Automaticity, as outlined earlier, describes a cell's ability to raise spontaneously (depolarize) the resting membrane potential above the threshold value to initiate an action potential. Enhanced automaticity resulting in tachycardia may result from an increase in the slope of phase 4 depolarization or a decrease (less negative) in the resting membrane potential. Activation of p-adrenoceptors, hypokalemia, and stretching of cardiac cells all increase the slope of phase 4 depolarization and may serve as the trigger for enhanced automaticity. It is also possible for tissue that normally does not have pacemaking capabilities to develop inappropriate spontaneous diastolic depolarization and serve as an ectopic focus for impulse generation.
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