Ventricular Fibrillation in Emergency Medicine Treatment & Management

Updated: Jan 12, 2021
  • Author: Keith A Marill, MD, MS; Chief Editor: Erik D Schraga, MD  more...
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Prehospital Care

Because of the critical importance of early defibrillation, prehospital care is vital for arrests due to ventricular fibrillation (VF) that occur outside the hospital.

Interventions that impact survival and outcome of resuscitation include the following:

  • Witnessed or early recognition of an arrest

  • Early activation of emergency medical services (EMS) system

  • Bystander CPR slows the degeneration of VF and improves survival.

  • Automated external defibrillator (AED) application and defibrillation by trained personnel in the field

  • Early access to trained EMS personnel capable of performing CPR, defibrillation, and advanced cardiac life support (ACLS)

Bystander CPR

Traditionally, CPR consists of artificial respirations and chest compressions. Mounting evidence demonstrates that high quality chest compressions are the critical action to provide some cardiac perfusion during CPR, and artificial respirations are less important. [16, 17, 18, 19] Interruption of chest compressions to perform artificial respirations by a single resuscitator causes a loss of cardiac perfusion pressure, and even after restarting compressions, it may take some time before the previously obtained perfusion pressure is restored.

Other concerns exist regarding the recommendation of artificial ventilations routinely for VF arrest. Rescuers may be prone to hyperventilate the victim, which may lead to increased intrathoracic pressure, and resulting decreased coronary perfusion and survival. [20] Bystanders may be more likely to perform CPR that involves only chest compressions and no artificial respirations.

Current American Heart Association (AHA) guidelines recommend immediate treatment with 30 chest compressions prior to any artificial ventilations.

Untrained lay rescuers should continue to provide chest compressions only with an emphasis on "push hard and fast." This should continue until an AED arrives or healthcare providers are ready to take over care.

Trained lay rescuers should provide 30 compressions to 2 artificial breaths.

Healthcare providers should perform cycles of 30 chest compressions to 2 ventilations until an advanced airway is placed. After that, chest compressions can be performed continuously along with provision of one breath every 6 to 8 seconds.

AHA guidelines reflect developments in this ongoing area of research, including the "cardiocerebral resuscitation" approach, also summarized after the AHA algorithm (see Emergency Department Care). [21] This approach emphasizes minimal interruption of continuous chest compressions (CCC) for victims of witnessed cardiac arrest.  More recent data do not suggest a difference in outcome between performance of CPR by EMS providers with chest compressions that are continuous or interrupted by artificial ventilations. [22]

It is important to note the arguments above apply to the use of artificial respirations for initial resuscitation of VF circulatory arrest. Future research may confirm the importance of artificial respirations for respiratory, drowning, traumatic, or other causes of arrest. It is becoming clear that the optimal treatment for these conditions with grossly different etiologies will differ and "one size will not fit all."

Automated external defibrillator (AED) application and defibrillation by trained personnel in the field

AEDs have revolutionized prehospital VF management because they decrease the time to defibrillation. This is accomplished by having the units prepositioned in the field where cardiac arrests are likely to occur (eg, airports, casinos, jails, malls, stadiums, industrial parks), eliminating the need for rhythm-recognition training and increasing the number of trained personnel and laypeople that can defibrillate at the scene.

Unfortunately, even for a group of patients at high risk for VF/VT, placement of an AED in the home was not associated with improved mortality. [23] AEDs were also unhelpful in the hospital setting where early access to a manual defibrillator and trained personnel are available. They may even be detrimental to the resuscitation and survival of patients with nonshockable rhythms such as pulseless electrical activity and asystole. [24, 25]

AEDs are programmed to recognize three shockable rhythms: coarse ventricular fibrillation, fine ventricular fibrillation, and rapid ventricular tachycardia. Modern units have a sensitivity greater than 95% and specificity approaching 100% for the three shockable rhythms. The greatest difficulty is in distinguishing fine ventricular fibrillation from asystole.

AEDs can also be used for children. A pediatric dose-attenuating system should be used, if available, for children up to the age of 8 years, and a conventional AED can be used for children at or older than 8 years or with a corresponding weight of at least 25 kg (55 lb).


Emergency Department Care


Electrical external defibrillation remains the most successful treatment of ventricular fibrillation (VF). A shock is delivered to the heart to uniformly and simultaneously depolarize a critical mass of the excitable myocardium. The objective is to interfere with all reentrant arrhythmia and to allow any intrinsic cardiac pacemakers to assume the role of primary pacemaker. [26]

Successful defibrillation largely depends on the following two key factors: duration between onset of VF and defibrillation, and metabolic condition of the myocardium. VF begins with a coarse waveform and decays to a fine tracing and eventual asystole. These electrical changes that occur over minutes are associated with a depletion of the heart's energy reserves. CPR slows the progression of these events, but defibrillation is the primary treatment to interrupt the process and return the heart to a perfusing rhythm.

Defibrillation success rates decrease 5-10% for each minute after onset of VF. The likelihood of defibrillation success can also be predicted based on the smoothness of the VF tracing. In strictly monitored settings where defibrillation was most rapid, 85% success rates have been reported.

Factors that affect the energy required for successful defibrillation include the following:

  • Paddle size: 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.

  • Paddle-to-myocardium distance (eg, obesity, mechanical ventilation): Position one paddle below the outer half of the right clavicle and one over the apex (V4-V5). Artificial pacemakers or implantable defibrillators mandate use of anterior-posterior paddle placement.

  • 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 may lower the chest wall impedance and decrease the defibrillation threshold.

Biphasic defibrillation

Biphasic defibrillation has a number of advantages over monophasic defibrillation including increased likelihood of defibrillation success for a given shocking energy. [27] While this has not translated into a proven survival benefit thus far, if less shocks are required, there may be less interruption of CPR. Lower energy shocks associated with biphasic defibrillation may lead to less myocardial stunning after repeated defibrillation attempts. Furthermore, smaller and lighter defibrillation units are required to produce a biphasic waveform, and this is an important advantage for portable AED units.

The optimal energy for first and subsequent defibrillation attempts with a biphasic pulse remains unproven. Escalating energy levels have been associated with increased VF conversion and termination. Unfortunately, no improvement in survival was noted. [28]

Operators are advised to use the energy protocols associated with individual devices, or to begin with 200 J and consider escalating energy dose with subsequent shocks, if necessary.

Predefibrillation Safety

Rescuers must remember to ensure the safety of everyone around the patient before each shock is applied. Prior to 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.


The goal is to use the minimum amount of energy required to overcome the threshold of defibrillation. Excessive energy may cause myocardial injury.

Defibrillation causes the serum creatine phosphokinase level 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 normal limits unless an infarction has caused myocardial injury.

Postcountershock myocardial depression

If contraction is reestablished following defibrillation, a period may occur of low cardiac output, termed postcountershock myocardial depression. Cardiac output recovery may take minutes to hours.

CPR is important immediately after shock delivery. Many victims demonstrate asystole or pulseless electrical activity (PEA) for the first several minutes after defibrillation. CPR can convert these rhythms to a perfusing rhythm.

Provision of immediate CPR post defibrillation is a change included in the new AHA algorithm below.

"Priming the pump" predefibrillation CPR

Patients with VF for 4-5 minutes or more at the time defibrillation becomes available may benefit from a 1- to 3-minute period of CPR prior to initial defibrillation. The theoretical benefit of this intervention is "to prime the pump" by restoring some oxygen and other critical substrates to the myocardium to allow successful contraction post defibrillation. The clinical benefit of this intervention remains uncertain, but it has now been included as an optional protocol for Emergency Medical Services (EMS) in the AHA ACLS guidelines. [18, 29, 30]

AED units that can analyze the smoothness of the VF waveform are now available. These units essentially estimate the duration of fibrillation and likelihood of defibrillation success and advise immediate CPR or defibrillation depending on the reading.

Unfortunately, an initial EMS study using VF waveform analysis to guide the decision for initial therapy with immediate defibrillation or 2 minutes of CPR demonstrated no significant survival benefit over standard immediate defibrillation therapy. [31]

Precordial chest thump has been studied in a number of case series for patients in pulseless VT and VF. It has been found to convert VT and VF to a perfusing rhythm in some cases, but it has also been reported to accelerate VT, and to convert VT to VF and VF to asystole in other cases. This intervention is no longer routinely recommended. [32]

AHA Algorithm

The following summarizes the AHA algorithm [18] :

  • Activate emergency response system.

  • Initiate CPR and give oxygen when available.

  • Verify patient is in VF as soon as possible (ie, AED and quick look with paddles).

  • Defibrillate once: For adults, use a device specific or 200 J for biphasic waveform and 360 J for monophasic waveform; for children, 2 J/kg

  • Resume CPR immediately without pulse check and continue for 5 cycles. One cycle of CPR equals 30 compressions and 2 breaths; 5 cycles of CPR should take roughly 2 minutes (compression rate 100 per minute). Do not check for rhythm/pulse until 5 cycles of CPR are completed.

  • During CPR, minimize interruptions while securing intravenous access and performing endotracheal intubation. Once the patient is intubated, continue CPR at 100 compressions per minute without pauses for respirations, and administer respirations at 8-10 breaths per minute.

  • Check rhythm after 2 minutes of CPR.

  • Repeat a single defibrillation if still VF or pulseless VT with rhythm check. Use the same dose as the initial defibrillation for adults, and use 4 J/kg for this and all subsequent defibrillations for children.

  • Resume CPR for 2 minutes immediately after defibrillation.

  • Continuously repeat the cycle of (1) rhythm check, (2) defibrillation, and (3) 2 minutes of CPR

  • Administer vasopressor: Give vasopressor during CPR before or after shock when intravenous or intraosseous access is available. Administer epinephrine 1 mg every 3–5 minutes. Consider administering vasopressin 40 units once instead of the first or second epinephrine dose.

  • Administer antidysrhythmics. Give antidysrhythmic during CPR before or after shock. Administer amiodarone 300 mg IV/IO once, then consider administering an additional 150 mg once. Instead of or in addition to amiodarone, administer lidocaine 1-1.5 mg/kg first dose, then additional 0.5 mg/kg doses up to a maximum total of 3 mg/kg.

  • If there is undulating polymorphic ventricular tachycardia suggestive of torsades de pointes (TdP), administer 1-2 g magnesium IV/IO.

  • Administer sodium bicarbonate 1 mEq/kg IV/IO in cases of known or suspected preexistent hyperkalemia or tricyclic antidepressant overdose.

  • Lidocaine and epinephrine can be administered through the endotracheal (ET) tube if IV/IO attempts fail. Use 2.5 times the IV dose.

In addition, correct the following if necessary and/or possible:

  • Hypovolemia

  • Hypoxia

  • Hydrogen ion (acidosis) - Consider bicarbonate therapy.

  • Hyperkalemia/hypokalemia and metabolic disorders

  • Hypoglycemia (Check fingerstick or administer glucose.)

  • Hypothermia (Check core rectal temperature.)

  • Toxins

  • Tamponade, cardiac (Check with ultrasonography.)

  • Tension pneumothorax (Consider needle thoracostomy.)

  • Thrombosis, coronary or pulmonary - Consider thrombolytic therapy if suspected.

  • Trauma

Refractory or recurrent VF

Lack of response to standard defibrillation algorithms is challenging.

After initial amiodarone bolus, consider continued amiodarone therapy with 1 mg/min IV for 6 hours, then 0.5 mg/min for 18 hours.

If ongoing ischemia is the suspected cause of recurrent VF, consider emergent cardiac catheterization and possible angioplasty even in the absence of STEMI, and intra-aortic balloon pump placement.

For patients with prolonged and refractory in-hospital cardiogenic arrest that included VF/VT, it has been shown that extracorporeal cardiopulmonary resuscitation was associated with improved neurologically intact survival. [33] This study was performed in a large tertiary center with an ongoing protocol for this advanced experimental care.

Postresuscitative care

Antidysrhythmics used successfully should be continued. Maintain amiodarone at 0.5-1 mg/min and lidocaine at 1-4 mg/min.

Control any hemodynamic instability by administering vasopressors as indicated.

Check for complications (eg, aspiration pneumonia, CPR-related injuries).

Establish the need for emergent interventions (eg, thrombolytics, antidotes, decontamination).

Cardiocerebral resuscitation

"Cardiocerebral resuscitation" is the term used to describe one cutting edge method for resuscitation that has yielded an improvement in survival. [21, 34] Based on the latest resuscitation research for all phases of resuscitation, the three pillars of this approach can be summarized as follows:

  1. Cardiopulmonary resuscitation without mouth-to-mouth ventilations, or continuous chest compressions (CCC), for all patients with witnessed cardiac arrest.

  2. EMS to administer 200 CCC before and after a single defibrillation for patients with arrest for greater than 5 minutes (circulatory phase of arrest [35] ). Cycle to be repeated three times prior to endotracheal intubation. Epinephrine to be given as soon as intravenous or intraosseous access available.

  3. Postresuscitation care to include targeted temperature management particularly to avoid hyperthermia, although the ideal hypothermic target remains uncertain. [36] Urgent cardiac catheterization including percutaneous coronary intervention as needed, unless it is otherwise contraindicated.


Consult a cardiologist or intensivist for continued inpatient ICU care.


Medical Care

Resuscitated patients must be admitted to an intensive care unit and monitored because of high risk of a recurrence. They require stabilization and monitoring for possibility of a coexistent emergency or complication.

Evaluation of ischemic injury to the CNS, myocardium, and other organs is essential.

Patients typically have an underlying etiology that must be investigated and treated.

Up to approximately half of cardiac arrest survivors have evidence of an acute MI. Both emergent thrombolytic therapy and percutaneous transluminal coronary angioplasty (PTCA) have been used to treat these patients; however, CPR for greater than 10 minutes is considered a relative contraindication to thrombolysis. Furthermore, thrombolytic therapy has not proven beneficial when administered unselectively to all cardiac arrest patients. [37] Cardiology consultation is warranted for all survivors of cardiac arrest, and efforts at revascularization should be attempted selectively, as indicated. [38, 39]

Patients who remain comatose post resuscitation may benefit from 12-24 hours of controlled hypothermia therapy at 32-34 degrees Centigrade (89.6-93.2 degrees Fahrenheit) or at least euthermia and avoidance of fever. Hypothermia can be accomplished with chemical sedation and paralysis to prevent shivering and an external cooling blanket or ice. Hypothermia therapy improved both neurologic outcome and mortality in two initial trials, but this result was not observed in a more recent study. [36, 40, 41]

Implantable cardioverter-defibrillator (ICDs) are recommended for patients at risk for recurrent VF because they effectively provide early defibrillation. Patients with VF arrest who receive ICDs have improved survival compared with those receiving only medications. However, patients with ICDs may also require oral antidysrhythmic therapy to minimize recurrent device activation.



In the setting of acute myocardial infarction, beta-adrenergic blocking therapy with agents such as metoprolol decrease the likelihood of ventricular dysrhythmias including ventricular fibrillation, and they lower overall mortality. Consider administering a beta-adrenergic blocking agent during acute myocardial infarction unless contraindicated by bradycardia, heart block, congestive heart failure, or reactive airway disease.