Ventricular Fibrillation Treatment & Management

Updated: Jun 06, 2018
  • Author: Sandeep K Goyal, MD, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Treatment

Approach Considerations

Acute ventricular fibrillation (VF) is treated according to Advanced Cardiac Life Support (ACLS) protocols. [81, 82] ) Interest in improving rates of public cardiopulmonary resuscitation (CPR) training—with a special emphasis on the use of early defibrillation with automated external defibrillators (AEDs) by public service personnel (eg, police, fire, airline)—is widespread. [2] 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). Pharmacotherapy or surgical treatment (eg, operable coronary artery disease [CAD]) may be appropriate in some cases, whereas radiofrequency ablation is effective in a variety of disorders.

Antiarrhythmic drugs appear to be beneficial for individuals with unsuccessful initial early CPR and defibrillation attempts when these agents are administered early. [83]  When defibrillation and antiarrhythmic medications are ineffective, potential additional survival benefit may be seen with other interventions, such as percutaneous coronary intervention (PCI) and extracorporeal CPR. [83]

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 who receive only medication. [84, 85, 86, 87]

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Defibrillation

External electrical defibrillation remains the most successful treatment for ventricular fibrillation (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 two key factors: the duration of the VF and the metabolic condition of the myocardium. The 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. Unfortunately, VF waveform measures do not appear to be useful for differentiating ischemic from nonischemic cardiac arrest etiology. [88]

Consequently, early defibrillation is vital; emergency medical services (EMS) personnel can perform defibrillation at the scene, long before the patient could be seen at the emergency department (ED). In addition, the placement of automated external defibrillators (AEDs) in public places such as airports, casinos, and restaurants allows prompt use of these devices by trained laypersons.

Defibrillation success rates decrease about 5%-10% for each minute after the onset of VF. In strictly monitored settings where defibrillation was performed most promptly, success rates of 85% have been reported.

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 affected, 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 the 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 (3.15-4.92 inches) for an adult, 8-10 cm (3.15-3.94 inches) for a child, and 4.5-5 cm (1.77-1.97 inches) for an infant. Position one paddle below the outer half of the right clavicle and one over the cardiac apex (V4 -V5) (see the following image).

Position of the paddle electrodes during defibrill Position of the paddle electrodes during defibrillation/cardioversion, position of the heart, and flow of intrathoracic energy during delivery of the electric shock are shown.

Before initiating 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 (CPK) 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 is actually not appropriate in both. Use it only for witnessed, monitored arrests in which no defibrillator is immediately available.

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ACLS Algorithm

Cardiopulmonary resuscitation

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 automated external defibrillator (AED). Initiate cardiopulmonary resuscitation (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 100-120 per minute—with complete recoil in between.

In a secondary analysis of data from the Circulation Improving Resuscitation Care trial to evaluate preshock pause and termination of ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT) 5s postshock (TOF) and return of organized rhythm (ROOR) with mechanical load-distributing band (LDB)-CPR and manual (M)-CPR, Olsen et al found that for first shocks with LDB-CPR, preshock pause duration was associated with TOF but that there was no association for the rate of ROOR. [89] For M-CPR, in which no shocks were given during continuous chest compressions, there were no significant associations between preshock pause duration and TOF or ROOR. [89]

Note that a growing body of research has found no benefit from ventilation in CPR for out-of-hospital cardiac arrest. [90, 91] 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. [92] The American Heart Association (AHA) currently recommends the use of chest compression-only CPR ("hands-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 one (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 three (3) cycles of CPR, and then check the rhythm.

Additional actions

While minimizing interruption of chest compression, do the following [81] :

  • Consider placement of an advanced airway (continuous chest compressions can be given after an advanced airway is in place)

  • Consider waveform capnography

  • Obtain intravenous (IV) or intraosseous (IO) access

  • Consider administering vasopressors and antiarrhythmics

  • Correct reversible causes

Vasopressors (epinephrine or vasopressin) are given per the asystole/pulseless electrical activity (PEA) advanced cardiac life support (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 three (3) doses or 3 mg/kg. If torsade de pointes is present, consider administering magnesium sulfate, loading dose 1-2 g IV/IO.

Treat the following underlying provocative abnormalities, if present:

  • Myocardial infarction

  • 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. [93] If amiodarone was not used earlier, consider giving 15 mg/min for 10 minutes, followed by 1 mg/min for 6 hours, and then 0.5 mg/min for 18 hours. Reported defibrillation 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

Careful postresuscitative care is essential to survival, because studies have shown a 50% repeat in-hospital arrest rate for people admitted after a ventricular fibrillation (VF) event. Multiple randomized trials have confirmed the benefit of treating myocardial ischemia, heart failure, and electrolyte disturbances.

Important considerations

Resuscitated patients must be admitted to an intensive care unit (ICU) and closely 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.

Assess for complications (eg, aspiration pneumonia, cardiopulmonary resuscitation [CPR]-related injuries), and establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).

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. [20, 94] Traditionally, a target temperature of 32°-34°C (89.6°-93°F) 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 (91.4°F) did not confer a benefit as compared with a targeted temperature of 36°C (96.8°F). [95]  During therapeutic hypothermia in patients with aborted arrhythmic sudden cardiac death (SCD), a prolonged T-wave peak to T-wave end (Tpeak-Tend) interval and QTc interval may predict the development of VF in the follow-up period. [96]

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 implantable cardioverter-defibrillator (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.

An analysis of data from the Israeli ICD Registry suggests that the presence of anemia in patients with ICDs is an independent factor that increases the risk for ventricular arrhythmias over the long term. [97]  Clinically at-risk patients with anemia were older, had more advanced heart failure symptoms, and/or had atrial fibrillation. At 2.5 years of follow-up, patients with lower hemoglobin levels had significantly greater rates of appropriate shocks than those with higher hemoglobin levels, and the presence of anemia was associated not only with a significant 56% increased risk for first appropriate ICD shock but also with a greater risk for all-cause mortality and hospitalizations for, or deaths from, heart failure. [97]

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Radiofrequency Ablation

Radiofrequency ablation (RFA) is indicated for prevention of ventricular fibrillation (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 [34]

  • 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 placement of an implantable cardioverter-defibrillator (ICD).

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 ventricular fibrillation (VF) that does not have a clear and readily reversible cause should undergo placement with an implantable cardioverter-defibrillator (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.

In a comparative effectiveness study of ICD therapy in survivors of in-hospital cardiac arrest, investigators linked data from a national inpatient cardiac arrest registry with Medicare files and identified 1200 adults who were discharged after surviving an in-hospital cardiac arrest due to VF or pulseless ventricular tachycardia (VT) and who otherwise met traditional inclusion and exclusion criteria for secondary prevention ICD trials. [98] Using an optimal match propensity-score analysis, the investigators evaluated the association between ICD treatment and long-term mortality and found that ICD therapy in survivors of in-hospital cardiac arrest due to a pulseless ventricular rhythm is associated with lower long-term mortality. [98]

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. [84, 99, 100] 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. [101]

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 (LVEF) of less than 35%, whether due to ischemic or nonischemic cardiomyopathy. [102, 103]

Findings from a study of subcutaneous ICD (S-ICD) in 60 patients following its introduction in Japan as an alternative to conventional transvenous ICD (TV-ICD) in February 2016 show it is safe and effective in those at high risk of sudden cardiac death. [104] Of 56 patients who underwent a postprocedure defibrillation test, VF was induced in 55 patients (98%), with 100% termination by a single 65-J shock. No complications related to the procedure or infection were noted. During a median follow-up period of 275 days, one patient (1.7%) received an appropriate shock for VF with termination, but five patients (8.3%) received an inappropriate shock from myopotential (n = 3) or T-wave (n = 1) oversensing or for detection of a supraventricular tachycardia (n = 1). [104] These preliminary findings for S-ICD require more studies.

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 three-vessel disease and chronic heart failure. [10]

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 ventricular fibrillation (VF), screen for hypertrophic cardiomyopathy (HCM) in young patients who are at high suspicion for HCM, particularly those who are prospective candidates for competitive-level athletics. [30]

Coventional risk factors for sudden cardiac death (SCD) in HCM include the following:

  • Syncope

  • Abnormal blood pressure response (ie, hypotension) to exercise

  • Nonsustained or sustained ventricular tachycardia (VT)

  • Paroxysmal supraventricular tachycardia (PSVT)

  • Paroxysmal atrial fibrillation (PAF)

  • Family history of sudden cardiac death (SCD) from suspected or diagnosed HCM

Nonconventional risk factors for an increased risk of SCD in HCM include the following:

  • Magnetic resonance imaging (MRI)-based scar: Extensive late gadolinium enhancement (LGE) by contrast cardiac MRI has been introduced as an independent marker of sudden death (SD) in HCM. [105]  The risk increases linearly with respect to the percentage (%) LGE of the left ventricular (LV) myocardium: 15% LGE conveys a two-fold increase in risk. Extensive LGE acts as a risk factor even in the absence of conventional markers, identifying patients at SD risk who otherwise would not be considered candidates for implantable cardioverter-defibriIlators (ICDs). [105]  Absent or focal LGE is associated with low risk and is a source of reassurance. [105]

  • LV apical aneurysms: LV apical aneurysms are relatively uncommon in HCM. However, they are associated with an increased risk of SCD due to monomorphic VT, and placement of an ICD may be justified. [106]

When HCM 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 ventricular tachycardia/ventricular fibrillation (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 placement of an implantable cardioverter-defibrillator (ICD).

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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