 There is one reason that we talk about the electrical activity of the heart. One, and it's so we can talk about the mechanical activity of the heart. The electrical activity initiates the mechanical activity. And really the mechanical activity is what is important. Why do we even need a heart? Dude, rip that thing out and throw it on the ground. Just kidding. Don't do it. Your heart is needed to pump all that blood through your body, and that's what's coming next. We're going to talk next about perfusion and exchange and how we can maintain blood pressure so that we can do exchange of goodies and nutrients at the cellular level. So your heart is kind of important, and its ability to pump blood is kind of important. All of this electrical stuff initiates the actual contraction. There are two terms that you need to be really comfortable with talking about what happens in our heart. And there are terms that should be familiar to you. Cystalline refers to contraction. So if we're going to talk about ventricular cystalline, we're going to talk about the events, the things that are going on when the ventricles are contracting. We also can talk about ventricular diastole. What happens when the ventricles relax? And at what stage does all this depolarization, repolarization stuff happen? You can imagine that the atria depolarizing, sending the electrical message through the myocardium of the atria, do you agree that that electrical message is going to initiate contraction or atrial cystalline? Repolarization of the atria, do you agree that that's going to be associated with atrial diastole, atrial relaxation? We're going to look at contraction and relaxation. We're going to look at the two characteristics that result from contraction, or that we can evaluate during contraction and relaxation. And those are pressure and volume. And we can talk about pressure and volume because we're talking about fluids here inside the heart. So let's go back to this picture, which is our lovely, what's that thing called? It's our lovely this thing. Oh, Crikey's, what did I just do? I want to get that out of there. Nobody knows what I'm doing right now. There, I just wanted that to go away. This is draft number two because that was a mistake. All right, so we've got our electrical activity that is ultimately going to stimulate the mechanical stuff that we're going to look at right now. We start at the point where everything is relaxed, and that is actually sort of arbitrary as all cycles. Like where are we going to begin evaluating the events in a cycle? You always have to start somewhere arbitrary because the whole thing goes in a circle. If at any point you're like, wait a second, what happened right before this? Stop and go back and look and see if you can figure out what happened right before this because all of it has this really lovely cause and effect. Like first this happens, then this happens. We're going to start with complete relaxation of your atria and your ventricles, and we're going to call it ventricular diastole and atrial diastole. So the whole thing should be relaxed at where we're going to begin this process or this conversation. During atrial and ventricular systole, I mean diastole when everything is relaxed, we're going to have this passive filling of both chambers. Now think about that for a second. Your chambers at one point they contract, yes, and push blood to various locations. When they relax, we're going to have, like the act of relaxing really does increase the volume of that space and we're going to make space for more blood if blood wants to come in or is available to come in. During atrial and ventricular diastole, blood passively enters the heart. And when I say passively, I mean nobody's pushing it in. There's a little bit of a push coming from the veins because blood is being returned to the heart and there's a little bit of pressure that's bringing that blood in. But the act of relaxation creates space for that blood, so it really is a pretty automatic thing that we end up with this filling. During diastole, guess what's going to happen? Dude, your awesome auto-rhythmic cells in the SA node are going to depolarize because of their pacemaker potential. Because of those leaky, funny channels, they're going to depolarize and eventually they're going to generate an action potential. That means that the whole atria, both sides, the atria will depolarize, which sends the message, hey guys, it's time to contract. The action potential is going to pass through those intercalated discs into contractile cells and atrial contraction or atrial systole is going to begin. Why did it begin? Because of the P wave. The auto-rhythmic cells depolarized, causing contraction of your atria. Now think through what you're going to imagine the atria are contracting. What's going to happen to the pressure inside the atria as they contract and make the volume smaller? Do you agree that pressure is going to increase in the atria during atrial systole? Totally. And the blood that's in the atria, where's it going to go? Super convenient. Dude, let's squish that blood into the ventricles. Do you agree with that? The ventricles, meanwhile, are relaxed. So we're in a position right now to literally squish as much blood as we possibly can as the atria contract. They're going to squish as much blood as possible into the ventricles. At the end of atrial systole, we've pushed in so much blood into the ventricles that we have a volume of blood in there that is known as end diastolic volume. And the end diastolic volume is the amount of blood in the ventricles. It's the volume of blood in the ventricles at the end of ventricular diastole. It's not at the end of atrial diastole. Atrial systole has pushed in as much blood as can fill. But think about that for a second. What if the ventricles were going through systole at the same time as the atria? Do you agree that the atria, well, look at the sizes and we can decide who's going to win. If the atria were contracting and the ventricles were contracting, we couldn't have a very large end diastolic volume. So it's super convenient to let the ventricles not start contracting yet as they fill with blood while the atria contract. The maximum amount of blood that they can hold is end diastolic volume. And then what happens? Dudes, we end up with the action potential passing through the AV node into the AV bundle down the bundle branches and up the brkinje fibers. And so the ventricles are starting to depolarize. What is that going to cause to happen? Dude, we're going to end up with ventricular systole. Ventricular systole happens and it takes a bit for the message to get through the ventricles, but then once we get through ventricles start contracting from the bottom up. And that has to do with the arrangement of those auto-rhythmic fibers. So they start contracting, do you agree with this? A couple of things happen when ventricular systole begins. First of all, the blood, if it has an option, dude, it's going to get out. It's like the walls are getting in here, like we're getting squished, pressures increasing. Let me out of here. They're going to, the blood is going to try to get back into the atria. It's going to try to flow backwards. Who stops that? The AV valves. The AV valves, I'm just going to say this now. We're going to talk about it again. But the AV valves, the act of the blood pushing against those AV valves creates a turbulence. And that turbulent sound is what you hear in the heart sounds. So that first sound you hear is the lub of the heartbeat. And it's actually the turbulence created when those AV valves are shutting to prevent, and they shut, not because they're like, okay guys, it's time for us to shut, ready go. They shut because the blood is pushing backwards and the valves have no choice. It's like the one-way door, they're headed out, but the act of heading out grabs those valves and snaps them shut and no more blood can get out. So for a brief moment, you actually have the AV valves closed because the pressure was increasing. And you also have the semi-lunar valves closed. And remember the semi-lunars are the ones that close off the ventricles to the big arteries that are going to take the blood somewhere else, either to the lungs or to the body. The semi-lunar valves, as pressure increases, the semi-lunar valves are like, we can't hold and outbursts the blood through the semi-lunar valves. The blood goes out through the semi-lunar valves and you have like the generation of the maximum force of contraction in your ventricles. As ventricular systole sort of finishes, you're going to end up, can you imagine, do you agree, that your ventricles are going to like squeeze out all the blood that they can possibly squeeze out. And what you end up with at that point is a volume known as end systolic volume. Do you agree that the end systolic volume is like at the end of ventricular systole, we squeeze out all the blood that's possible and the volume in the ventricles is really low. Ventricular systole happens, we repolarize our ventricles, which means our ventricles now go back into ventricular diastole. Do you agree at this point? If we're going to go back into ventricular diastole, what happens to the pressure in there? The pressure is going to decrease as everything kind of relaxes. We can allow more blood to come in. There's one thing that happens. This is actually going, if we relaxed, we pushed all that blood out, and it goes out the arteries, pulmonary artery or the aortic trunk. I mean the aortic, the ascending aorta, pulmonary trunk. Either way, it's going out some big old arteries. And when it relaxes again, do you agree that the blood is going to be like, dude, you were sending me this way, but I changed my mind, I want to go back? Who's going to keep it from going back? The semilunar valves. And it makes sense. The relaxation, the blood's going to try to come back. Semi-lunar valves are going to snap shut after a look, dog pound, you got to go forward. We've got other mechanisms in place to actually allow and promote. Yes, please do continue on, go forward. And we have that as the ventricles relax in diastole, the AV valves are going to open, and that's going to allow blood to continue filling from the ventricle or the atria, which also were already relaxed. And we're back to the beginning again. Did you follow all of that? What you should do before moving on, and I can't remember which direction I go, not that one, not that one. Maybe it's this one. Ah, this is the direction that I go. You should go back and look at this thing now. Now go back and look at this and see what you can piece out as a result of what you're seeing here. We're going to talk about heart sounds next, and then a couple more measurements, and then we're done. After this, everything is reviewed. You've got the electrical activities, and you've got the mechanical events that are initiated because of the electrical activities, and now we're just going to see, we're going to remind ourselves of what kinds of things are we going to expect to happen, and what kinds of things can we measure as a result of this.