The cardiac action potential differs from the action potentials present in other body sections. It is a brief change in membrane potential across the cells of the heart, caused by movement of charged atoms that are so-called ions, in and outside the cell via proteins referred to as ion channels (C.A.P, 2017). The action potentials that are in other electrically excitable cells like nerves differ from cardiac action potential in that action potentials vary within the heart because different cells have different ion channels.
For a case in point, as Theeplab.com (2017) states, nervous and the non-peace maker cardiac cells that are called muscle cells depend on the opening of channels of Na in order to facilitate the depolarization phase, while the cardiac peace-maker cells depend on Ca ions in depolarization. In fact, ions transfer from the intracellular context to the extracellular context and vice versa, are what makes it possible for polarization and depolarization of peace-maker cells and the cardiac cells of the muscle. Through the cellular membrane, the ions get transferred, aiding in the maintenance of the different charges in and outside the cell.
The main forces that facilitate the transfer of ions across the membrane of the cells are chemical and electrical potential. Chemical potential causes downward movement of ion concentration gradient. On the other hand, electrical potential cause particles that are similarly charged to move away. Changes in voltage of every single cardiac cell are represented by the action potential because of their true resting potential, fast in depolarizing, and having prolonged plateau phase like shown in the figure below (Daily & Yin, 2017).
Phase 0 is the rapid depolarization where there are increased sodium ions and decreased potassium ions conductance. Phase 1 is the initial depolarization consisting of decreased ions of sodium and increased ions of potassium conductance. Phase 2 consists of plateau phase with increased Ca++ conductance (Petrosky et.al, 2013). Phase 3 indicates depolarization with increased ions of potassium and decreased Ca++ conductance. The last phase is the resting phase where there are increased ions of potassium, decreased ions of sodium, and decreased Ca++ conductance.
And so, since the movement of distinct ions in and out of the cells determines the actions potentials, the conductance of these ions is what alters the action potentials. Sodium channel blockers are used in non-nodal tissue in order to decrease the fast inward movement of ions of sodium, in turn decreasing the slope of phase 0 and the depolarization size (Rohr, 2004). The principal effect causing this change is referred to as conduction velocity. Like the action potentials, the article on Cardiac Action Potentials (2017) elucidates that, changes in conductance of membrane by potassium and calcium ions changes the slow response of action potentials, and in this case, calcium channel blockers are used to reduce the slope of phase 4, in turn decreasing the rate at which spontaneous depolarization reduces the rate of firing of the peacemaker. This kind of drugs when used, also decrease the slope of phase 0 that in turn alters the velocity of conduction that is within the AV node.
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