Medscape is available in 5 Language Editions – Choose your Edition here.


Ventricular Fibrillation Treatment & Management

  • Author: Sandeep K Goyal, MD; Chief Editor: Jeffrey N Rottman, MD  more...
Updated: Apr 29, 2014

Approach Considerations

Acute ventricular fibrillation (VF) is treated according to Advanced Cardiac Life Support (ACLS) protocols. (See the current ACLS guidelines.[72, 73] ) Interest in improving rates of public cardiopulmonary resuscitation (CPR) training—with a special emphasis on use of early defibrillation with automatic external defibrillators (AEDs) by public service personnel (eg, police, fire, airline)—is widespread.[74] 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). Medication therapy or surgical treatment (eg, operable coronary artery disease [CAD]) may be appropriate in some cases, while radiofrequency ablation is effective in a variety of disorders.

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 receiving only medication.[75, 76, 77, 78]



External electrical defibrillation remains the most successful treatment for 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 2 key factors: the duration of VF and the metabolic condition of the myocardium. 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.

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

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

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 effected, 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 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 for an adult, 8-10 cm for a child, and 4.5-5 cm for an infant. Position one paddle below the outer half of the right clavicle and one over the cardiac apex (V4 -V5).

Before 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 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 actually is appropriate in neither. Use it only for witnessed, monitored arrests in which no defibrillator is immediately available.


ACLS Algorithm


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 AED. Initiate 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/minute—with complete recoil in between.

It should be noted that a growing body of research has found no benefit from ventilation in CPR for out-of-hospital cardiac arrest.[79, 80] 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.[81] The American Heart Association (AHA) currently recommends the use of chest compression-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 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 3 cycles of CPR, and then check the rhythm.

Additional actions

While minimizing interruption of chest compression, do the following[72] :

  • Consider placement of an advanced airway (continuous chest compressions can be given after an advanced airway is in place)
  • Consider capnography
  • Obtain intravenous (IV) or intraosseous (IO) access
  • Consider vasopressors and antiarrhythmics
  • Correct reversible causes

Vasopressors (epinephrine or vasopressin) are given per the asystole/pulseless electrical activity 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 3 doses or 3 mg/kg. If torsade de pointes is present, consider magnesium sulfate, loading dose 1-2 g IV/IO.

Treat the following underlying provocative abnormalities, if present:

  • MI
  • 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.[82] If amiodarone was not used earlier, consider giving 15 mg/min for 10 minutes, followed by 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours. Reported 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

Resuscitated patients must be admitted to an intensive care unit and 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.

Check for complications (eg, aspiration pneumonia, CPR-related injuries), and establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).

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

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.[14, 83] Traditionally, a target temperature of 32-34°C 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 did not confer a benefit as compared with a targeted temperature of 36°C.[84]

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 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.


Radiofrequency Ablation

Radiofrequency ablation is indicated for prevention of 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 [26]
  • 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 ICD placement.

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 VF that does not have a clear and readily reversible cause should be implanted with an 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.

A multiorganizational task force that includes the American College of Cardiology and the American Heart Association has developed guidelines for the use of ICDs.[85] These guidelines are updated annually.[86]

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.[87, 75, 88] 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.[89]

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 of less than 35%, whether due to ischemic or non-ischemic cardiomyopathy.[85, 90]

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 3-vessel disease and chronic heart failure.[5]

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 VF, screen for hypertrophic cardiomyopathy in young patients who are at high suspicion for hypertrophic cardiomyopathy, particularly those who are prospective candidates for competitive-level athletics.[22] Features in the history that indicate increased risk include the following:

  • Syncope
  • Abnormal blood pressure response (ie, hypotension) to exercise
  • Nonsustained or sustained VT
  • Paroxysmal supraventricular tachycardia (PSVT)
  • Paroxysmal atrial fibrillation
  • Family history of sudden cardiac death from suspected or diagnosed hypertrophic cardiomyopathy

When hypertrophic cardiomyopathy 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 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 ICD placement.

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.

Contributor Information and Disclosures

Sandeep K Goyal, MD Clinical Fellow in Cardiac Electrophysiology, Division of Cardiovascular Medicine, Vanderbilt University Medical Center

Sandeep K Goyal, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, American Medical Association, Heart Rhythm Society

Disclosure: Nothing to disclose.


Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.


Robert E Fowles, MD Clinical Professor of Medicine, University of Utah College of Medicine; Consulting Staff, Intermountain Medical Center and LDS Hospital; Director and Consulting Staff, Department of Cardiology, Salt Lake Clinic

Robert E Fowles, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association

Disclosure: Nothing to disclose.

Brian Olshansky, MD Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

  1. Warnes CA, Roberts WC. Sudden coronary death: relation of amount and distribution of coronary narrowing at necropsy to previous symptoms of myocardial ischemia, left ventricular scarring and heart weight. Am J Cardiol. 1984 Jul 1. 54(1):65-73. [Medline].

  2. Anthony R, Daubert JP, Zareba W, Andrews ML, McNitt S, Levine E. Mechanisms of ventricular fibrillation initiation in MADIT II patients with implantable cardioverter defibrillators. Pacing Clin Electrophysiol. 2008 Feb. 31(2):144-50. [Medline].

  3. Menegazzi JJ, Callaway CW, Sherman LD, Hostler DP, Wang HE, Fertig KC, et al. Ventricular fibrillation scaling exponent can guide timing of defibrillation and other therapies. Circulation. 2004 Feb 24. 109(7):926-31. [Medline].

  4. Rissanen V. Coronary atherosclerosis in cases of coronary death as compared with that occurring in the populatiom. A study of a medico-legal autopsy series of coronary deaths and violent deaths. Ann Clin Res. 1975 Dec. 7(6):412-25. [Medline].

  5. Holmes DR Jr, Davis K, Gersh BJ, et al. Risk factor profiles of patients with sudden cardiac death and death from other cardiac causes: a report from the Coronary Artery Surgery Study (CASS). J Am Coll Cardiol. 1989 Mar 1. 13(3):524-30. [Medline].

  6. Bigger JT Jr, Fleiss JL, Kleiger R, et al. The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction. Circulation. 1984 Feb. 69(2):250-8. [Medline].

  7. Tung RT, Shen WK, Hammill SC, Gersh BJ. Idiopathic ventricular fibrillation in out-of-hospital cardiac arrest survivors. Pacing Clin Electrophysiol. 1994 Aug. 17(8):1405-12. [Medline].

  8. Belhassen B, Viskin S. Idiopathic ventricular tachycardia and fibrillation. J Cardiovasc Electrophysiol. 1993 Jun. 4(3):356-68. [Medline].

  9. Bikkina M, Larson MG, Levy D. Prognostic implications of asymptomatic ventricular arrhythmias: the Framingham Heart Study. Ann Intern Med. 1992 Dec 15. 117(12):990-6. [Medline].

  10. Sharma B, Asinger R, Francis GS, et al. Demonstration of exercise-induced painless myocardial ischemia in survivors of out-of-hospital ventricular fibrillation. Am J Cardiol. 1987 Apr 1. 59(8):740-5. [Medline].

  11. Cobb LA, Baum RS, Alvarez H 3rd, Schaffer WA. Resuscitation from out-of-hospital ventricular fibrillation: 4 years follow-up. Circulation. 1975 Dec. 52(6 Suppl):III223-35. [Medline].

  12. Larsen L, Markham J, Haffajee CI. Sudden death in idiopathic dilated cardiomyopathy: role of ventricular arrhythmias. Pacing Clin Electrophysiol. 1993 May. 16(5 Pt 1):1051-9. [Medline].

  13. Maron BJ, Wolfson JK, Epstein SE, Roberts WC. Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy. J Am Coll Cardiol. 1986 Sep. 8(3):545-57. [Medline].

  14. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002 Feb 21. 346(8):549-56. [Medline].

  15. Corrado D, Basso C, Thiene G, et al. Spectrum of clinicopathologic manifestations of arrhythmogenic right ventricular cardiomyopathy/dysplasia: a multicenter study. J Am Coll Cardiol. 1997 Nov 15. 30(6):1512-20. [Medline].

  16. Pilichou K, Nava A, Basso C, Beffagna G, Bauce B, Lorenzon A, et al. Mutations in desmoglein-2 gene are associated with arrhythmogenic right ventricular cardiomyopathy. Circulation. 2006 Mar 7. 113(9):1171-9. [Medline].

  17. McKenna WJ, Beiras AC, Lado MP. The cardiomyopathies. Br Heart J. 1994 Dec. 72(6 Suppl):S1. [Medline]. [Full Text].

  18. [Guideline] Marcus FI, McKenna WJ, Sherrill D, Basso C, Bauce B, Bluemke DA, et al. Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria. Circulation. 2010 Apr 6. 121(13):1533-41. [Medline]. [Full Text].

  19. Chizner MA, Pearle DL, deLeon AC Jr. The natural history of aortic stenosis in adults. Am Heart J. 1980 Apr. 99(4):419-24. [Medline].

  20. Kligfield P, Levy D, Devereux RB. Arrhythmias and sudden death in mitral valve prolapse. Am Heart J. 1987 May. 113(5):1298-307. [Medline].

  21. Driscoll DJ, Edwards WD. Sudden unexpected death in children and adolescents. J Am Coll Cardiol. 1985 Jun. 5(6 Suppl):118B-121B. [Medline].

  22. Myerburg RJ, Mitrani R, Interian A Jr, Castellanos A. Identification of risk of cardiac arrest and sudden cardiac death in athletes. Estes NA, Salem DN, Wang PJ, eds. Sudden Cardiac Death in the Athlete. Armonk, NY: Futura Publishing; 1996. 25.

  23. Young D, Mark H. Fate of the patient with the Eisenmenger syndrome. Am J Cardiol. 1971 Dec. 28(6):658-69. [Medline].

  24. Bezzina CR, Pazoki R, Bardai A, Marsman RF, de Jong JS, Blom MT, et al. Genome-wide association study identifies a susceptibility locus at 21q21 for ventricular fibrillation in acute myocardial infarction. Nat Genet. 2010 Aug. 42(8):688-91. [Medline].

  25. Watanabe H, Nogami A, Ohkubo K, Kawata H, Hayashi Y, Ishikawa T, et al. Electrocardiographic characteristics and SCN5A mutations in idiopathic ventricular fibrillation associated with early repolarization. Circ Arrhythm Electrophysiol. 2011 Dec. 4(6):874-81. [Medline].

  26. Knecht S, Sacher F, Wright M, Hocini M, Nogami A, Arentz T, et al. Long-term follow-up of idiopathic ventricular fibrillation ablation: a multicenter study. J Am Coll Cardiol. 2009 Aug 4. 54(6):522-8. [Medline].

  27. Yokokawa M, Good E, Crawford T, Chugh A, Pelosi F Jr, Latchamsetty R, et al. Reasons for failed ablation for idiopathic right ventricular outflow tract-like ventricular arrhythmias. Heart Rhythm. 2013 Aug. 10(8):1101-8. [Medline].

  28. Viskin S, Rosso R, Rogowski O, Belhassen B. The "short-coupled" variant of right ventricular outflow ventricular tachycardia: a not-so-benign form of benign ventricular tachycardia?. J Cardiovasc Electrophysiol. 2005 Aug. 16(8):912-6. [Medline].

  29. P Doppalapudi H. Idiopathic focal epicardial ventricular tachycardia originating from the crux of the heart. Heart Rhythm. 2009 Jan. 6(1):44-50.

  30. Nanthakumar K, Massé S, Umapathy K, Dorian P, Sevaptsidis E, Waxman M. Cardiac stimulation with high voltage discharge from stun guns. CMAJ. 2008 May 20. 178(11):1451-7. [Medline]. [Full Text].

  31. Zipes DP. Sudden cardiac arrest and death following application of shocks from a TASER electronic control device. Circulation. 2012 May 22. 125(20):2417-22. [Medline].

  32. Wever EF, Hauer RN, Oomen A, et al. Unfavorable outcome in patients with primary electrical disease who survived an episode of ventricular fibrillation. Circulation. 1993 Sep. 88(3):1021-9. [Medline].

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

  34. Moss AJ. Clinical management of patients with the long QT syndrome: drugs, devices, and gene-specific therapy. Pacing Clin Electrophysiol. 1997 Aug. 20(8 Pt 2):2058-60. [Medline].

  35. Splawski I, Timothy KW, Sharpe LM, Decher N, Kumar P, Bloise R, et al. Ca(V)1.2 calcium channel dysfunction causes a multisystem disorder including arrhythmia and autism. Cell. 2004 Oct 1. 119(1):19-31. [Medline].

  36. Priori SG, Napolitano C, Memmi M, Colombi B, Drago F, Gasparini M, et al. Clinical and molecular characterization of patients with catecholaminergic polymorphic ventricular tachycardia. Circulation. 2002 Jul 2. 106(1):69-74. [Medline].

  37. Watanabe H, Chopra N, Laver D, Hwang HS, Davies SS, Roach DE, et al. Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans. Nat Med. 2009 Apr. 15(4):380-3. [Medline]. [Full Text].

  38. Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med. 1979 Nov 15. 301(20):1080-5. [Medline].

  39. Moore JP, Kannankeril PJ, Fish FA. Isoproterenol administration during general anesthesia for the evaluation of children with ventricular preexcitation. Circ Arrhythm Electrophysiol. 2011 Feb. 4(1):73-8. [Medline].

  40. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol. 1992 Nov 15. 20(6):1391-6. [Medline].

  41. Gussak I, Antzelevitch C, Bjerregaard P, et al. The Brugada syndrome: clinical, electrophysiologic and genetic aspects. J Am Coll Cardiol. 1999 Jan. 33(1):5-15. [Medline].

  42. Kapplinger JD, Tester DJ, Alders M, Benito B, Berthet M, Brugada J, et al. An international compendium of mutations in the SCN5A-encoded cardiac sodium channel in patients referred for Brugada syndrome genetic testing. Heart Rhythm. 2010 Jan. 7(1):33-46. [Medline]. [Full Text].

  43. Wilde AA, Antzelevitch C, Borggrefe M, Brugada J, Brugada R, Brugada P, et al. Proposed diagnostic criteria for the Brugada syndrome. Eur Heart J. 2002 Nov. 23(21):1648-54. [Medline].

  44. Brugada J, Brugada R, Brugada P. Right bundle-branch block and ST-segment elevation in leads V1 through V3: a marker for sudden death in patients without demonstrable structural heart disease. Circulation. 1998 Feb 10. 97(5):457-60. [Medline].

  45. Priori SG, Gasparini M, Napolitano C, Della Bella P, Ottonelli AG, Sassone B, et al. Risk stratification in Brugada syndrome: results of the PRELUDE (PRogrammed ELectrical stimUlation preDictive valuE) registry. J Am Coll Cardiol. 2012 Jan 3. 59(1):37-45. [Medline].

  46. Belhassen B, Glick A, Viskin S. Efficacy of quinidine in high-risk patients with Brugada syndrome. Circulation. 2004 Sep 28. 110(13):1731-7. [Medline].

  47. McNally B, Robb R, Mehta M, Vellano K, Valderrama AL, Yoon PW, et al. Out-of-hospital cardiac arrest surveillance --- Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005--December 31, 2010. MMWR Surveill Summ. 2011 Jul 29. 60(8):1-19. [Medline].

  48. Holmberg M, Holmberg S, Herlitz J. The problem of out-of-hospital cardiac-arrest prevalence of sudden death in Europe today. Am J Cardiol. 1999 Mar 11. 83(5B):88D-90D. [Medline].

  49. Becker LB, Han BH, Meyer PM, et al. Racial differences in the incidence of cardiac arrest and subsequent survival. The CPR Chicago Project. N Engl J Med. 1993 Aug 26. 329(9):600-6. [Medline].

  50. Gillum RF. Sudden cardiac death in Hispanic Americans and African Americans. Am J Public Health. 1997 Sep. 87(9):1461-6. [Medline].

  51. Schatzkin A, Cupples LA, Heeren T, et al. Sudden death in the Framingham Heart Study. Differences in incidence and risk factors by sex and coronary disease status. Am J Epidemiol. 1984 Dec. 120(6):888-99. [Medline].

  52. Gordon T, Kannel WB. Premature mortality from coronary heart disease. The Framingham study. JAMA. 1971 Mar 8. 215(10):1617-25. [Medline].

  53. Kuller LH. Sudden death--definition and epidemiologic considerations. Prog Cardiovasc Dis. 1980 Jul-Aug. 23(1):1-12. [Medline].

  54. Winkle RA. The effectiveness and cost effectiveness of public-access defibrillation. Clin Cardiol. 2010 Jul. 33(7):396-9. [Medline].

  55. McCullough PA, Thompson RJ, Tobin KJ. Validation of a decision support tool for the evaluation of cardiac arrest victims. Clin Cardiol. 1998 Mar. 21(3):195-200. [Medline].

  56. Lombardi G, Gallagher J, Gennis P. Outcome of out-of-hospital cardiac arrest in New York City. The Pre- Hospital Arrest Survival Evaluation (PHASE) Study. JAMA. 1994 Mar 2. 271(9):678-83. [Medline].

  57. Waalewijn RA, de Vos R, Koster RW. Out-of-hospital cardiac arrests in Amsterdam and its surrounding areas: results from the Amsterdam resuscitation study (ARREST) in 'Utstein' style. Resuscitation. 1998 Sep. 38(3):157-67. [Medline].

  58. Cronier P, Vignon P, Bouferrache K, et al. Impact of routine percutaneous coronary intervention after out-of-hospital cardiac arrest due to ventricular fibrillation. Crit Care. 2011 May 11. 15(3):R122. [Medline].

  59. Hollenbeck RD, McPherson JA, Mooney MR, Unger BT, Patel NC, McMullan PW Jr, et al. Early cardiac catheterization is associated with improved survival in comatose survivors of cardiac arrest without STEMI. Resuscitation. 2014 Jan. 85(1):88-95. [Medline].

  60. Mateen FJ, Josephs KA, Trenerry MR, et al. Long-term cognitive outcomes following out-of-hospital cardiac arrest: A population-based study. Neurology. 2011 Sep 14. [Medline].

  61. Surawicz B. Ventricular fibrillation. J Am Coll Cardiol. 1985 Jun. 5(6 Suppl):43B-54B. [Medline].

  62. Thompson RJ, McCullough PA, Kahn JK. Prediction of death and neurologic outcome in the emergency department in out-of-hospital cardiac arrest survivors. Am J Cardiol. 1998 Jan 1. 81(1):17-21. [Medline].

  63. McCullough PA, Prakash R, Tobin KJ. Application of a cardiac arrest score in patients with sudden death and ST segment elevation for triage to angiography and intervention. J Interv Cardiol. 2002 Aug. 15(4):257-61. [Medline].

  64. Turitto G, Ahuja RK, Caref EB, el-Sherif N. Risk stratification for arrhythmic events in patients with nonischemic dilated cardiomyopathy and nonsustained ventricular tachycardia: role of programmed ventricular stimulation and the signal-averaged electrocardiogram. J Am Coll Cardiol. 1994 Nov 15. 24(6):1523-8. [Medline].

  65. Brugada P, Geelen P. Some electrocardiographic patterns predicting sudden cardiac death that every doctor should recognize. Acta Cardiol. 1997. 52(6):473-84. [Medline].

  66. Gibson RS, Watson DD, Craddock GB. Prediction of cardiac events after uncomplicated myocardial infarction: a prospective study comparing predischarge exercise thallium-201 scintigraphy and coronary angiography. Circulation. 1983 Aug. 68(2):321-36. [Medline].

  67. Risk stratification and survival after myocardial infarction. N Engl J Med. 1983 Aug 11. 309(6):331-6. [Medline].

  68. Zheutlin TA, Steinman RT, Mattioni TA, Kehoe RF. Long-term arrhythmic outcome in survivors of ventricular fibrillation with absence of inducible ventricular tachycardia. Am J Cardiol. 1988 Dec 1. 62(17):1213-7. [Medline].

  69. Buxton AE, Waxman HL, Marchlinski FE, Untereker WJ, Waspe LE, Josephson ME. Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias. Circulation. 1984 Mar. 69(3):532-40. [Medline].

  70. Iesaka Y, Nogami A, Aonuma K, Nitta J, Chun YH, Fujiwara H, et al. Prognostic significance of sustained monomorphic ventricular tachycardia induced by programmed ventricular stimulation using up to triple extrastimuli in survivors of acute myocardial infarction. Am J Cardiol. 1990 May 1. 65(16):1057-63. [Medline].

  71. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med. 1999 Dec 16. 341(25):1882-90. [Medline].

  72. Morrison LJ, Deakin CD, Morley PT, Callaway CW, Kerber RE, Kronick SL, et al. Part 8: advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2010 Oct 19. 122(16 Suppl 2):S345-421. [Medline].

  73. Hazinski MF, Nolan JP, Billi JE et al. Part 1: executive summary: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2010 Oct 19. 122(16 Suppl 2):S250-75. [Medline].

  74. White RD, Hankins DG, Bugliosi TF. Seven years'' experience with early defibrillation by police and paramedics in an emergency medical services system. Resuscitation. 1998 Dec. 39(3):145-51. [Medline].

  75. Domanski MJ, Sakseena S, Epstein AE, et al. Relative effectiveness of the implantable cardioverter-defibrillator and antiarrhythmic drugs in patients with varying degrees of left ventricular dysfunction who have survived malignant ventricular arrhythmias. AVID Investigators. Antiarrhythmics Ver. J Am Coll Cardiol. 1999 Oct. 34(4):1090-5. [Medline].

  76. Lessmeier TJ, Lehmann MH, Steinman RT, et al. Outcome with implantable cardioverter-defibrillator therapy for survivors of ventricular fibrillation secondary to idiopathic dilated cardiomyopathy or coronary artery disease without myocardial infarction. Am J Cardiol. 1993 Oct 15. 72(12):911-5. [Medline].

  77. Meissner MD, Lehmann MH, Steinman RT, et al. Ventricular fibrillation in patients without significant structural heart disease: a multicenter experience with implantable cardioverter- defibrillator therapy. J Am Coll Cardiol. 1993 May. 21(6):1406-12. [Medline].

  78. Maron BJ, Shen WK, Link MS, et al. Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. N Engl J Med. 2000 Feb 10. 342(6):365-73. [Medline].

  79. Rea TD, Fahrenbruch C, Culley L, Donohoe RT, Hambly C, Innes J, et al. CPR with chest compression alone or with rescue breathing. N Engl J Med. 2010 Jul 29. 363(5):423-33. [Medline].

  80. Iwami T, Kitamura T, Kawamura T, Mitamura H, Nagao K, Takayama M, et al. Chest compression-only cardiopulmonary resuscitation for out-of-hospital cardiac arrest with public-access defibrillation: a nationwide cohort study. Circulation. 2012 Dec 11. 126(24):2844-51. [Medline].

  81. Ewy GA, Sanders AB. Alternative approach to improving survival of patients with out-of-hospital primary cardiac arrest. J Am Coll Cardiol. 2013 Jan 15. 61(2):113-8. [Medline].

  82. Hassan TB, Jagger C, Barnett DB. A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation. Emerg Med J. 2002 Jan. 19(1):57-62. [Medline]. [Full Text].

  83. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002 Feb 21. 346(8):557-63. [Medline].

  84. Nielsen N, Wetterslev J, Cronberg T, Erlinge D, Gasche Y, Hassager C, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013 Dec 5. 369(23):2197-206. [Medline].

  85. [Guideline] Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd, Freedman RA, Gettes LS, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation. 2008 May 27. 117(21):e350-408. [Medline].

  86. [Guideline] Tracy CM, Epstein AE, Darbar D, Dimarco JP, Dunbar SB, Estes NA 3rd, et al. 2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2012 Oct 2. 60(14):1297-313. [Medline]. [Full Text].

  87. Cappato R. Secondary prevention of sudden death: the Dutch Study, the Antiarrhythmics Versus Implantable Defibrillator Trial, the Cardiac Arrest Study Hamburg, and the Canadian Implantable Defibrillator Study. Am J Cardiol. 1999 Mar 11. 83(5B):68D-73D. [Medline].

  88. The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997 Nov 27. 337(22):1576-83. [Medline].

  89. Matsue Y, Suzuki M, Nishizaki M, Hojo R, Hashimoto Y, Sakurada H. Clinical implications of an implantable cardioverter-defibrillator in patients with vasospastic angina and lethal ventricular arrhythmia. J Am Coll Cardiol. 2012 Sep 4. 60(10):908-13. [Medline].

  90. Klein H, Auricchio A, Reek S, Geller C. New primary prevention trials of sudden cardiac death in patients with left ventricular dysfunction: SCD-HEFT and MADIT-II. Am J Cardiol. 1999 Mar 11. 83(5B):91D-97D. [Medline].

  91. Callaway CW. Epinephrine for cardiac arrest. Curr Opin Cardiol. 2013 Jan. 28(1):36-42. [Medline].

  92. Haïssaguerre M, Shoda M, Jaïs P, Nogami A, Shah DC, Kautzner J, et al. Mapping and ablation of idiopathic ventricular fibrillation. Circulation. 2002 Aug 20. 106(8):962-7. [Medline].

  93. Huang J, Rogers JM, Killingsworth CR, Singh KP, Smith WM, Ideker RE. Evolution of activation patterns during long-duration ventricular fibrillation in dogs. Am J Physiol Heart Circ Physiol. 2004 Mar. 286(3):H1193-200. [Medline].

  94. Kuller LH. Sudden death--definition and epidemiologic considerations. Prog Cardiovasc Dis. 1980 Jul-Aug. 23(1):1-12. [Medline].

  95. Maron BJ, Epstein SE, Roberts WC. Causes of sudden death in competitive athletes. J Am Coll Cardiol. 1986 Jan. 7(1):204-14. [Medline].

  96. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med. 1996 Dec 26. 335(26):1933-40. [Medline].

  97. Murphy JG, Gersh BJ, Mair DD, et al. Long-term outcome in patients undergoing surgical repair of tetralogy of Fallot. N Engl J Med. 1993 Aug 26. 329(9):593-9. [Medline].

  98. Tanno K, Miyoshi F, Watanabe N, Minoura Y, Kawamura M, Ryu S, et al. Are the MADIT II criteria for ICD implantation appropriate for Japanese patients?. Circ J. 2005 Jan. 69(1):19-22. [Medline].

  99. Yoon G, Quitania L, Kramer JH, Fu YH, Miller BL, Ptácek LJ. Andersen-Tawil syndrome: definition of a neurocognitive phenotype. Neurology. 2006 Jun 13. 66(11):1703-10. [Medline].

Epsilon wave on the electrocardiogram of a patient with arrhythmogenic right ventricular dysplasia.
Ventricular fibrillation appeared during rapid atrial fibrillation in a patient with Wolff-Parkinson-White syndrome.
Ventricular fibrillation in a patient with a left ventricular assist device (LVAD).
Table 1. Long QT syndrome diagnostic criteria
Category Criteria Points
Electrocardiographic Findings Corrected QT interval ≥480 ms 3
460-479 ms 2
450-459 ms (in males) 1
Torsade de pointes 2
T wave alternans 1
Notched T waves in three leads 1
Low heart rate for age (resting rate below second percentile 0.5
Clinical History Syncope With stress 2
Without stress 1
Congenital deafness 0.5
Family History Family members with definite long QT syndrome 1
Unexplained SCD before age 30 in immediate family members without definite long QT syndrome 0.5
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[33]


≤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

Table 2: Outcome according to initial cardiac arrest score
Cardiac Arrest Score In-hospital mortality rate (%) Neurologic Recovery (%)
0 90 3
1 71 17
2 42 57
3 18 89
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.