Functions of Sodium and Potassium in the Heart
The cardiac action potential refers to a momentary change in the voltage of cell membranes found in the heart as a result of the movement of ions outside and inside the cells through ion channels such as calcium, potassium and sodium. Potassium channels in the heart are responsible for making the voltage to become more negative (repolarization) while the sodium channels make the voltage more positive (depolarization). The sequence of upward and downward movement of both sodium and potassium ions takes place in fives phases.
Phase 0 is where depolarization occurs, and positive changes take place transversely through cell membranes. The whole process lasts for 20 minutes in the sinoatrial node cells (SAN) and 2 minutes in the ventricular cells (Rudy, 2008, p. 113). Sodium-ion channels are activated in the ventricular cells, causing an increase in the cell voltage. An increase in voltage up to a threshold potential of -70mV leads to the opening of sodium ion channels which further causes a large influx of sodium into the cell increasing the voltage to +50mV resulting to cell depolarization. In SAN cells, the activation of L-type calcium channels causes an increase in cell voltage leading to subsequent depolarization in SAN cells.
Deactivation of sodium ion channels begins at phase 1 where their movements are restricted into the cells. The potassium channels block sodium channels using its two components, such as the gate and the filter. At this stage, the filter blocks the passage of sodium ions and allows only the movement of potassium ions. The gate opens and closely swiftly allowing a flow of potassium ions out of the cells making the ventricular membrane to become negative through repolarization (Sherwood, 2012). The membrane begins to repolarize at phase 2 due to a balance of charge caused by the inward and outward movement of sodium and potassium channels. Potassium channels facilitate the flow of potassium out of the cell while the L-Type calcium channels, which was activated at phase 0, allows calcium ions to move into the cell. Movement of calcium ions into the cell acts as an opposing force to changes made by potassium ion, causing the cell to remain moderately constant due to depolarization and repolarization.
Rapid repolarization takes place at phase 3 due to the closure of L-Type calcium ion channels. Potassium ion channels remain open, causing an increase in potassium ion movement into the cell and a subsequent increase in outward positive current of the cell. Potassium ion eliminates sodium and calcium ions and restores the membrane potential through cell repolarization (Soares et al., 2015). Potassium ion channels remain open until the next action potential is triggered by either calcium or sodium ion channels. Action in phase 4 takes place when the ventricular cell is at rest. The cell voltage is constant at this stage due to a balance between the intracellular and extracellular ions. At this stage, the membrane is permeable to potassium ion whose movement is allowed in and out of the cell through leaked channels. In contrast, other ions are blocked by activity pumps such as sodium-calcium exchanger and sodium-potassium pump (Crichton, 2008, p. 162). It is also a stage where the membrane potential gradually becomes positive until it gets depolarized by an action potential originating from adjacent cells.
Alteration of the controlled flow and movement of potassium and sodium ions in the cell can predispose the patient to cardiac arrhythmia. It is a disease caused by the uncontrolled rate of heartbeat, making the heart rate to be too slow, too fast or a combination of fast and slow. The irregular heartbeat may also predispose patients to heart failure or stroke, and in extreme cases, it can lead to sudden death, also known as sudden arrhythmic death syndrome (SADS).