Health and medicine
Find out exactly how your autonomic nervous system has a chronotropic effect (i.e. timing) that changes the delay between the contraction of the atria and the ventricles! Rishi is a pediatric infectious disease physician and works at Khan Academy. Created by Rishi Desai.
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- i love these videos. do you have any made for the Bowditch/Treppe staircase? i'm not really getting that and you are AWESOME at explaining.(10 votes)
- No, unfortunately there are no videos on this site for that topic. I'm sure YouTube has some good ones, though!(4 votes)
- isnt the downward part of the AV node's action potential supposed to be 3? I know you named it 3 in previous vids and 1 in others. please let me know. You guys are doing something magical with khan academy!!(7 votes)
- Is this effect not called dromotropic effect?(4 votes)
- Dromotropes are agents that affect the conduction speed of the AV node, while chromotopes are those that change heart rate. While dromotropes are often also chormotropes; however this is not always the case.(4 votes)
- At5:37, Dr. Rishi says "neurotransmitter" but drew an axon terminal. Did Dr. Rishi mean "axon terminal" instead of "neurotransmitter"?(3 votes)
- No, he said neurotransmitter because the axon terminals send neurotransmitters, which are norepinephrine and acetylcholine in this video, to communicate with the other cell.
You could watch this video, https://www.khanacademy.org/science/health-and-medicine/human-anatomy-and-physiology/nervous-system-introduction/v/neuronal-synapses-chemical, at8:53to learn more about how the neuron communicate with other cells with neurotransmitters.(4 votes)
- Which phase/s of the action potential here for the specialized cardiomyocytes in the AV node is responsible for the PR interval and the delay in conduction?(3 votes)
- It would be phase 0 and and about half way down the slope of phase 1. Once the action potential for the AV pacemaker cell has reached the apex, the Purkinje cells are going to have their action potential almost immediately. The ventricular cardiac myocytes will then contract.
You can see a good image here: http://tmedweb.tulane.edu/pharmwiki/lib/exe/fetch.php/apd_ecg.png?w=600&tok=9d495d(3 votes)
- So why in these videos do you guys skip phases 1 and 2? I'm just curious because I feel that only showing three of the phases can be misleading in terms of studying.(2 votes)
- The reason that only phase 4, 0 and 3 are shown in this video is because Dr. Desai is showing the action potential of the AV node and, for this type of a cell, phases 1 and 2 are missing. If you look at an action potential for a cardiac myocyte, you will see all 4 phases represented. To see all of the phases, look at11:30on the video "Action potentials in cardiac myocytes".(3 votes)
So I'm going to draw for you a quick figure to show you exactly what happens with the AV node. So this is our AV node over time, right? And we've got zero millivolts here-- positive and negative. And you know the AV node is actually going to look really similar to what the SA node looks like. But there are a couple of key differences. As I draw them, I'm going to highlight them. So one is that there's a shallow increase. So this is of course the first phase. This is phase 4. And it increases very, very kind of subtly, and then it finally gets to that threshold, right? So it finally reaches this threshold point where the voltage-gated calcium channels flip open, and it rises again. But it's kind of shallow once again. And it gets up to this point and then goes back down. And so that's your phase 0 right here and your phase 1. So what are the differences exactly? Well, one difference is that there's a shallow phase 4. And why is it so shallow? What's the reason behind that? Well, remember that the AV node has a heart rate that it would like to set, and it's relatively on the low side. It's somewhere between 40 and 60. So compared to the SA node, it's a lower heart rate, which means it's going to be a longer heartbeat. So the fact that it's a shallow phase 4 kind of alludes to the fact that the AV node likes to keep a low heart rate. I'll write down arrow. But I want to also point out that usually, under normal circumstances, this doesn't really matter a whole lot because the SA node is in charge of the heart rate. And so even though it's a low heart rate, we don't really care about this phase 4 usually because the SA node is in charge. So unless the SA node is out on a holiday or something, this doesn't matter so much because the SA node is in charge. So that means that we can kind of draw our attention to the other two parts, right? Because that means phase 0 and phase 1 still matter. And there's one key difference there that I want to point out, and that is that you also have kind of a shallow phase 0. So think about that. If the phase 0 is shallow and we know this is the action potential, right-- this is the action potential-- well, what implications does that have? What does that mean? Well, the slope of the action potential-- and this is actually kind of an interesting idea to get your head around-- the slope of the action potential is going to affect conduction velocity. Because really that's where the ions are kind of leaking into the neighbor cells. So if this was really, really steep, you'd have a fast conduction velocity. And if it's shallow, like this one is, you have a kind of low conduction velocity. So the effect of this is going to be a low conduction velocity, meaning that ions are taking kind of a while to get over to neighboring cells and trigger their action potentials. So going from cell, to cell, to cell, it's going to be kind of sluggish through that AV node. And now you might be thinking, well, wait a second. We've talked about this in a way before because this sluggishness, this decreased conduction velocity, this is the explanation, we think, for the delay. So you remember in the AV node, you have a delay. And usually it's about 0.1 seconds. And this is the reason why. Because this phase 0 is going up so sluggishly, so slowly, that it actually creates a delay between the atria and the ventricles. A delay that-- it might seem initially that it's kind of a waste of time, but really it matters because you want to create that delay so the ventricles don't squeeze too early. So this is how you create that delay. You have that shallow phase 0. So now, let me actually make a little space. And I'm going to ask you to think about something from the cell's perspective. So imagine now you have a cell-- I'm going to draw it out for you. And this is our cell right here. And our cell is kind of doing its own thing and letting-- we're going to actually look at phase 0. Actually, let me write that here. This is going to be phase 0. So in phase 0, what's happening? Well, our cell has these voltage-gated calcium channels. And that's actually really important. So we talk about calcium channels, and sometimes I haven't done a great job of kind of clarifying voltage-gated versus non-voltage-gated. But remember in phase 4, those calcium ions are coming through kind of normal channels. But these ones are voltage-gated, meaning they kind of quickly flip on, but then they also quickly flip off. And so these voltage-gated calcium channels are going to let calcium in during phase 0. So calcium is going to kind of flood inside the cell. And that's the reason that you're getting that rise in the membrane potential, right? It's rising up, up, up. And so the calcium's coming in. And these cells, interestingly, have little receptors on them. You might be kind of now guessing where this is all going to go. These receptors are for a neurotransmitter that's coming from the sympathetic nerve. So sympathetic nerves are actually coming down and landing on the AV node just as they did on the SA node, right? So they're kind of landing here, and they're letting off their norepinephrine. Their norepinephrine is coming in here. And on the other side, you have receptors as well. So you've got little receptors on this side as well. And there are also nerves here. And as I said before, I'm drawing it kind of as two different sides of the cell, but you know that's just the way I'm drawing it. It has nothing to do with the reality of it. It's not like the cell actually organizes one side to be for the sympathetics and the other side to be for the parasympathetics. But that's definitely how my mind kind of sees it just because I guess I'm adversarial. And you have a little signal coming in from the parasympathetic nerve on this side, and a competitive signal coming in on this side. And actually let me just make sure I'm super clear here. This neurotransmitter is acetylcholine. And so the sympathetic nerve is telling this cell to allow more calcium to come in quickly. And the parasympathetic nerve is basically putting on the brakes and saying, no, don't let calcium come in quite so fast. So these two are competing back and forth. Let me make a little bit of space here. So going back up to our picture, I'm going to ignore phase 4 because we know, again, the heart rate is really going to be dominated by the SA node. So we don't have to worry about phase 4 so much because, really, the interesting bit begins there. So if the sympathetics won out, then you'd have a rise that would go pretty quick like that, and then it would fall like that, OK? And if the parasympathetics won, it would actually be the opposite, right? It would rise more slowly because less calcium is coming in over a given period of time. And then it's going to go down like that. So really what we're looking at is the slope going up or is the slope going down depending on whether the sympathetics or parasympathetics are in charge. And now if I said that the slope is related to the conduction velocity, if we-- do you remember we said that earlier? The conduction velocity is going to be affected by the slope of the line. Well, then basically what you're going to be doing is changing the amount of delay. So now let me actually play this out, and you'll see how cool this gets in just a moment. And let's make a little bit of space on our canvas. So here we go. If we have now three scenarios, OK-- we're going to do a baseline scenario. And we're going to do two scenarios with one sympathetics in control and one with parasympathetics in control. And I'm going to show you kind of the number of heartbeats you get. So at baseline, let's say you have, I don't know, let's say four heartbeats. And this would be-- let's say these little white arrows represent atrial systole. So this is when the atria are contracting-- atrial systole. And let's say in another color, let me do blue, this represents ventricular systole. So this is when the ventricles are contracting. So that will be ventricular systole. Ventricular systole-- when the ventricles contract. And we know that's going to happen about a tenth of a second later usually. So this delay is usually about 0.1 seconds. So if I was to kind of watch this over time I'd have, of course, another ventricle systole there, another one right there, and a fourth one right there. Now, if sympathetics are kind of driving this cell-- let's say actually I'm running, right? So this is a scenario where I'm running. And I'm being chased or maybe I'm chasing someone. And over the same time frame, what would happen? Well, I'll have, in this case, I'll have more atrial systoles, right? Because my SA node is going to fire more frequently. The heart rate's going to go up. So I'm going to have, instead of just four, maybe I'll have-- I don't know, I'm going to have to see I guess. I'll have maybe-- looks like six, six heartbeats. And that's because the big difference is SA node affects heart rate. And if I was to draw in now my ventricles, I would draw something like this. And you see these ventricular systoles are happening right after the atrial systoles, which is actually really interesting because this points out that I have kind of a smaller delay. Maybe my delay is, I don't know, maybe 0.08 seconds-- slightly less than 0.1 second. So now parasympathetics, you have basically the opposite problem or the opposite change. I shouldn't call it a problem. It's not really a problem, right? You'd have, let's say, three heartbeats in the span of time we're following. And if you were to see the ventricles they contract, but they contract with a much longer delay. So if you were to kind of measure out this delay, instead of 0.1 seconds, now this is let's say 0.1 or maybe 0.2 seconds. Maybe it's double. So you can see that the SA node had a change in heart rate, and the AV node, because of this sympathetic or parasympathetic drive, had a change in delay. So these are the two kind of big changes that you see when sympathetic and parasympathetic nerves are acting on the SA node and AV node.