Ventricular Fibrillation Treatment & Management

  • Author: Michael E Zevitz, MD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Oct 12, 2011
 

Medical Care

  • Advanced cardiac life support (ACLS): In the event of cardiac arrest, the immediate implementation of ACLS guidelines is indicated. See the 2010 Advanced Life Support Guidelines.[15, 16] Interest in improving rates of public ACLS training—with a special emphasis on use of early defibrillation by public service personnel (eg, police, fire, airline)—is widespread. These measures can help achieve the greatest public health benefits in the fight against sudden death.
  • Defibrillation
    • External electrical defibrillation remains the most successful treatment of VF. A shock is delivered to the heart in order 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: duration between onset of VF and defibrillation and the metabolic condition of the myocardium. VF waveform usually begins with a relatively high amplitude and frequency; it then degenerates to smaller and smaller amplitude until asystole after approximately 15 minutes, possibly from depletion of the heart's energy reserves. Consequently, early defibrillation is vital; emergency response teams can perform defibrillation before arrival at the ED.
    • 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 most rapid.
    • Factors that increase the energy required for successful defibrillation include the following:
      • Time before defibrillation begins
      • Paddle size
      • Paddle-to-myocardium distance (eg, obesity, mechanical ventilation)
      • Use of conduction fluid (eg, disposable pads, electrode paste/jelly)
      • Contact pressure
      • Elimination of 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 apex (V4 -V5).
    • Artificial pacemakers or ICDs necessitate the use of anteroposterior paddle placement.
    • Before any defibrillation, remove all patches and ointments from the chest wall because they create a risk of fire or explosion.
    • 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 contraction is reestablished following defibrillation, a period of low cardiac output (ie, postcountershock myocardial depression) may occur. Cardiac output recovery may take minutes to hours.
    • Defibrillation causes serum creatine phosphokinase levels to increase proportionate 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 precordial thump is less appropriate for VF than for VT, it really is appropriate in neither. Use it only for witnessed monitored arrests in which no defibrillator is immediately available.
  • Algorithm
    • Activate emergency response system, dial 911 or emergency number, and retrieve automatic external defibrillator (AED).
    • Open airway and if patient is pulseless, initiate CPR by giving 30 chest compressions and 2 breaths until AED/defibrillator arrive. Chest compressions should be hard and fast at a rate of 100/minute.
    • Connect AED/defibrillator and check for shockable rhythm.
    • Deliver 1 defibrillation shock to the patient (AED, by specific; monophasic adult, 200 J; child, 2 J/kg or equivalent biphasic energy).
    • Resume CPR immediately—give 3 cycles of CPR, then check rhythm.
    • If patient is in asystole, and CPR has been initiated for 5 cycles, in debate, obtain IV access, give vasopressor, and deliver either epinephrine or vasopressin per asystole/pulseless electrical activity ACLS algorithm.
    • If shockable rhythm is present, continue CPR while defibrillator is charging.
    • Deliver 1 shock as before; resume CPR immediately after shock.
    • When intravenous access/IO access is available, give vasopressor during CPR (before or after the shock)—Epinephrine 1 mg IV/IO, repeat every 3-5 minutes, or vasopressin (one-time dose) 40 U IV/IO to replace first or second dose of epinephrine.
    • Give 5 cycles of CPR, then check rhythm.
    • If rhythm is not shockable, go to asystole/PEA algorithm. If rhythm is shockable, continue CPR while defibrillator is charging.
    • Give 1 shock as before, then resume CPR immediately after the shock.
    • Consider antiarrhythmic agents; give during CPR (before or after the shock).
      • Amiodarone 300 mg IV/IO once, then consider additional 150 mg IV/IO once, or lidocaine 1-1.5 mg/kg IV/IO first dose, then 0.5-0.75 mg/kg IV/IO, maximum 3 doses or 3 mg/kg.
      • Consider magnesium sulfate, loading dose 1-2 g IV/IO for torsade de pointes.
    • After 5 cycles of CPR, check rhythm.
    • Repeat algorithm as before if patient pulseless without spontaneous rhythm.
  • Treat underlying provocative abnormalities or VF: MI, hypovolemia, hemorrhagic shock, anoxia/hypoxia, pneumothorax/hemothorax, hypercalcemia, drug overdose (narcotic, tricyclic antidepressant, cocaine, barbituate), carbon monoxide poisoning, hyperkalemia, etc.
  • Refractory VF
    • Lack of response to standard defibrillation algorithms is challenging. Addition of magnesium and/or procainamide is often ineffective.
    • If not used earlier, consider the following amiodarone-loading protocol: 15 mg/min for 10 minutes, followed by 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours.
    • Such reported alternatives 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
    • Continue successfully used antiarrhythmics. Maintain lidocaine at 1-4 mg/min, or amiodarone at 0.5 mg/min.
    • Control any hemodynamic instability.
    • Administer vasopressors as indicated.
      • Postdefibrillation arrhythmias (mainly 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).
      • Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).
  • Medical stabilization: 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. Treatment of myocardial ischemia, heart failure, and electrolyte disturbances are all justified by the results of multiple randomized trials investigating acute MI and CHF. Empiric beta-blockers are reasonable in many circumstances because of favorable properties discussed in Causes. Empiric antiarrhythmics, including amiodarone, should not supersede ICD placement unless control of recurrent VT is needed while the patient is hospitalized.
Next

Surgical Care

Most survivors of VF should be treated with ICDs. Transvenous ICDs can be placed with minimal morbidity and mortality.

  • Radiofrequency ablation: Now routinely available, radiofrequency ablation is indicated for patients with AV bypass tracts, bundle-branch block VT, RVOT tachycardia, idiopathic LV tachycardia, and more rare forms of automatic foci VT (which almost never cause VF). Unfortunately, most cases of VF are not amenable to radiofrequency ablation and require ICD placement. VF is an exception because of preexcited tachycardias in patients with WPW syndrome. In these patients, successful catheter ablation of the accessory pathway(s) is the appropriate therapy.
  • Several multicenter trials have examined the prophylactic use of ICD therapy in patients at high risk for VF.
    • The annual VF rate in patients with these devices has been reduced from 25% to 1-2%. ICD placement is beneficial in high-risk patients in whom electrophysiologic-guided therapy with antiarrhythmics has failed. In several studies comparing ICD placement with antiarrhythmic therapy in patients with VT/VF and/or prior cardiac arrest, ICD placement has been shown to be associated with significantly decreased mortality rate.[17, 18]
    • The use of ICDs as primary prevention for VF is still being investigated in ongoing trials. Newer ICDs have pacing capabilities and have addressed bradyarrhythmias either causing or complicating VT or VF.
    • Currently, the transvenous approach to implantation is universally applied and favored over the thoracotomy implants. In the Multicenter Automatic Defibrillation Implantation Trial (MADIT) 1, prophylactic use of ICDs in patients with a history of MI, LVEF of less than 35%, documented episode of nonsustained VT, and inducible nonsuppressible VT had a 54% reduction in mortality during any follow-up interval compared with patients treated with conventional medical therapy. In MADIT 2, the ICD conferred a 31% reduction in mortality in patients with prior MI and LVEF of 30% or less. In MADIT 2, there was no requirement for nonsustained VT or EPS.[19, 20]
  • 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 CASS study illustrated that patients with significant 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 CHF.[10] By itself, CABG only prevents recurrent VF if the ejection fraction is normal and ischemia was the cause of the arrest. Even in these patients, ICDs are frequently placed after CABG.
    • 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, however, given the efficacy of ICDs.
    • Aortic valve replacement is associated with improved outcome in patients with hemodynamically significant valvular stenosis and well-preserved ventricular function. In patients with MVP associated with significant valvular regurgitation and LV dysfunction, malignant tachyarrhythmias, such as VT and VF, have been reported. These patients are candidates for mitral valve replacement.
    • Orthotopic heart transplantation is indicated in patients with SCD and refractory heart failure, in whom significant improvement in actuarial survival is expected. Given a limited donor service, this form of treatment is expected to be beneficial for very few people who survive VF.
    • Patients with long QT syndrome who do not respond to beta-blockers are candidates for ICD placement or high thoracic left sympathectomy.
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Consultations

  • A cardiologist should always participate in the care of these patients. Cardiac electrophysiologists should also be involved in the care of these patients, which generally involves ICD placement.
  • Other consultants include an interventional cardiologist and cardiac surgeon. Such consultations are made on a case-by-case basis.
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Diet

  • Patients with CAD are advised to follow a diet low in fat and cholesterol. Patients with severe heart failure should monitor their fluid and sodium intake.
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Proceed to Medication
 
 
Contributor Information and Disclosures
Author

Michael E Zevitz, MD  Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice

Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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

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

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

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Figure A shows neurologic outcome stratified by initial cardiac arrest score. Neurologic recovery is defined as discharged home and ability to care for self. Figure B shows overall survival stratified by initial cardiac arrest score.
Epsilon wave in 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).
 
 
 
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