Ventricular Fibrillation in Emergency Medicine Medication

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

Medication Summary

Treatment goals are to electrically terminate ventricular fibrillation (VF) so that an organized electrical rhythm follows and restores cardiac output. Success rates significantly decrease as the duration of ischemia increases. Drug therapy to facilitate defibrillation may consist of vasopressors, antidysrhythmics, electrolytes, and other agents.

The theoretical benefit of vasopressor medicines, such as epinephrine and vasopressin, is that they increase coronary perfusion pressure. Coronary perfusion pressure is the difference between aortic and right atrial pressure during the relaxation phase of CPR, and it determines myocardial blood flow. Higher levels of coronary perfusion pressure are associated with increased survival in animal models of VF arrest.

Vasopressors, such as epinephrine, increase coronary perfusion pressure; however, no vasopressors have been proven to increase survival in humans. Nevertheless, they are recommended due to possible benefit. Epinephrine, 1 mg, is recommended every 3-5 minutes once IV or IO access is established, and vasopressin, 40 units, may be administered once instead of the first or second epinephrine dose. Higher doses of epinephrine, 0.1-0.2 mg/kg, have been studied, but they are not clearly beneficial compared with the standard 1-mg dose.[33] Recent data suggest no synergistic effect of administering vasopressin in addition to epinephrine.[34, 35]

Antidysrhythmic agents are recommended when initial defibrillation and vasopressor medicines fail or after successful defibrillation to prevent recurrence. Potential benefits of antidysrhythmic therapy include lowering the threshold for defibrillation and preventing immediate or delayed VF recurrence. Potential risks of antidysrhythmic therapy include hypotension due to decreased myocardial contractility or vascular tone, bradycardia, or asystole. No antidysrhythmic agent has been proven to improve survival to hospital discharge from VF arrest, but amiodarone may increase the likelihood of at least temporarily regaining a perfusing rhythm.[36, 37]

The mechanism of action of most antidysrhythmic agents is to alter the conductance of ions, such as sodium and potassium, across myocardial cell membrane ion conducting channels. Amiodarone and other Vaughn-Williams class III agents decrease the repolarizing flow of potassium across the cell membrane and cause a prolongation of the depolarized period. The cell is refractory to further excitation during this period and may not be able to conduct the VF waveform, thus breaking the reentrant cycle of excitation. Other class III agents that have been studied in cardiac arrest include bretylium and sotalol, but they have not been consistently shown to provide benefit.[38, 39]

Lidocaine is a Vaughn-Williams class IB agent that alters the depolarizing flow of sodium across the cell membrane and may be particularly effective in an ischemic or acidotic environment. Procainamide is a Vaughn-Williams class IA agent that affects both sodium and potassium flow across the cell membrane and may also rarely be used for refractory or recurrent VF.

Additional alternative medications include magnesium sulfate, propranolol, and sodium bicarbonate. Magnesium may be particularly important in stabilizing the cell membrane and in preventing after-depolarizations that are important in the genesis of torsades de pointes. Propranolol or other beta-adrenergic blocking agents may have a calming effect on the myocardium for patients with recurrent persistent VF often described as VF storm. Bicarbonate is useful to block the effects of tricyclic antidepressant overdose, to treat hyperkalemia that may be causing ventricular dysrhythmias, or to treat acidosis associated with prolonged cardiac arrest.

Next

Vasopressors/sympathomimetics

Class Summary

Augment both coronary and cerebral blood flow present during low-flow state associated with CPR.

Epinephrine (Adrenalin)

 

Increases coronary perfusion pressure but has not been proven to increase survival in cardiac arrest.

Vasopressin (Pitressin)

 

A nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction. Its effects on outcome have not been proven to differ from epinephrine in VF arrest. It may be used instead of the first or second dose of epinephrine during cardiac arrest resuscitation. Since it lasts longer than epinephrine, vasopressin is used only once.

Previous
Next

Antidysrhythmics

Class Summary

These agents alter electrophysiologic mechanisms responsible for dysrhythmia.

Lidocaine (Xylocaine, Dilocaine)

 

Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue.

Amiodarone (Cordarone)

 

Acute actions after IV bolus are to inhibit AV conduction and prolong the AV refractory period; IV amiodarone usually causes a decrease in systemic vascular resistance with coronary and peripheral vasodilatation and variable depressant effects on cardiac contractility. Eventually amiodarone lengthens the duration of repolarization (QT interval corrected for pulse rate) and refractory period in most cardiac tissue. Amiodarone improves the return of spontaneous circulation from VF arrest by uncertain mechanisms, but it has not been shown to improve survival to hospital discharge. When administered chronically, multiple other effects occur on adrenergic tone, thyroid function, and other systems.

Bretylium

 

Class III antidysrhythmic agent previously used for VF refractory to defibrillation, epinephrine, and lidocaine. Bretylium may increase the fibrillation threshold and ventricular myocardial refractory period by decreasing potassium conductance. Has catecholamine-releasing properties and adverse effects and is not used as initial treatment. Currently not commercially available in the United States.

Procainamide (Procanbid)

 

Vaughn-Williams class IA antidysrhythmic that blocks both sodium and potassium conducting channels. Myocardiac excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity, and it widens the QRS interval. Procainamide also increases the refractory period of atria and ventricles with associated lengthening of the QT interval. Procainamide is used to treat both supraventricular and ventricular dysrhythmias.

Previous
Next

Electrolytes

Class Summary

These agents are considered therapeutic alternatives for refractory VF. Patients with persistent or recurrent VF following antidysrhythmic administration should be assessed for underlying electrolyte abnormalities as a cause for their refractory dysrhythmia. Among electrolyte abnormalities associated with VF are hyperkalemia, hypokalemia, and hypomagnesemia. Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VF secondary to other medications. Magnesium sulfate acts as an antidysrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VF caused by hyperkalemia.

Magnesium sulfate

 

Deficiency in this electrolyte is associated with SCD and can precipitate refractory VF. Magnesium supplementation is used to treat torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF.

Sodium bicarbonate (Neut)

 

Only when the patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant, or phenobarbital overdose. Routine use not recommended.

Calcium chloride

 

Useful in treatment of hyperkalemia, hypocalcemia, or calcium channel blocker toxicity. Moderates nerve and muscle performance by regulating the action potential excitation threshold.

Previous
 
 
Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

References
  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].

 
Previous
Next
 
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.
 
Medscape Consult
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.