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Ventricular fibrillation (VF) causes uncoordinated quivering of the ventricle with no useful contractions. It causes immediate syncope and death within minutes. Treatment is with cardiopulmonary resuscitation, including immediate defibrillation.
Ventricular fibrillation is due to multiple wavelet reentrant electrical activity and is manifested on ECG by ultrarapid baseline undulations that are irregular in timing and morphology (see Figure: Atrial fibrillation in Wolff-Parkinson-White syndrome.).
VF is the presenting rhythm for about 70% of patients in cardiac arrest and is thus the terminal event in many disorders. Overall, most patients with VF have an underlying heart disorder (typically ischemic cardiomyopathy, but also hypertrophic or dilated cardiomyopathies, arrhythmogenic right ventricular dysplasia [ARVD], or Brugada syndrome). Risk of VF in any disorder is increased by electrolyte abnormalities, acidosis, hypoxemia, or ischemia.
VF is much less common among infants and children, in whom asystole is the more common presentation of cardiac arrest.
Treatment is with cardiopulmonary resuscitation, including defibrillation. The success rate for immediate (within 3 min) defibrillation is about 95%, provided that overwhelming pump failure does not preexist. When it does, even immediate defibrillation is only 30% successful, and most resuscitated patients die of pump failure before hospital discharge.
Patients who have VF without a reversible or transient cause are at high risk of future VF events and of sudden death. Most of these patients require an implantable cardioverter-defibrillator; many require concomitant antiarrhythmic drugs to reduce the frequency of subsequent episodes of ventricular tachycardia and VF.
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