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) trainingwith 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]

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 lowerenergy 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.

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 fast2 inches or
more, at a rate of at least 100/minutewith 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-compressiononly 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.

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
32-34C 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 33C did not confer a benefit
as compared with a targeted temperature of 36C.[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.

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.

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.

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.

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.
MEDICATION
Medication Summary
In acute ventricular fibrillation (VF), drugs (eg, vasopressin, epinephrine,
amiodarone) are used after 3 defibrillation attempts are performed to restore
normal rhythm. Amiodarone can also be used on a long-term basis in patients
who refuse an implantable cardioverter-defibrillator (ICD) or who are not
candidates for an ICD. However, amiodarone has not been shown to be of value
for primary prevention of VF in patients with a depressed left ventricular (LV)
ejection fraction.
Antidysrhythmics, Ia
Class Summary
Class Ia antiarrhythmics increase the refractory periods of the atria and
ventricles. Myocardial excitability is reduced by an increase in the threshold for
excitation and inhibition of ectopic pacemaker activity.
View full drug information
Procainamide (Procanbid, Pronestyl, Pronestyl [SR])
Procainamide is a third-line drug of choice for VF. This drug is generally not
recommended for VF patients, but because of its long loading time, it can be
used to prevent recurrences of VF or for treatment of sustained ventricular
tachycardia (VT).
Antidysrhythmics, Ib
Class Summary
Class Ib antidysrhythmics suppress automaticity of conduction tissue by
increasing the electrical stimulation threshold of the ventricle and His-Purkinje
system and by inhibiting spontaneous depolarization of the ventricles during
diastole by a direct action on the tissues. Class Ib antidysrhythmics block the
initiation and conduction of nerve impulses by decreasing the neuronal

membrane's permeability to sodium ions, resulting in inhibition of depolarization,

with resultant blockade of conduction.
View full drug information
Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach)
Lidocaine is a local anesthetic and a class Ib antiarrhythmic agent that increases
the electrical stimulation threshold of the ventricle, suppressing the automaticity
of conduction through the tissue. Class Ib agents particularly shorten the action
potential. Lidocaine may be tried in patients with VT due to ischemia.
Antidysrhythmics, III
Class Summary
Class III antidysrhythmics prolong the action potential duration. Some agents in
this class inhibit adrenergic stimulation (alpha- and beta-blocking properties);
affect sodium, potassium, and calcium channels; and prolong the action potential
and refractory period in myocardial tissue. These effects result in decreased
atrioventricular (AV) conduction and sinus node function.
View full drug information
Amiodarone (Pacerone, Cordarone, Nexterone)
Amiodarone is a class III antiarrhythmic agent indicated for the management of
life-threatening recurrent VF.
Amiodarone may be administered intravenously or orally.
Recurrent VF that is not due to a reversible cause can be treated with
intravenous (IV) amiodarone. It decreases AV conduction and sinus node
function. It also prolongs action potential and refractory period in myocardium
and inhibits adrenergic stimulation. Amiodarone can also be used orally on a
long-term basis in patients who refuse ICDs, are not candidates for ICDs, or have
frequent ventricular arrhythmias.
Antidysrhythmics, V
Class Summary
Class V antidysrhythmics have a mechanism of action different from those of
agents in classes I-IV; in many cases their mechanism of action is unknown.
View full drug information
Magnesium sulfate

Magnesium acts as an anti-arrhythmic agent and diminishes the frequency of

premature ventricular contractions, particularly when secondary to acute
ischemia. Clinical trials have been inconclusive in demonstrating its ability to
improve mortality rates in the setting of refractory VF.
Vasopressors
Class Summary
These agents augment the coronary and cerebral blood flow that is present
during the low-flow state associated with hemodynamic compromise from VF.
View full drug information
Epinephrine (Adrenalin)
Epinephrine is considered to be the single most useful drug in cardiac arrest,
although it has never been shown to benefit long-term survival or functional
recovery. Epinephrine stimulates alpha, beta1, and beta2 receptors, resulting in
relaxation of smooth muscle, cardiac stimulation, and dilation of muscle
vasculature.
View full drug information
Vasopressin (ADH, Pitressin)
Vasopressin is a peptide hormone that regulates the body's retention of water by
increasing water absorption in the collecting duct of the kidney nephron. It also
increases arterial blood pressure by affecting peripheral vascular resistance.
Vasopressin has an off-label indication for VF that is causing pulseless arrest.
This agent may improve vital organ blood flow, cerebral oxygen delivery, the
patient's ability to be resuscitated, and the patient's neurologic recovery.