Although they are controversial, experimental and clinical observations suggest that ventricular fibrillation is also a re- entrant phenomenon. Unlike ventricular tachycardia, during which a single activation wavefront circulates around a fixed barrier, ventricular fibrillation is caused by multiple simultaneous rotors that travel around functional barriers of refractory tissue, moving continuously throughout the myocardium to create very rapid, irregular, and ineffective activation. Like postinfarction arrhythmias, the ventricular tachycardia in patients with nonischemic cardiomyopathy is often the result of reentry in a zone of patchy fibrosis. Unlike reentry, which can usually be induced and terminated by premature beats, automatic rhythms tend not to be influenced by pacing. Changes in heart rate at the onset of ventricular tachycardia may also provide insight into the arrhythmia mechanism.
Reentrant tachycardias are usually stable because of a fixed conduction time around the circuit.
In contrast, automaticity often shows warm-up, with progressive acceleration during the first few seconds of the tachycardia. Abnormal automaticity may play a role in a number of clinical arrhythmia syndromes. These slow-fast rhythms are probably the result of abnormal automaticity in ischemic Purkinje fibers. More rapid ventricular tachycardia is also a frequent complication of acute ischemia, reperfusion, or both. It is likely that abnormal automaticity in ischemic myocardium is responsible for many of these episodes.