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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]

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Defibrillation

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.

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ACLS Algorithm

CPR

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.

Defibrillation

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.

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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.

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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.

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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.

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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.

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Consultations

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.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Acknowledgements

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

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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]



Scoring:



≤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
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