 Hey there and welcome. In this video, we're going to break down this animation bit by bit to get a better grasp on the fundamental underlying electrophysiology. So here's a cardiac mysight and over here, we've got a graph registering the charge difference across its membrane. If the charge is more negative inside than outside the cell, there's a negative charge difference. We call this a negative trans membrane potential or TMP. Between contractions, the resting state of a cardiac mysight has a steady TMP of negative 90 millivolts. This is because the cell is mostly permeable to potassium in this state by leaky channels specific for this cation. Potassium's preferred TMP is negative 92 millivolts, so if the cell is mostly permeable to potassium, this is where the TMP will sit. We'll use these three bars to record the movement of ions through their specific transporters in the membrane. The top three are potassium, calcium and sodium. A waveform upward means influx and down means efflux. The first step toward generating a cardiac mysight action potential is flow into the cell of cations through gap junctions. This is the action potential from neighboring cells, which begins in the pacemaker cells of the atria. Movement in of cations makes the inside of the cell more positively charged relative to the outside of the cell. More cations inside means a less negative TMP over the first several milliseconds of the cycle. Negative 70 millivolts is the threshold for voltage-gated sodium channels to open up. As the concentration of sodium is much higher outside the cell, these rush in down their concentration gradient. Ions want equalized concentrations to change the gradient from this to a balance. These sodium channels are only capable of opening for a few milliseconds at a time, not long enough to equilibrate the levels of sodium inside and outside the cell. They have been open long enough, however, to manifest a change in the TMP from negative 70 to positive 20. This change from negative to positive is called depolarization. This rapid change to positive TMP activates our next phase, opening of voltage-gated potassium channels. These open and potassium moves out of the cell, down its concentration gradient, in an initial burst. This burst is seen as a downward notch in the action potential. Very shortly afterward, voltage-gated calcium channels open, and calcium moves into the cell, down its concentration gradient. Again, there's an initial rush, followed by a steady flow. And you can see here that these two processes are happening simultaneously. Potassium going out, calcium coming in. Cat ions in, make the TMP more positive. Cat ions out, making the TMP more negative. In other words, calcium wants to depolarize the cell, turn the TMP from negative to positive, and potassium wants to repolarize TMP from positive to negative. Their cross-purposes creates this plateau phase in the cardiac myocyte action potential. The calcium channels stay open for a little while, but as with the sodium channels, they stick to a time limit, after a short while they begin to close. This leaves only the potassium channels open, which allows potassium to achieve its goal of repolarizing the cell. Back we go, down to the cells resting TMP. The time between these action potentials depends on your heart rate, which is regulated by many different factors. Before too long, another action potential will arrive from a neighboring cell, and the process will repeat. Let's watch that happen for a few cycles. One final thing worth mentioning is the numbers given to each phase of the cardiac myocyte action potential. Each major vector has a number, from 0 to 1, 2, 3, and then 4, the resting phase. As always, thanks for watching, and we'll see you next time.