Action potential at the heart
The basis of electrical excitation of the heart is the so-called action potential. It represents the biologically temporally limited change of an electrical voltage across the cell membrane, which ends in a muscle action, in this case the heartbeat. With a duration of about 200 to 400 milliseconds depending on the respective heart rate, i.e. the number of heartbeats per minute, the action potential at the heart is longer than that of a skeletal muscle or nerve cell.
This protects the heart from overexcitation. Starting from a certain rest potential, a basic voltage of about minus 90 millivolts, which is applied to the membranes of the cells, the action potential at the heart goes through four phases of excitation formation. Different ion channels work together to change the electrical voltage on the outside of the cells.
These are mostly transport proteins that are located in the skin of the cells and transport different smallest charged particles across their membrane. This alters the electrical voltage on the cell and thus creates the action potential at the heart. In the first phase, the so-called depolarisation phase, the transport capacity for positively charged sodium particles increases.
These now flow into the interior of the cells and lead to an increase in voltage from about minus 90 millivolts to plus 30 millivolts. By shifting the electrical charge into the positive range, specific calcium channels in the heart are opened. This results in an influx of calcium particles into the heart cells.
This second phase represents the long plateau phase typical of the heart. Here the excitation is carried and prevents, among other things, the entry of additional superfluous action potentials. It ensures the controlled pumping performance of the heart and protects against cardiac arrhythmia.
In the third phase, the repolarization phase, the electrical voltage slowly returns towards the resting potential of minus 90 millivolts. Through an energy-consuming process, the inflowing sodium particles are actively transported out of the cell against the concentration gradient above the cell, and the outflowing potassium particles are transported back into the cell. This process continues until the original resting potential has settled down again. The cell is now ready for a new action potential.
Action potential at the sinus node
The excitation origin of the action potential at the heart is in the so-called sinus node. This is located in the right atrium of the heart near the junction of the superior vena cava, which transports the blood from the upper body circulation to the heart. The sinus node consists of modified muscle cells that generate the action potential necessary for excitation.
They thus form the natural pacemaker of our heart. These are rapidly excitable cells with a natural frequency of about 60 to 80 beats per minute. This natural frequency can be registered in the form of a pulse.
From there, the resulting action potential takes its course via certain anatomical structures to lead to a contraction, a heartbeat, in the working muscles of the heart. The number of beats per minute can be adapted to the load on the human body. The sympathetic nervous system, an autonomic nervous system that is activated primarily with increasing load, leads to an increase in the incoming action potential.
If the opposite, the so-called parasympathetic nervous system, is activated, which plays a role especially in resting phases of the body, the number of action potentials towards the heart is reduced. The heartbeat slows down. Drugs and the body’s own hormones, such as adrenaline, also influence this system.
