By Pappano A.J., Wier W.G.
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The action potential is characterized by a large-amplitude, steep upstroke, which is produced by the activation of the fast Na+ channels. The effective refractory period begins at the upstroke of the action potential and persists until about midway through phase 3. Slow-response action potentials may be recorded from normal sinoatrial (SA) and atrioventricular (AV) nodal cells and from abnormal myocardial cells that have been partially depolarized. The action potential is characterized by a less negative resting potential, a smaller amplitude, and a less steep upstroke than is the fast-response action potential.
In atrial cells, therefore, the outward K+ current exceeds the inward Ca++ current early in the plateau, whereas the outward and inward currents remain equal for a much longer time in ventricular myocytes. Hence the plateau of the action potential is much less pronounced in atrial than in ventricular myocytes (Figure 2-16). The delayed rectifier K+ currents (IKr and IKs) are activated near the end of phase 0, but activation is very slow. Therefore these outward IK currents tend to increase gradually throughout the plateau.
The amplitudes and upstroke slopes gradually increase as action potentials are elicited later and later in the relative refractory period. The recovery of full excitability is much slower than for the fast response. Impulses that arrive early in the relative refractory period are conducted much more slowly than those that arrive late in that period. The lengthy refractory periods also lead to conduction blocks. Even when slow responses recur at a low repetition rate, the fiber may be able to conduct only a fraction of those impulses.