Ventricular fibrillation and ventricular tachycardia

Also known as: Vfib, Vtach, wide complex tachycardias

Related conditions: Pulseless ventricular tachycardia, monomorphic ventricular tachycardia, polymorphic ventricular tachycardia

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1. Description of the problem

Early diagnosis and rapid defibrillation of ventricular fibrillation (Vfib) and pulseless ventricular tachycardia can significantly increase chances for survival. Advanced cardiac life support (ACLS) emphasizes high-quality CPR. Ventricular tachycardia (Vtach) will be divided clinically into stable and unstable. A patient with unstable ventricular tachycardia should undergo rapid synchronized cardioversion (timed on QRS complex). Stable Vtach can be managed pharmacologically.

Clinical features

Vfib is rapid totally incoordinate contraction of ventricular fibers; the EKG shows chaotic electrical activity and clinically the patient has no pulse. Vtach is defined by QRS greater than or equal to .12 secs and a rate of greater than or equal to 100 beats per minute. There are three clinical types: pulseless, hemodynamically unstable and hemodynamically stable. If there is any doubt of polymorphic versus monomorphic Vtach in the hemodynamically unstable patient, treat like Vfib.

Key management points
  • Assess airway, breathing and circulation.

  • In a pulseless patient, begin immediate CPR and attach AED or external defibrillator. If Vtach or Vfib, prepare for defibrillation.

  • If pulse is present, attach EKG or defibrillator and evaluate rhythm. If patient is unstable and not polymorphic Vtach, prepare for synchronized cardoversion.

  • Once stable, assess underlying cause of arrhythmia, treat hypotension, electrolytes, etc.

2. Emergency Management

Determine whether patients has pulse or not. If no pulse, begin immediate CPR while placing AED or defibrillator. As action to restore circulation begins, think of what caused the arrest. ACLS says H’s and T’s: hypoxia, hypokalemia, hyperkalemia, hypovolemia, hydrogen ion acidosis, hypothermia, toxins, tension pneumothorax, and thrombosis (coronary and pulmonary).

3. Diagnosis

Diagnostic considerations

Diagnosis by EKG for all ventricular arrythmias.

Vfib is defined by totally incoordinate contraction of ventricular fibers, reflected on EKG by chaotic electrical activity.

Pulseless Vtach will be treated like Vfib.

Wide complex tachycardia (other than pulseless Vtach and Vfib) needs to be separated into stable or unstable; regular or irregular. Hemodynamic instability examples include: altered mental status, ischemic chest discomfort, acute heart failure, respiratory distress, hypotension or other signs of shock. Wide complex tachycardia is defined as a QRS greater than .12 secs and can be Vtach (monomorphic and polymorphic), supraventricular tachycardia with aberrancy, a pre-excitation tachycardia or a ventricular paced rhythm. Vtach diagnosis is supported by evidence of AV dissociation, wide complexes greater than 140 ms, and axis is positive or negative in all leads. Monomorphic Vtach has one morphology of QRS complexes. Polymorphic Vtach has progressive changes in QRS complex, which means multiple morphologies. Polymorphic Vtach with a prolonged QT (greater than 450 msec when heart rate corrected) is called torsades de pointes (
Figure 1).

Figure 1.

EKGs for Vtach, Vfib, polymorphic Vtach, and torsades de pointes

How do I know this is what the patient has?

Vfib is easily diagnosed by EKG; just do not forget to check EKG leads during the code to be sure they do not come unattached.

A wide complex tachycardia that is regular could be Vtach, SVT with aberrancy, pre-excited tachycardia or a v-paced rhythm. A wide complex tachycardia that is irregular may be atrial fibrillation with aberrancy, pre-excited atrial fibrillation, polymorphic vtach or torsades de pointes. If the etiology of the rhythm cannot be determined, the rate is regular and the QRS is monomorphic, then adenosine 6-12 mg IV can be given. If SVT it will convert or slow; if no response then it is Vtach. (Always have patient attached to defibrillator when giving adenosine in this clinical scenario.) Do not give adenosine to unstable patients or those with irregular or regular polymorphic wide complex tachycardias. In these scenarios adenosine could lead to Vfib.

Consider expert cardiology/electrophysiology consultation if diagnosis not clear.

4. Specific Treatment

Vfib/pulseless Vtach: Begin CPR while attaching AED or defibrillator; continue while charging. Biphasic defibrillation use 120 to 200 joules; it is acceptable to use maximum dose if unsure, For monophasic defibrillators use 360 joules. After defibrillation continue CPR for 2 minutes before checking pulse. If no return to circulation, defibrillate again and check pulse in 2 minutes. After two shocks epinephrine should be used, 1 mg IV every 3-5 minutes, Remember, circulation time with CPR for IV drugs is 1-2 minutes. Amiodarone may be considered when Vfib/pulseless Vtach is unresponsive to CPR, defibrillation, and vasopressors. The dose of amiodarone will be 300 mg IV. Once return to circulation occurs, treat hypoxia, hypotension, electrolytes; early diagnosis and treatment of ST-segment myocardial infarction; and therapeutic hypothermia for comatose survivors.

Vtach with unstable patient: Proceed with synchronized cardioversion 100 joules (monophasic or biphasic) if monomorphic. If irregular wide complex, polymorphic or torsades de pointes, defibrillate like Vfib.

Vtach that is monomorphic with stable patient: Treat with procainamide, amiodarone or sotalol (doses in next section). Verapamil is contraindicated for wide complex tachycardia unless known to be supraventricular in origin. If drug therapy fails, elective cardioversion is an option. Consider seeking expert consultation; burst overdrive pacing of the right ventricle may be an option for therapy.

Vtach that is polymorphic requires defibrillation as described above. Polymorphic Vtach with a prolonged QT can be treated with magnesium 1-2 mg over 15 minutes. Correct electrolyte imbalance; consider drug overdose, tricyclic antidepressants, or congenital prolonged QT syndrome. If QT is not prolonged, then myocardial ischemia is the likely culprit. IV amiodarone and beta blockers may reduce the frequency of recurrence. Consult cardiology for possible need of coronary intervention. If there is any doubt whether rhythm is monomorphic or polymorphic in an unstable patient, do not delay shock delivery; provide high-energy unsynchronized shocks as for Vfib.

Drugs and dosages

Adenosine may be used as a diagnostic maneuver in stable monomorphic wide complex tachycardia in a dose of 6 mg IV fast push, may repeat with 12 mg. Adenosine is contraindicated in asthma, WPW, polymorphic Vtach, irregular Vtach or Vtach from ischemia. Side effects are hypotension, bronchospasm, chest discomfort (the drug will cause a temporary pause.)

Procainamide can be used in hemodynamically stable monomorphic Vtach in a dose of 20 to 50 mg/min until arrhythmia is suppressed, hypotension, QRS prolonged by 50%, or total dose of 17 mg/kg. Side effects are bradycardia, hypotension, torsades de pointes. Avoid with QT prolongation and CHF.

Amiodarone can be used in refractory Vfib, hemodynamically stable monomorphic Vtach, or polymorphic Vtach with normal QT interval. Dose for Vfib is 300 mg IV, second dose 150 mg. For Vtach the dose is 150 mg IV and repeat if necessary. Start infusion at 1 mg/min for 6 hours, then 0.5 mg/min for 6 hours. Side effects are bradycardia, hypotension and phlebitis.

Sotalol can be used in hemodynamically stable monomorphic Vtach. Dose is 1.5 mg/kg over 5 minutes. Side effects are bradycardia, hypotension, torsades de pointes. Avoid in patients with prolonged QT and CHF.

Lidocaine can used for hemodynamically stable monomorphic Vtach. Initial dose is 1-1.5 mg/kg IV, repeat dose is 0.5-0.75 mg/kg IV up to maximum cumulative dose of 3 mg/kg. Side effects are slurred speech, altered levels of consciousness, seizures and bradycardia.

Magnesium can be used for polymorphic Vtach associated with QT prolongation, also called torsades de pointes. Dose is 1-2 mg IV over 15 minutes. Side effects are hypotension, CNS toxicity, respiratory depression. Follow levels and watch closely with concomitant renal dysfunction.

5. Disease monitoring, follow-up and disposition

Expected response to treatment

In Vfib/pulseless Vtach the majority of resuscitative efforts do not result in return to circulation. Vtach response to therapy depends on underlying etiology. Key to treatment past antiarrhythmics and electricity will be identifying possible causes (defined in pathophysiology section).

Incorrect diagnosis

If front-line arrhythmia therapy fails or clinical situation deteriorates, reconsider diagnosis. Reevaluate EKG, clinical history and presentation. Seek expert help.


Treament for underlying cause; follow up with cardiology and/or electrophysiology.


The vast majority of adult cardiac arrests from Vfib and pulseless Vtach are secondary to myocardial ischemia, around 250,000 people per year. These arrhythmias are the most common cause of death in acute myocardial infarction. Primary Vfib (not associated with an MI) needs evaluation by an electrophysiologist. Vtach accounts for 80% of wide complex tachycardias, while 15-30% of wide complex tachycardias may be the result of SVT with abnormal interventricular conduction. Prior history of MI, heart failure or recent angina in one study meant a 95% chance that the wide complex tachycardia is the result of Vtach.

Idiopathic Vtach (absent structural heart disease) occurs in around 10% of cases and prognosis is excellent with beta blocker therapy. Vtach occurs in areas of scar from prior MI, the risk of development depending on severity of myocardial necrosis, LV dysfunction and the degree of septal involvement. Thus stable Vtach is more likely from an arrhythmogenic focus in an old scar. Therapy should be focused on underlying hypoxia, electrolytes, etc. Other possible causes of monomorphic Vtach include: dilated cardiomyopathy, hypertrophic cardiomyopathy, myocarditis, RV dysplasia, drug toxicity and electrolyte abnormalities.

Polymorphic Vtach in the setting of a normal QT is usually secondary to acute coronary ischemia or myocardial infarction. Outside of congenital syndromes such as long QT syndrome, polymorphic Vtach from prolonged QT occurs most frequently following exposure to a QT-prolonging drug. Significant QT prolongation occurs in 1-10% of patients receiving QT-prolonging anti-arryhthmics and even more with non-cardiovascular QT-prolonging agents. Risk factors for torsades are female gender, hypokalemia, bradycardia, recent conversion from atrial fibrillation especially with a QT0prolonging drug, CHF, digitalis, baseline QT prolongation, subclinical QT syndrome or severe hypomagnesemia. Congenital QT syndrome occurs in 5/10,000 people.


See section on pathophysiology; hard to separate for arrhythmias.


See above for details.

Special considerations for nursing and allied health professionals.

For the patient with no pulse, immediate CPR is the key to survival post arrest.

What's the evidence?

For Vfib arrest, high-quality CPR and defibrillation have been proven to increase survival to hospital disharge. Vascular access, drug delivery, advanced airway should not cause significant disruptions in CPR or delay defrbrillation.

Amiodarone is the first-line antiarrhythmic during cardiac arrest, as it has been shown to improve return to circulation. Two observational studies have shown that magnesium can terminate torsades de pointes, it is not likely to be effective in terminating irregular or polymorphic Vtach with a normal QT interval. For stable Vtach, IV antiarrhythmic drugs or elective cardioversion is recommended. Lidocaine has been found to be less effective than amiodarone, sotalol or procainamide. Procainamide and sotalol should be avoided with QT prolongation. Procainamide should be avoided in CHF. At this time there is no conclusive evidence that one drug is better for termination of monomorphic Vtach. ICD should be considered with sustained Vtach, but no survival benefit has been shown if the ejection is greater than 35%.

Neumar, R. “Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”. Circulation. vol. 122. 2010. pp. s729-s767. This is highly recommended reading for all.

Pellegrini, C. “Clinical management of ventricular tachycardia”. Curr Probl Cardiol. vol. 35. 2010. pp. 453-504. Review article for Vtach.

Marill, K. “Adenosine for wide-complex tachycardia: Efficacy and safety”. Crit Care Med. vol. 37. 2009. pp. 2512-2518.

Tzivoni, D. “Treatment of torsades de pointes with magnesium sulfate”. Circulation. vol. 77. 1988. pp. 392-397.

Kudenchuk. ” Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation”. N Engl J Med. vol. 341. 1999. pp. 871-8.

Somberg, J. “Intravenous lidocaine versus intravenous amiodarone for incessant ventricular tachycardia”. Am J Cardiol. vol. 90. 2002. pp. 853-859.

Tomlinson, DR. “Intravenous amiodarone for the pharmacological termination of hemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?”. Emerg Med J. vol. 25. 2008. pp. 15-18.