Hello, welcome to Bite Size Med. This video is on the cardiac action potential, and in part 1, we're going to look at the ventricular action potential. Action potentials are how excitable cells, like nerve and muscle cells, communicate. The action potentials of nerves and skeletal muscles look similar, but in cardiac muscles, they've got different phases. And there are two kinds.
One is in the muscles of the atria and the ventricles, where they've got this plateau. The length of this plateau would be shorter in the atria. The other is in the pacemaker of the heart, that's the sinoatrial node.
In this video, we're going to be looking at the parts of the ventricular action potential, and in part 2, we'll look at the sinoatrial node. To understand cardiac action potentials, you've got to know some basics about membrane potentials and about action potentials in neurons. I will leave links to videos I've got on that stuff in the description box below in case you need them.
But I am going to do a quick recap of some things that you'll need to know. The action potentials are brief changes in the membrane potential. At rest, that membrane potential is usually negative. When stimulated, ion channels open and different ions move between the environments inside the cell and outside. like sodium, potassium, and here in cardiac muscle, calcium as well.
When the channels open, the ions move along their electrochemical gradient. Since they carry a charge, when they move, they change the membrane potential. This is the action potential in a neuron. It has a negative resting membrane potential of around negative 70 millivolts.
When the membrane potential becomes less negative and more positive, that's depolarization. When it returns to the original negativity, that's repolarization. And if it becomes more negative than that, it's called hyperpolarization. In a neuron, these three phases are mainly caused by the movement of sodium and potassium.
When the membrane potential reaches threshold from a stimulus, the sodium channels open and sodium enters the cell, causing depolarization. they get inactivated very quickly, so the membrane potential starts becoming more negative again. Also, by the time the action potential reaches a peak, the potassium channels open. The gradient for potassium directs it out of the cell, so potassium leaving the cell would bring the membrane potential back towards the resting membrane potential.
This is repolarization. These channels are slow to close, so the potential becomes more negative than that. that's hyperpolarization.
Then the channels close and it comes back to rest again. That's a neuron's action potential. Now let's see how things are different in the cells of cardiac muscle. Already you can see it looks different. There's an upstroke and a downstroke but in between there's a notch and a plateau so the duration of the action potential is obviously longer.
In cardiac muscle the resting membrane potential is a little more negative than a neuron, at around negative 90mV. The upstroke means the potential is becoming less negative and more positive. That's depolarization. The slight dip after is repolarization. But then there's a sustained period of depolarization.
That creates the plateau. Finally, there's repolarization back to the resting membrane potential. The upstroke is phase 0. The little notch that's repolarization is phase 1. The plateau is phase 2. The late repolarization is phase 3. And phase 4 is rest.
Those are the five phases of a cardiac action potential. Now let's see how they happen. There are three important ions, sodium, potassium, and calcium. They use different channels during the action potential. The sodium channels are called fast channels because they open and close quickly.
The calcium channels are the slow L-type calcium channels. When the channels open, the gradient is such that sodium and calcium enter the cell from the extracellular fluid to the intracellular fluid. The third ion is potassium, and it uses different channels at different points in the curve, but to simplify it, let's just look at the direction of current. sets the direction in which potassium moves.
Potassium's gradient is such that it leaves the cell during the action potential. The depolarization is from the opening of sodium channels. Sodium enters the cell, making the inside less negative and more positive, so the upstroke, up to around positive 20 millivolts. There's also a contribution from calcium through the calcium channels towards the end of the upstroke. The sodium channels get inactivated quickly, so the potential starts falling.
as potassium now starts leaving the cell. A positive ion leaving makes the membrane potential more negative. That is phase 1, the notch, the initial repolarization. But calcium ions are entering the cell while potassium ions are leaving. These two currents balance each other resulting in sustained depolarization creating the plateau.
That's phase 2. The calcium channels are slow to open and slow to close. So at the end of the plateau, the calcium channels close. Potassium leaving the cell causes the potential to become more negative again.
Repolarization. That's phase three. And then the membrane potential reaches its resting value again. That's phase four.
So those are the five phases of the action potential. Now just like neuronal action potentials, cardiac action potentials also have a refractory period. That's a time period where a second stimulus if given cannot elicit another action potential. This usually extends the duration of the action potential itself. There is an absolute and a relative refractory period.
The absolute refractory period is for most of the duration of the action potential until a portion of the final repolarization is complete. This is when a second stimulus, no matter how strong it is, can't initiate another action potential because the sodium channels are inactivated. From this point until when the cell is almost completely polarized again is the relative refractory period, where a second stimulus, if stronger than usual, may elicit another action potential.
So this would be an action potential in a contractile cell of the heart. Its job is to make the cardiac muscle cells contract. During the plateau phase, there's a calcium influx that happens. This entry of calcium stimulates a receptor on the surface of the sarcoplasmic reticulum, which is a calcium storage center inside the cell. This is a calcium release channel, which now lets calcium exit the sarcoplasmic reticulum and the intracellular calcium rises.
That's then going to result in the sliding of thin filaments over thick filaments, making the muscle contract. And that process is excitation-contraction coupling. These action potentials spread between the cells through gap junctions, ensuring that all the cells of the atria contract together and all the cells of the ventricles contract together.
But like I said this was in contractile cells. Conducting cells like in the sinoatrial node, have something a little different. And we'll look at that in part two.
I hope this video was helpful. If it was, you can give it a like and subscribe to my channel. Thanks for watching and I'll see you in the next one.