All about the Conduction System of the Heart, ECG, and the Cardiac Cycle. A very nice read.
Early repolarization occurs when the voltage-gated Na+ channels close and a small number of voltage-gated K+ channels open. Diffusion of Na+ into the cell stops, and there is some movement of K+ out of the cell. These changes in ion movement result in an early, but mall repolarization.
The plateau phase occurs as voltage-gated Ca2+ channels continue to open, and the diffusion of Ca2+ into the cell counteracts the potential change produced by the diffusion of K+ out of the cell. The plateau phase ends and final repolarization begins as the voltage-gated Ca2+ channels close, and many voltage-gated K+ channels open. Diffusion of Ca2+ into the cell decreases and diffusion of K+ out of the cell increases. These changes cause the membrane potential to return to its resting level.
Action potentials in cardiac muscle exhibit a refractory period, like that of action potentials in skeletal muscle and in neurons. The refractory period lasts about the same length of prolonged action potential in cardiac muscle. The prolonged action potential and refractory period allow cardiac muscle to contract and almost complete relaxation to take place before another action potential can be produced. Also, the long refractory period in cardiac muscle prevents titanic contractions from occurring, thus ensuring the rhythm of contraction and relaxation for cardiac muscle. Therefore, action potentials in cardiac muscle are different from those in skeletal muscle because of the plateau phase, which makes the action potential and it’s refractory period last longer.
The sinoatrial (SA) node, which functions as a pacemaker of the heart, is located in the superior walls of the right atrium and initiates the contraction of the heart. The SA node is the pacemaker because it produces action potentials at a faster rate than other areas of the heart. The action potentials of the SA node acts as a stimulus to adjacent areas of the heart. Also, the SA node action potentials have characteristics that are somewhat different from action potentials in the rest of the cardiac muscle. The SA node has a larger number of voltage-gated Ca2+ channels than other areas of the heart. As soon as the resting
membrane potential is reestablished after an action potential, some of the voltage-gated Ca2+ channels open spontaneously. As they open, Ca2+ begin to diffuse into the cell and cause depolarization. The depolarization stimulates additional voltage-gated Ca2+ channels to open and voltage-gated Na+ channels to open. Thus, additional Ca2+ and Na+ diffuse into the cell and cause further depolarization. Quickly, threshold is reached and another action potential is produced. Drugs called Ca2+ channel blocking agents are used to treat some types of tachycardia (rapid heart rate) and arrhythmia (abnormal rhythm) because they block Ca2+ channels and slows the rate of action potential production.