Automaticity, as outlined earlier, describes a cell’s abil-ity to raise spontaneously (depolarize) the resting mem-brane 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 β- 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 spon-taneous diastolic depolarization and serve as an ectopic focus for impulse generation.
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