What are the risk factors for sudden cardiac death (SCD) in patients with ventricular fibrillation (VF)?

Which specialist consultations are beneficial for patients with ventricular fibrillation (VF)?


Which organizations have issued cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) guidelines for patients with ventricular fibrillation (VF)?

What is the AHA adult cardiac arrest algorithm for ventricular fibrillation (VF)?

According to AHA guidelines, when can termination of resuscitation in out-of-hospital cardiac arrest (OHCA) be considered?

What are the AHA guidelines for defibrillation in patients with ventricular fibrillation (VF)?

What are the AHA guidelines for airway control and ventilation in patients with ventricular fibrillation (VF)?

What are the AHA guidelines for the administration of drugs during cardiac arrest in patients with ventricular fibrillation (VF)?

According to ACC/AHA/HRS guidelines, what are the class I recommendations for implantable cardioverter-defibrillator (ICD) therapy for ventricular fibrillation (VF)?

According to ACC/AHA/HRS guidelines, what are the class IIa recommendations for implantable cardioverter-defibrillator (ICD) therapy for ventricular fibrillation (VF)?

According to ACC/AHA/HRS guidelines, what are the class III recommendations against implantable cardioverter-defibrillator (ICD) therapy for ventricular fibrillation (VF)?

What are the HRS/EHRA/APHRS treatment guidelines for idiopathic ventricular fibrillation (VF)?

What are the ESC treatment guidelines for idiopathic ventricular fibrillation (VF)?


What is the role of medications in the treatment of ventricular fibrillation (VF)?

Which medications in the drug class Vasopressors are used in the treatment of Ventricular Fibrillation?

Which medications in the drug class Antidysrhythmics, V are used in the treatment of Ventricular Fibrillation?

Which medications in the drug class Antidysrhythmics, III are used in the treatment of Ventricular Fibrillation?

Which medications in the drug class Antidysrhythmics, Ib are used in the treatment of Ventricular Fibrillation?

Which medications in the drug class Antidysrhythmics, Ia are used in the treatment of Ventricular Fibrillation?