Ventricular Fibrillation

Ventricular fibrillation (VF) is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle fibres contract randomly causing a complete failure of ventricular function. Most cases of ventricular fibrillation occur in patients with pre-existing known heart disease but the precise nature of the underlying cause of ventricular fibrillation is not currently known.

• Ventricular fibrillation is the most commonly identified arrhythmia in cardiac arrest patients.
• The incidence of VF parallels the incidence of ischaemic heart disease, with a peak incidence of VF occurring in people aged 45-75 years.¹
• An estimated 3-9% of cases of ventricular tachycardia (VT) and VF occur in the absence of myocardial ischaemia. Up to 15% of patients younger than 40 years who experience VF have no underlying structural heart disease.

Risk factors

• VF is most often associated with coronary artery disease and as a terminal event. VF may be due to acute myocardial infarction or ischaemia, or occur because of a chronic infarct scar.
• When documentation is available, it often shows that rapid VT precedes VF.
• VF can occur during any of the following conditions or situations:
  • Antiarrhythmic drug administration
  • Hypoxia
  • Ischaemia
  • Atrial fibrillation
  • Very rapid ventricular rates in the pre-excitation syndrome
  • Electrical shock administered during cardioversion
  • Electrical shock caused by accidental contact with improperly grounded equipment
  • Competitive ventricular pacing to terminate VT

• Patients may have a history of chest pain, fatigue, palpitations and other non-specific complaints.
• There may be known diagnosis or suggestion of pre-existing heart disease, e.g. coronary artery disease, cardiomyopathy, valvular heart disease, myocarditis, congenital heart disease, Long QT syndrome, Wolff-Parkinson-White syndrome or Brugada syndrome.

• Arrhythmias associated with cardiac arrest are divided into two groups:
  • Shockable rhythms (VF/VT).
  • Non-shockable rhythms: asystole and pulseless electrical activity (PEA): see article on advanced life support which covers the resuscitation guidelines from the Resuscitation Council.
• Other causes of sudden collapse such as aortic dissection and pulmonary embolism.

• Cardiac enzymes (eg, creatine kinase, myoglobin, troponin).
• Electrolytes, calcium and magnesium. Severe metabolic acidosis, hypokalaemia, hyperkalaemia, hypocalcaemia, and hypomagnesaemia are some of the conditions that can increase the risk for arrhythmia and sudden death.
• Drug levels (e.g. quinidine, procainamide, tricyclic antidepressants, digoxin). Most of the antiarrhythmia medications also have a proarrhythmic effect.
• Toxicology screen: drugs that can lead to vasospasm-induced ischemia, e.g. cocaine.
• Thyroid-stimulating hormone: hyperthyroidism can lead to tachycardia and tachyarrhythmias.
• ECG²: evidence of MI, prolonged QT interval, short PR, WPW pattern or other conditions.
• Chest x-ray: signs of left heart failure, pulmonary hypertension.
• Echocardiography: underlying structural abnormalities and cardiac dysfunction.
• Nuclear imaging techniques.
  • Resting thallium Tl or technetium Tc 99m scintigraphy: assessing myocardial damage after MI.
  • Exercise nuclear scintigraphy: very sensitive in detecting the presence, extent and location of myocardial ischemia.
• Coronary angiography:
  • Cardiac catheterisation in patients who survive VF to assess the state of ventricular function and severity and extent of coronary artery disease.
  • Coronary angiography can also help identify coronary artery anomalies and other forms of congenital heart disease - to identify patients who may benefit from revascularisation by angioplasty or coronary artery bypass grafting.

See Cardiac Arrest protocols

Medical stabilisation

Patients who survive the initial episode of VF require a full evaluation of left ventricular function, myocardial perfusion and electrophysiological instability.

• Careful post-resuscitation care is essential to survival because recurrence rates average at about 50%.
• Treatment of myocardial ischaemia, heart failure and electrolyte disturbances.
• Empirical beta-blockers are often given.
• Most survivors of VF should be treated with implantable cardioverter defibrillators (ICD). Transvenous ICDs can be placed with minimal morbidity and mortality.
• Radiofrequency ablation: most cases of VF are not amenable to radiofrequency ablation and require ICD placement.
• By itself, CABG only prevents recurrent VF if the ejection fraction is normal and ischemia was the cause of the arrest. Even in these patients, ICDs are frequently placed after CABG.

• Central nervous system ischaemic injury
• Myocardial injury
• Post-defibrillation arrhythmias
• Aspiration pneumonia
• Defibrillation injury to self or others
• Injuries from CPR and resuscitation
• Skin burns
• Death

• Prognosis for survivors of VF strongly depends on the time elapsed between onset and medical intervention (prognosis is poor without intervention by 4-6 minutes after onset of VF) as well as on the particular aetiology for the VF.
• Early defibrillation often makes the difference between long-term disability and functional recovery.
• Death and disability after successful resuscitation correlate with the degree of central nervous system damage occurring during the event.
• VF that occurs within the first 48 hours of the onset of acute myocardial infarction has no bearing on prognosis, but VF that occurs more than 48 hours after acute myocardial infarction is associated with a high rate of recurrence and a poorer prognosis.
• After resuscitation, the prognosis is largely dependent on haemodynamic stability, early neurological recovery and duration of the resuscitation.
• Education and training of non-health care professional in basic life support and the use of automated external defibrillators in public places will probably have the greatest impact on improving survival rates.
• A major adverse outcome from a VF event is anoxic encephalopathy, which occurs in 30-80% of patients.