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Ventricular Fibrillation in Emergency Medicine

  • Author: Keith A Marill, MD; Chief Editor: Erik D Schraga, MD  more...
Updated: Dec 30, 2015


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

Ventricular fibrillation is shown in the rhythm strip below.

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


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

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

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

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

All fibrillation is not the same. VF begins as a coarse, irregular deflection on the ECG, then degenerates to a fine, irregular pattern, and eventually becomes asystole. This progression of electrocardiographic abnormalities reflects the electrical and energetic changes described above. The probability of successful defibrillation decreases as the VF waveform becomes smoother with time.[1]




United States

The incidence of sudden cardiac death in the United States is approximately 300,000 cases per year. The distribution of rhythms found in patients with cardiac arrest depends largely on the average duration of the arrest state and, thus, the emergency medical system (EMS) response times. In monitored settings, such as casinos, where average response times are less than 5 minutes, the initial rhythm is ventricular fibrillation in approximately 70% of patients.[2] A circadian pattern of sudden cardiac death has also been reported.

The incidence of VF seems to be decreasing based on multiple reports. This may, in part, be due to improved treatment of coronary artery disease and acute myocardial infarction, internal cardioverter defibrillator placement in patients at high risk,[3] or other unknown factors.


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



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

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

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


Postresuscitation death and disability after successful resuscitation directly correlate with the amount of CNS damaged during the event. Without intervention, by 4-6 minutes after onset of VF, the prognosis is poor. Few survive when VF lasts more than 8 minutes without intervention. Prediction rules have been developed to predict favorable neurologic survival from cardiac arrest.[5, 6]

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

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


Complications include the following:

  • CNS ischemic injury
  • Myocardial injury
  • Postdefibrillation arrhythmias
  • Aspiration pneumonia
  • Defibrillation injury to self or others
  • Injuries from CPR and resuscitation
  • Skin burns
  • Damage to implanted electronics (eg, AICD, pacemaker)
  • Death


Black males have the highest incidence of sudden cardiac death.


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


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

Contributor Information and Disclosures

Keith A Marill, MD Faculty, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor, Harvard Medical School

Keith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Received ownership interest from Medtronic for none; Received ownership interest from Cambridge Heart, Inc. for none; Received ownership interest from General Electric for none. for: GE; Medtronic; Cambridge Heart.


A Antoine Kazzi, MD Deputy Chief of Staff, American University of Beirut Medical Center; Associate Professor, Department of Emergency Medicine, American University of Beirut, Lebanon

A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Aaron A Bright, MD Assistant Professor of Clinical Emergency Medicine, Department of Emergency Medicine, LAC+USC Medical Center, Keck School of Medicine of the University of Southern California

Aaron A Bright, MD is a member of the following medical societies: American College of Emergency Physicians, Los Angeles County Medical Association

Disclosure: Nothing to disclose.

Mazen K Khalil, MD Post Doctoral Research Fellow, Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation

Mazen K Khalil, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Department of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, National Association of EMS Physicians

Disclosure: Medical Director for: SironaHealth.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

Steven A Conrad, MD, PhD Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

  1. Menegazzi JJ, Callaway CW, Sherman LD. Ventricular Fibrillation Scaling Exponent Can Guide Timing of Defibrillation and Other Therapies. Circulation. 2004. 109(7):926-31. [Medline].

  2. Valenzuela TD, Roe DJ, Nichol G. Outcomes of rapid defibrillation by security officers after cardiac arrest in casinos. N Engl J Med. 2000. 343(17):1206-9. [Medline].

  3. Hulleman M, Berdowski J, de Groot JR, van Dessel PF, Borleffs CJ, Blom MT, et al. Implantable cardioverter-defibrillators have reduced the incidence of resuscitation for out-of-hospital cardiac arrest caused by lethal arrhythmias. Circulation. 2012 Aug 14. 126(7):815-21. [Medline].

  4. Becker LB, Ostrander MP, Barrett J, Kondos GT. Outcome of CPR in a large metropolitan area--where are the survivors?. Ann Emerg Med. 1991 Apr. 20(4):355-61. [Medline].

  5. Chan PS, Spertus JA, Krumholz HM, Berg RA, Li Y, Sasson C, et al. A validated prediction tool for initial survivors of in-hospital cardiac arrest. Arch Intern Med. 2012 Jun 25. 172(12):947-53. [Medline]. [Full Text].

  6. Coppler PJ, Elmer J, Calderon L, et al; Post Cardiac Arrest Service. Validation of the Pittsburgh Cardiac Arrest Category illness severity score. Resuscitation. 2015 Apr. 89:86-92. [Medline].

  7. Link MS, Wang PJ, Pandian N. An experimental model of sudden death due to low-energy chest-wall impact (commotio cordis). N Engl J Med. 1998. 338(25):1805-11. [Medline].

  8. Young KD, Gausche-Hill M, McClung CD. A prospective, population-based study of the epidemiology and outcome of out-of-hospital pediatric cardiopulmonary arrest. Pediatrics. 2004. 114(1):157-64. [Medline].

  9. Swor RA, Jackson RE, Tintinalli JE. Does advanced age matter in outcomes after out-of-hospital cardiac arrest in community-dwelling adults?. Acad Emerg Med. 2000. 7(7):762-8. [Medline].

  10. Mosier J, Itty A, Sanders A, Mohler J, Wendel C, Poulsen J, et al. Cardiocerebral resuscitation is associated with improved survival and neurologic outcome from out-of-hospital cardiac arrest in elders. Acad Emerg Med. 2010 Mar. 17(3):269-75. [Medline].

  11. Robinson SM, Mackenzie-Ross S, Campbell Hewson GL. Psychological effect of witnessed resuscitation on bereaved relatives. Lancet. 1998. 352(9128):614-7. [Medline].

  12. Bobrow BJ, Clark LL, Ewy GA, Chikani V, Sanders AB, Berg RA. Minimally interrupted cardiac resuscitation by emergency medical services for out-of-hospital cardiac arrest. JAMA. 2008 Mar 12. 299(10):1158-65. [Medline].

  13. Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): an observational study. Lancet. 2007 Mar 17. 369(9565):920-6. [Medline].

  14. Field JM, Hazinski MF, Sayre MR, Chameides L, Schexnayder SM, Hemphill R. Part 1: executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 2. 122(18 Suppl 3):S640-56. [Medline].

  15. 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].

  16. Aufderheide TP, Sigurdsson G, Pirrallo RG, Yannopoulos D, McKnite S, von Briesen C, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation. 2004 Apr 27. 109(16):1960-5. [Medline].

  17. Ewy GA, Kern KB. Recent advances in cardiopulmonary resuscitation: cardiocerebral resuscitation. J Am Coll Cardiol. 2009 Jan 13. 53(2):149-57. [Medline].

  18. Nichol G, Leroux B, Wang H, et al; ROC Investigators. Trial of continuous or interrupted chest compressions during CPR. N Engl J Med. 2015 Dec 3. 373(23):2203-14. [Medline].

  19. Bardy GH, Lee KL, Mark DB, Poole JE, Toff WD, Tonkin AM, et al. Home use of automated external defibrillators for sudden cardiac arrest. N Engl J Med. 2008 Apr 24. 358(17):1793-804. [Medline].

  20. Forcina MS, Farhat AY, O'Neil WW, Haines DE. Cardiac arrest survival after implementation of automated external defibrillator technology in the in-hospital setting. Crit Care Med. 2009 Apr. 37(4):1229-36. [Medline].

  21. Chan PS, Krumholz HM, Spertus JA, Jones PG, Cram P, Berg RA, et al. Automated external defibrillators and survival after in-hospital cardiac arrest. JAMA. 2010 Nov 17. 304(19):2129-36. [Medline].

  22. Truong JH, Rosen P. Current concepts in electrical defibrillation. J Emerg Med. 1997 May-Jun. 15(3):331-8. [Medline].

  23. Schneider T, Martens PR, Paschen H. Multicenter, randomized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Circulation. 2000. 102(15):1780-7. [Medline].

  24. Stiell IG, Walker RG, Nesbitt LP, Chapman FW, Cousineau D, Christenson J, et al. BIPHASIC Trial: a randomized comparison of fixed lower versus escalating higher energy levels for defibrillation in out-of-hospital cardiac arrest. Circulation. 2007 Mar 27. 115(12):1511-7. [Medline].

  25. Wik L, Hansen T, Fylling F. Delaying Defibrillation to Give Basic Cardiopulmonary Resuscitation to Patients With Out-of-Hospital Ventricular Fibrillation. A Randomized Trial. JAMA. 2003. 289(11):1389-95. [Medline].

  26. Huang Y, He Q, Yang LJ, Liu GJ, Jones A. Cardiopulmonary resuscitation (CPR) plus delayed defibrillation versus immediate defibrillation for out-of-hospital cardiac arrest. Cochrane Database Syst Rev. 2014 Sep 12. 9:CD009803. [Medline].

  27. Freese JP, Jorgenson DB, Liu PY, Innes J, Matallana L, Nammi K, et al. Waveform analysis-guided treatment versus a standard shock-first protocol for the treatment of out-of-hospital cardiac arrest presenting in ventricular fibrillation: results of an international randomized, controlled trial. Circulation. 2013 Aug 27. 128(9):995-1002. [Medline].

  28. Gertsch M, Hottinger S, Hess T. Serial chest thumps for the treatment of ventricular tachycardia in patients with coronary artery disease. Clin Cardiol. 1992 Mar. 15(3):181-8. [Medline].

  29. Shin TG, Choi JH, Jo IJ, Sim MS, Song HG, Jeong YK, et al. Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: A comparison with conventional cardiopulmonary resuscitation. Crit Care Med. 2011 Jan. 39(1):1-7. [Medline].

  30. Kellum MJ, Kennedy KW, Barney R, Keilhauer FA, Bellino M, Zuercher M, et al. Cardiocerebral resuscitation improves neurologically intact survival of patients with out-of-hospital cardiac arrest. Ann Emerg Med. 2008 Sep. 52(3):244-52. [Medline].

  31. Weisfeldt ML, Becker LB. Resuscitation after cardiac arrest: a 3-phase time-sensitive model. JAMA. 2002 Dec 18. 288(23):3035-8. [Medline].

  32. Nielsen N, Wetterslev J, Cronberg T, et al; TTM Trial Investigators. Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med. 2013 Dec 5. 369(23):2197-206. [Medline].

  33. Gueugniaud PY, Mols P, Goldstein P. A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. N Engl J Med. 1998. 339(22):1595-1601. [Medline].

  34. Wenzel V, Krismer AC, Arntz R. A Comparison of Vasopressin and Epinephrine for Out-of-Hospital Cardiopulmonary Resuscitation. N Engl J Med. 2004. 350(2):105-16. [Medline].

  35. Callaway CW, Hostler D, Doshi AA. Usefulness of Vasopressin Administered With Epinephrine During Out-of-Hospital Cardiac Arrest. Am J Cardiol. 2006. 98(10):1316-21. [Medline].

  36. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med. 1999 Sep 16. 341(12):871-8. [Medline].

  37. Dorian P, Cass D, Schwartz B. Amiodarone as compared with Lidocaine for Shock-Resistant Ventricular Fibrillation. N Engl J Med. 2002. 346(12):884-90. [Medline].

  38. Nowak RM, Bodnar TJ, Dronen S. Bretylium tosylate as initial treatment for cardiopulmonary arrest: randomized comparison with placebo. Ann Emerg Med. 1981. 10(8):404-7. [Medline].

  39. Kovoor P, Love A, Hall J. Randomized double-blind trial of sotalol versus lignocaine in out-of-hospital refractory cardiac arrest due to ventricular tachyarrhythmias. Intern Med J. 2005. 35(9):518-25. [Medline].

  40. Bottiger BW, Arntz HR, Chamberlain DA, et al. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008 Dec 18. 359(25):2651-62. [Medline].

  41. Spaulding CM, Joly LM, Rosenberg A. Immediate coronary angiography in survivors of out-of-hospital cardiac arrest. N Engl J Med. 1997. 336(23):1629-33. [Medline].

  42. Sunde K, Pytte M, Jacobsen D, Mangschau A, Jensen LP, Smedsrud C, et al. Implementation of a standardised treatment protocol for post resuscitation care after out-of-hospital cardiac arrest. Resuscitation. 2007 Apr. 73(1):29-39. [Medline].

  43. Hypothermia after Cardiac Arrest Study Group. Mild Therapeutic Hypothermia to Improve the Neurologic Outcome after Cardiac Arrest. N Engl J Med. 2002. 346(8):549-56. [Medline].

  44. Bernard SA, Gray TW, Buist MD. Treatment of Comatose Survivors of Out-of-Hospital Cardiac Arrest with Induced Hypothermia. N Engl J Med. 2002. 346(8):557-63. [Medline].

  45. [Guideline] American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005 Dec 13. 112(24 Suppl):IV1-203. [Medline].

  46. Angelos MG, Menegazzi JJ, Callaway CW. Bench to Bedside: Resuscitation from Prolonged Ventricular Fibrillation. Acad Emerg Med. 2001. 8(9):909-24. [Medline].

  47. Bossaert LL. Fibrillation and defibrillation of the heart. Br J Anaesth. 1997 Aug. 79(2):203-13. [Medline].

  48. Cohen TJ. Innovative emergency defibrillation methods for refractory ventricular fibrillation in a variety of hospital settings. Am Heart J. 1993 Oct. 126(4):962-8. [Medline].

  49. Cummins RO, Eisenberg MS, Litwin PE, et al. Automatic external defibrillators used by emergency medical technicians. A controlled clinical trial. JAMA. 1987 Mar 27. 257(12):1605-10. [Medline].

  50. Eisenberg MS, Mengert TJ. Cardiac resuscitation. N Engl J Med. 2001. 344(17):1304-1313. [Medline].

  51. Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac arrhythmias. N Engl J Med. 2001. 345(20):1473-82. [Medline].

  52. Mogayzel C, Quan L, Graves JR, et al. Out-of-hospital ventricular fibrillation in children and adolescents: causes and outcomes. Ann Emerg Med. 1995 Apr. 25(4):484-91. [Medline].

  53. Mols P, Beaucarne E, Bruyninx J, et al. Early defibrillation by EMTs: the Brussels experience. Resuscitation. 1994 Mar. 27(2):129-36. [Medline].

  54. Weaver WD, Cobb LA, Copass MK, Hallstrom AP. Ventricular defibrillation -- a comparative trial using 175-J and 320-J shocks. N Engl J Med. 1982 Oct 28. 307(18):1101-6. [Medline].

  55. Weiss JN, Garfinkel A, Karagueuzian HS. Chaos and the Transition to Ventricular Fibrillation: a new approach to antiarrhythmic drug evaluation. Circulation. 1999. 99(21):2819-26. [Medline].

  56. White RD, Russell JK. Refibrillation, resuscitation and survival in out-of-hospital sudden cardiac arrest victims treated with biphasic automated external defibrillators. Resuscitation. 2002 Oct. 55(1):17-23. [Medline].

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