Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal resting membrane potential. The higher the reduction in membrane potential, the faster and more rapid the already abnormal automaticity. Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on afterdepolarizations (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: Early afterdepolarizations(EAD) and Delayed afterdepolarizations (DAD). When either of these afterdepolarizations become high enough to reach the membrane threshold, they result in a spontaneous "triggered" action potential. Hence for a triggered activity to occur, at least one action potential must precede it.
In pulseless ventricular tachycardia, the combination of increased automatically and/or triggered activity leads to a rate of contraction that is too rapid to result in adequate ventricular filling during diastole. This results in deficient cardiac output, inadequate perfusion of organs, and hemodynamic collapse.
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