Cardiac Action Potentials

Non-nodal Cell Action Potentials

Non-nodal action potentials, sometimes referred to as "fast response" action potentials, are characteristic of atrial and ventricular myocytes, and the fast-conducting Purkinje system in the ventricles. These action potentials have a true resting potential, a fast depolarization phase, and a prolonged plateau phase as shown below to the right.

Phase 0:    Rapid depolarization
            - increased Na⁺ and decreased K⁺
            conductances

Phase 1:    Initial repolarization
            - decreased Na⁺ and increased K⁺
            conductances*

Phase 2:    Plateau phase
            - increased Ca⁺⁺ conductance

Phase 3:    Repolarization
            - increased K⁺ and decreased Ca⁺⁺ conductances

Phase 4:    Resting potential
            - increased K⁺ and decreased Na⁺ and decreased Ca⁺⁺ conductances

* Phase 1 transient repolarization is produced by an outward movement of K⁺ through special K⁺ channels.

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Because action potentials are determined by the movement of different ions (ion currents) into and out of the cell, changes in the membrane conductance to these ions alter action potentials. Antiarrhythmic drugs that affect the movement of these ions are used to alter cardiac action potentials in order to prevent or stop arrhythmias. In non-nodal tissue, sodium-channel blockers decrease the fast inward movement of Na⁺, thereby decreasing the slope of phase 0 and the magnitude of depolarization. The principle effect of this change is a reduction in conduction velocity.

These drugs also increase the effective refractory period (ERP) by delaying the reactivation of fast-sodium channels. Potassium-channel blockers delay phase 3 repolarization, thereby lengthening the action potential duration and ERP.

Nodal Cell Action Potentials

Nodal action potentials, sometimes referred to as "slow response" action potentials, are characteristic of action potentials found in the sinoatrial node and atrioventricular (AV) node. These action potentials display automaticity, or pacemaker activity, and therefore undergo spontaneous depolarization. Their depolarization phase is slower and they have a shorter action potential duration than non-nodal, fast response action potentials. Furthermore, they have no phase 1 or phase 2.

Phase 0:    Depolarization
            - increased Ca⁺⁺ and decreased K⁺ conductances

Phase 3:    Repolarization
            - increased K⁺ and decreased Ca⁺⁺ conductances

Phase 4:    Spontaneous depolarization
            "Funny" currents (I_f) through slow Na⁺ channels
            - increased Ca⁺⁺ and decreased K⁺ conductances

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Like fast-response action potentials, changes in the membrane conductance to calcium and potassium ions alter slow-response action potentials. Calcium-channel blockers reduce the slope of phase 4, thereby decreasing the rate of spontaneous depolarization, which reduces the rate of pacemaker firing. These drugs also decrease the slope of phase 0, which slows conduction velocity within the AV node. The AV nodal ERP is also lengthened by calcium-channel blockers. Potassium-channel blockers delay phase 3 repolarization, thereby lengthening the action potential duration and ERP.

Revised 09/07/06