Ventricular Fibrillation in Emergency Medicine Medication

  • Author: Keith A Marill, MD; Chief Editor: David FM Brown, MD   more...
 
Updated: Jun 23, 2011
 

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.[22] Recent data suggest no synergistic effect of administering vasopressin in addition to epinephrine.[23, 24]

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.[25, 26]

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.[27, 28]

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.

View full drug information

Epinephrine (Adrenalin)

 

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

View full drug information

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.

View full drug information

Lidocaine (Xylocaine, Dilocaine)

 

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

View full drug information

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.

View full drug information

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.

View full drug information

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.

View full drug information

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.

View full drug information

Sodium bicarbonate (Neut)

 

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

View full drug information

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
Proceed to Follow-up
 
 
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 and Society for Academic Emergency Medicine

Disclosure: Medtronic Ownership interest None; Cambridge Heart, Inc. Ownership interest None; General Electric Ownership interest None

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 is a member of the following medical societies: American Academy of Emergency Medicine

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.

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 and Los Angeles County Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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

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

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

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD  Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency 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. Becker LB, Ostrander MP, Barrett J, Kondos GT. Outcome of CPR in a large metropolitan area--where are the survivors?. Ann Emerg Med. Apr 1991;20(4):355-61. [Medline].

  4. 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].

  5. 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. Mar 12 2008;299(10):1158-65. [Medline].

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

  7. 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. Nov 2 2010;122(18 Suppl 3):S640-56. [Medline].

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

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

  10. 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. Apr 24 2008;358(17):1793-804. [Medline].

  11. 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. Apr 2009;37(4):1229-36. [Medline].

  12. 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. Nov 17 2010;304(19):2129-36. [Medline].

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

  14. 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].

  15. 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. Mar 27 2007;115(12):1511-7. [Medline].

  16. 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].

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

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

  19. 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. Jan 2011;39(1):1-7. [Medline].

  20. 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. Sep 2008;52(3):244-52. [Medline].

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

  22. 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].

  23. 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].

  24. [Best Evidence] 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].

  25. 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. Sep 16 1999;341(12):871-8. [Medline].

  26. 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].

  27. 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].

  28. 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].

  29. 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].

  30. 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. Apr 2007;73(1):29-39. [Medline].

  31. 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].

  32. 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].

  33. 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].

  34. 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].

  35. 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. Mar 2010;17(3):269-75. [Medline].

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

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

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

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

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

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

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

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

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

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

  46. 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].

  47. White RD, Russell JK. Refibrillation, resuscitation and survival in out-of-hospital sudden cardiac arrest victims treated with biphasic automated external defibrillators. Resuscitation. Oct 2002;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 course 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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.