Pacemaking activity is regulated by both sympathetic and parasympathetic activity (see above). Therefore, factors that antagonize or enhance these effects can alter normal impulse formation, producing either bradycardia or tachycardia. Genetic mutations have also been found to alter normal pacemaking activity.
Under certain circumstances, abnormal activity can be generated by latent pacemakers, cells that show slow phase 4 depolarization even under normal conditions (eg, Purkinje cells). Such cells are
Early afterdepolarization (arises from the plateau) Delayed afterdepolarization (arises from the resting potential) Prolonged plateau 0 mV –70 0 mV –70 0.5 sec
FIGURE 14–5 Two forms of abnormal activity, early (top) and particularly prone to accelerated pacemaker activity, especially under delayed afterdepolarizations (bottom). In both cases, abnormal conditions such as hypokalemia. Abnormalities in impulse formation depolarizations arise during or after a normally evoked action can also be the result of afterdepolarizations (Figure 14–5). These can potential. They are therefore often referred to as “triggered” automaticity; be either early afterdepolarizations (EADs), which occur during that is, they require a normal action potential for their initiation.