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0:08
What s up, Taim talks med here. I ve now simplified all the most important high yield topics in heart physiology, so this is the Complete Cheat Code
0:18
We re doing this in 4 segments. This is the 1st video where we re going talk detailed about the different types of cardiac muscle, the action potentials of pace maker cells and contractile myocardium, and the general properties of our cardiomyocytes. The 2nd video will be about the cardiac cycle. The 3rd video we ll cover everything you need to know regarding the cardiac output. And in the 4th video we ll cover the regulation of the Heartbeat, covering all the
0:42
most important mechanisms that actually change the contractility and heart rate. Alright awesome. Alright, so I m starting this video assuming that you have some pre knowledge in the anatomy of the heart. I m basically assuming that you already know that the heart has 4 chambers, you know that the heart has 3 layers, endocardium, myocardium and the epicardium. I m basically assuming that
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you know that the heart is an organ in your chest. If you know that, you re good. Let s continue. Now the topic about heart muscle falls under electrophysiology, this is an extremely important topic and the reason why is because the heart is so special, it has the Intrinsic ability to spontaneously depolarize itself and cause the heart muscle to contract, it doesn t really depend upon the nervous system. We ll cover in the 4th video how the nervous system like the extrinsic
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innervation of the heart can speed up the heart rate or decrease the heart rate, as well as maybe increase the contractility. But again, I want you to understand something about the heart is that the heart exhibit something called automaticity. So it s able to depolarize itself continuously without external stimulation. How is it able to do that. Follow along, and I ll ask you that question again at the end of this video so you can answer it without any hesitation.
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In theory, we can classify cardiomyocytes into three primary functional categories based on their general roles in cardiac physiology. So in this area we can divide the muscle cells into three functional categories. First one being Pacemaker cells, we got contractile cells, and last one, many don t consider it as a classification on it s own, but the heart also exhibit some endocrine function as well. These are the three main muscle cells with
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their own primary function within the heart. Now, pacemaker cells. Pacemaker cells are cells located within the conductive system of the heart. So we can also call them nodal cells, or non contractile cells. These are the ones that generate automaticity. These are the ones that can spontaneously depolarize, generate action potentials. Alright now, where can you find these pacemaker cells? If you look here, the main node that makes up
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our normal rhythm is found at the superiorlateral border of the right atrium, called the SA node, just beneath the superior vena cava. The SA node is the main pacemaker - it sets the pace. When it generate impulses, it ll send impulses towards the left atrium through the interatrial bundle, aka bachmann's bundle. And it ll send impulses down through the internodal pathway towards the AV node. These pathways are just fast conducting pathways so the signals reach
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the contractile myocardium faster. Now the AV node is really interesting, because look where it s located. It s located at the junction between the atria and the ventricles, just behind the tricuspid valve, at the beginning of the interventricular septum. So it acts as a gateway for the impulses passing from the atria to the ventricles. After the AV node impulses are then sent down the ventricular septum as the bundle of HIS,
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which continues on as the Right Bundle Branch and the Left Bundle Branch. Then from there, the impulses are further conducted towards these breaking units called Purkinje Fibers. Now, these pacemaker cells are all special in their own way. The SA node primarily consists of pacemaker cells that are specialized for generating spontaneous action potentials. They have fewer contractile fibers and more ion channels, so we say it s the natural and primary
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pacemaker, which generates sinus rhythm of around 60-80 beats per minute. Sometimes if the SA node is damaged or if the electrical conduction system of the heart has problems then the secondary pacemaker which is the AV node sets the pace. If the AV node takes over it usually generates a slower HR at around 40-60 beats per minute. If the pacemaker cells in the AV node fails, there are theoretically some pacemaker cells within the av bundle, or the bundle of his aswell, denoted
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as tertirary pacemakers. Purkinje fibers, again, their job is to conduct the impulses towards the ventricular contractile myocardium to initiate contraction in a specific set of time. Now. When the SA node generates action potential, the electrical impulse travel throughout the conductive system to have the heart contract in a controlled manner, so that the blood fillings in the atria and ventricles work in a harmony. And this can only work if the
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velocity of the impulse conduction differ based upon the location of the cardiomyocytes. Within the conductive system, specifically in the atria, the transmission speed is about 1 meter/second. So almost immediately after the SA-node generates an impulse, it s transmitted to all atrial pacemaker cells. When the impulse reaches the AV-node, it slows down to about 0.1 meter/second, which is literally the lowest speed of impulse transmission
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throughout the heart. Now what s the significance of this? Because it has significance. One of the significance allowing for the AV node to delay the impulse before it sends the impulse down through the interventricular septum to the bundle of HIS, is because it wants to give time for Atria to contract, before the ventricles contract. I can t express how important this is. Because of this
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delay, it gives the atria enough adequate time to contract and push the blood into the ventricles. Because if the AV node didn t conduct the impulse slower, it would ve depolarized the myocardium in the ventricles while the atria are trying to empty their blood into the ventricle. If that s the case then as the ventricles are getting depolarized they might start contracting at the same time as the atria are contracting. That s counterintuitive. We don t want that. We want to
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allow for the atria to squeeze all the blood into the ventricles, then let the ventricles attain the blood then push it out towards the aorta and the pulmonary circulation. Now why is the conduction slower here? We know the purpose, it gives time for the atria to contract before the ventricles contract, but there s two microscopic reasons why. These nodal cells are riddled with a tons of gap
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junctions, which are basically channels which allow ions to pass from cell to cell. However, the AV node, which consist of a bundle for those nodal cells, it has a lot less of these gap junctions than these other nodal cells. So a lot less gap junctions, which means a lot less ions can flow from cell to cell that decreases the actual speed at which it s moving. So we say because of this, there s a greater resistance to conduction of excitatory
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ions from one conducting fiber to the next. That s one reason. That s why it s a little bit slower. Another one is because the nodal cells are in the AV junction are smaller, they have lower diameter. And if you know a little bit about conduction, we know that the larger diameter of the structure the faster the velocity of that conduction is gonna move. So the smaller the diameter, the slower the conduction speed. Okay. So again the transmission speed in the
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atria is about 1 m/s, it reaches the AV node, slows down to 0.1 m/s, then when the impulses finally reach the ventricles, the speed of conduction varies between 1-4 meters/seconds. It s so fast almost instantly all the contractile myocardium will contract at the same time. Now. Keeping this in mind. The working myocardium also has gap junctions, which means when they re depolarized, they can conduct the impulse in a speed of around 0.3-0.5 meters/second.
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So in case the conductive system is damage as a result of an infarction or a surgical error, then the working myocardial cells can transmit the impulses aswell, but in a slower rate, which can be problematic because some cells then after the damage will contract meanwhile the cells before the damage are already starting to relax. And here you see how this plays out in fractions of a second after initial depolarization at the SA-node, showing how many seconds
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it takes before the different parts in the heart receives that signal. There are just two things I wanna highlight here before we go further and talk about the other cardiomyocytes. Notice the delay in seconds between the atria and the ventricles. And I wanna ask you again, why is there a delay here? Because of the slow conduction at the AV node. The other thing I wanna mention here, and this is so important to know. Is that the AV bundle,
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has a special characteristic in that it can only do a one-way conduction, allowing only forward conduction from the atria to the ventricles. This prevents something called re-entry of cardiac impulses, meaning it prevents the impulses from going from the ventricles back into the atria. So, I wanna ask you now, why can t the impulses just travel from the atria down to the ventricles from the right side or the left side? Why does it have to go through the AV node and the AV bundle?
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This is because everywhere, except at the A-V bundle, the atrial muscle is separated from the ventricular muscle by a continuous fibrous barrier, as you see here. This barrier normally acts as an insulator to prevent passage of the cardiac impulse between atrial and ventricular muscle through any other route besides forward conduction through the A-V bundle itself. So when you start studying impulse diseases In the heart, you can come across an instance where
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there s an abnormal muscle bridge that penetrate the fibrous barrier elsewhere besides at the A-V bundle. If that that happens, what do you think is going to happen now? The cardiac impulse can re-enter the atria from the ventricles and cause a serious cardiac arrhythmia. Alright. That s the pacemaker cells, the second type of cells are the endocrine cardiomyocytes. These endocrine cells in the heart are located both in the atria and in the ventricles. These
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special cells contain secretory granules filled with hormones that are secreted out in response to stretch of the cardiomyocytes due to increase blood volume. They are the Atrial Natriuretic Peptide primarily from the atria, and B-type Natriuretic Peptide, secreted primarily from the ventricular cardiomyocytes. And since they re secreted in response to stretch, their primary function is to try to decrease the blood volume by decreasing sodium and
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water reabsorption from the kidneys, and promote vasodilation. We ll talk about these in a little more detailed in the last video where we cover the different ways the heart pumping is regulated. The third type of cardiomyocytes are the contractile cells. So these are the ones that consist of actual contractile proteins. So they consist of actin, and myosin and troponin and tropomyosin. They re also special because they contain something called Sarcoplasmic Reticulum.
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Now these contractile cardiomyocytes are arranged in a specific manner, and they have arms extending to the neigboring cell connected through something called intercalated discs, which is essentially made up of gap junctions and desmosomes, making it easier for signals to pass on to the next cell. And because the cardiomyocytes have these gap junctions, we say that the cardiomyocytes work as a functional syncytium, which basically means that it consists of a group of cells
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that function as a single unit while still maintaining their individual cellular role. Alright, now. Let s take one pacemaker cell, and one contractile cell, and draw an outline of each cell just like this. So we re looking at two different types of cells, a nodal cell and a contractile cell, and we re gonna see how these two cells are communicating and what s all these ion channels and stuff. And so let s draw a gap junction between these cells.
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And we ll use these two graphs to illustrate the voltage change and phases of each functional cell. There s a lot of graphs when it comes to cardiac physiology. But they make so much sense once you actually understand what happens at each phase. In each graph I ve denoted one line with longer dots and one with shorter dots. The one with longer dots means resting membrane potential, which essentially means each cell don t normally go below this level in respect to voltage change.
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And the shorter dotted lines represent threshold potential. Means when the voltage inside the cell reaches the voltage of threshold potential, it s gonna activate a certain function. Now, pacemaker cells don t really have a stable resting membrane potential. They re never really at rest, if that makes sense. It s kinda funny. It s funny, the pacemaker cells has funny sodium channels. I m not even kidding. I ve no idea why they re called funny sodium channels. But these
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channels, that are within the wall of the nodal cells, are very leaky. And they allow for a little bit of sodium to leak into the cell very very slowly. And because they re leaky, pacemaker cells don t really have any stable resting potential, so the lowest point at which the voltage can go to is around -60 mV before the voltage turns and starts to go towards the positive side again due to the slow sodium influx. When the membrane potential reaches around -55 mV,
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T-type Ca2+ channels starts to open and we now start getting calcium influx aswell. As these sodium and calcium ions starts coming into the cell look what happens. We start hitting the threshold potential. Now that we ve hit the threshold, the long lasting calcium channels opens up. These L-type calcium channels blasts open and we get a huge influx of calcium, depolarizing the cell up to around 30 mV. These voltage numbers can vary a little bit so you ll often see slight
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number differences in different sources. But now, what happens now? Now the cell is depolarized. We ve depolarized the cell. It didn t require any nervous system functioning. Isn t that beautiful? What happens now is that we ve accumulated all of these cations in the pacemaker cell. Once it s depolarized, it ll shoot these cations through the gap junctions into the next cell. Now the contractile cardiomyocyte is usually at rest at around -85 mV. So the resting membrane potential
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of the contractile myocardium is around -85 mV. When the cations flows in from the pacemaker cell, it starts to depolarize. It goes up and hits the threshold potential of right around -60mV.
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This threshold potential will now trigger the Voltage gated sodium channels to open up. While this is happening, if we now go back to the pacemaker cell. The L-type calcium channel will close, and potassium channels starts opening up, and we get an efflux of potassium which triggers repolarization. So potassium ions starts going out of the cell, which brings the membrane potential all the way back to -60 mV. Alright let s go back to our contractile
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myocardium. When the threshold potential reaches -60 mV, voltage gates sodium channel opens up, and we get a huge influx of sodium. So the membrane potential shoots up to about +40 mV. Again these numbers can vary a little bit, but the sodium influx will trigger a positive charge throughout the cell membrane, and when it reaches about +40 mV, potassium channels starts opening up, which brings potassium ions out from the cell. At the same time, these voltage gated
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sodium channels are now closing. So since we have potassium ions going out and no infux of sodium, the membrane potential of the working myocardium starts going down, or repolarize. Now, the contractile cells have something called T-tubules, which are packed with extracellular calcium. These T-tubules are equipped with something called dihydropyridine receptors, which are a form of l-type calcium channels. When they receive an impulse, these channels will open, and cause
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an influx of calcium. Now within the contractile cardiomyocyte, you ll find Sarcoplasmic Reticulum which contain a lot of calcium. The Sarcoplasmic Reticulum has something called Ryanodine Receptors on it. We say that there s a voltage gated coupling between the dihydropyridine receptor and the ryanodine receptor in that, when calcium flows in, it binds to the ryanodine receptor, activates it, and causes it to release a whole lot of calcium into the intracellular fluid.
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So two things happen when dihydropyridine receptors are activated. It causes influx of calcium necessary for contraction, and also necessary for activation of ryanodine receptors. Now we got a high amount of calcium ions in the cytoplasm. Now we wanna contract the cardiomyocyte. Inside of the cell, we got something called the troponin complex which is a complex of three regulatory proteins called troponin T, troponin I,
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and troponin C. Troponin T is a protein that binds to tropomyocin to help with the positioning. Troponin I is a protein that binds to actin, and because it s bound to actin, it prevents the myosin from binding to the actin in a relaxed state. Troponin C is a calcium sensitive protein that has four calcium-binding hands, and it also hold hands with Troponin I, so when troponin C is activated it changes the form of troponin I. Just remember TIC TAC for this one.
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So what happens is, when calcium binds to the troponin C, it causes it to change its form which lead to dislocation of troponin I. When that happens, tropomyosin leaves the binding site for myosin on actin leading to contraction of muscle, so the heart can squeeze the blood out to the systemic circulation. So the letter I in Troponin I is given due to its inhibitory character, and it s a really useful marker in the laboratory diagnosis of cardiac muscle damage.
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Now, while all of this is happening, the cells voltage Is neither going to increase nor decrease, because the rate at which calcium is flowing in is approximately the same as the rate of which potassium is flowing out. So all this happens during a plateau phase. Now we want to remove calcium from the intracellular space, because if it s there for a long time it s just going to keep binding and contracting the muscle
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cells. The heart will eventually become weak if it doesn t rest, so we need to get this Calcium into the Sarcoplasmic Rreticulum and out into the extracellular space. It does that with the help of calcium pumps. These calcium pumps are located in two places, in the cell membrane and in the wall of sarcoplasmic reticulum. Another name for them is SERCA, or sarcoplasmic reticulum Ca2+ ATPase,
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and PMCA, or Plasma Membrane Ca2+ ATPase. They re primarily going to use ATP to pump calcium into the Sarcoplasmic reticulum and out to the extracellular space. Now SERCA has a phospholamban attached to it, which is going to inhibit the pump. The SERCA pump is still somewhat active, but its efficiency is reduced due to the inhibitory effect of the unphosphorylated phospholamban. Only when the sympathetic nervous system gets activated, it ll phosphorylate and
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remove the phospholambans inhibition on SERCA and a lot more calcium will be pumped into SR, but that doesn t happen in basal conditions without sympatric stimulation. We ll talk about this in detail when we go through the regulation of heart pumping in a separate video. Alright. What else, how do we remove the calcium? In the wall of the myocardium, we ll find something called Sodium Calcium exchanger, which uses sodium gradient into the cell to transport
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calcium out of the cell. It s called secondary active transport, this mechanism, which depends on the sodium potassium pump activity. Now imagine if the sodium potassium pump keeps pumping sodium ions out of the cell, it ll decrease the concentration of sodium in the cytoplasm, the sodium can then easily be transported into the cell at the same time calcium is transported out. It s a really cool mechanism. And there re an abundance of
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these sodium calcium exchangers along the cell membrane, specially at the T-tubule area. Now, as calcium is going out, and potassium is keep getting pumped out, we ll now repolarize the cell all the way back to its resting membrane potential, which is around -85 mV. While all of this is happening, guess who s working? The funny sodium channels back here. And watch how the pacemaker cells don t have any resting membrane potential because of that. Also
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while the depolarization is happening, the contractile cardiomyocyte can send its impulses further to the next cell. So that s really it, that s how the heart is able to contract and relax without any external stimulation. Argiht, awesome. Now, let s take a closer look at these graphs, and divide these graphs into phases so that it makes so much more sense to understand them. The pacemaker cells can be divided into three phases.
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First one is the slow diastolic repolarization phase. Remember during the slow depolarization we got funny sodium channels pumping in sodium, as well as transient calcium channels pumping in calcium. Then we got a fast depolarization after the cell hits threshold potential, where the L type calcium channels open. When depolarization is done, we got repolarization, which pumps potassium out until it reaches around -60mV again, where the funny sodium channels starts working, and the
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cycle continues. For the contractile myocardium, we can divide it using numbers from 0-4. Phase 0 is depolarization, or rapid depolarization, which is due to the Na+ influx. So when an action potential arrives from a neighbouring cell, through gap junctions. The voltage within the cell increases slightly. When this increased voltage reaches the threshold potential of approximately ?60 mV, it causes the Na+ channels to open, and this produces a
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larger influx of sodium into the cell, rapidly increasing the voltage further to around +40 mV. All of this is happening in this phase. Phase 1 is the initial fast repolarization, where fast sodium channels close, and potassium ions opens. Now we re losing potassium, so we re only losing cations. Phase 2 is the plateau phase, where we re now getting calcium influx, which is electrically balanced with potassium efflux.
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So we re losing potassium and gaining calcium at a rate of which the electrical gradient is kept constant. And remember in this phase the cell is contracting. And after contraction, we want to further repolarize the cell, So phase 3 is the end fast repolarization, where L-type calcium channels are closed, and we get a further potassium efflux, as well as we re removing the calcium from the intracellular space back into the Sarcoplasmic
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reticulum and into the extracellular space. And now we re at phase 4, which is the resting membrane potential of approximately -85 mV as a result of the constant outward movement of potassium. So that s basically how we divide these graphs into phases. Now, the next thing I wanna talks about that is really important, is something we call refractory periods. Which basically just means a period of time when the contractile
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myocardium is unable to contract. So in the y axis 100% means that the cell is 100% able to respond to the next stimulus given, while 0% means it s not gonna respond to the next stimulus, no matter how much you try to stimulate it. Now, the excitability of contractile myocardium depends on the voltage gated sodium channels. And if you zoom in on a voltage gated sodium channel, you ll see that it has two gates. It has an extracellular activation gate which can open
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due to a simulation. And within the cell there s an inactivation gate which is not open by a stimulation, but it opens if the membrane potential becomes lower than -40 mV. Now, if we look at the phase with the resting membrane potential, the activation gate is closed, and the inactivated gate is open. Can we open this gate if we stimulate it? Absolutely. So in this stage we say the cell is 100% excitable. If we apply threshold or suprathreshold stimuli,
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the activation gate can respond to that stimulus, and open. Now, during the depolarization, both the activation and the inactivation gates are open so there s a sodium influx. If you stimulate this cell now at this stage, will the cell respond? Nope, it s already responding to the previous stimulus. So the cell is 0% excitable and because of that, we call this stage absolute refractory period. Now,
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once it s at the top. The inactivation gate is closed. It starts closing gradually once you get above -40 mV. And since we re still above -40 mV, the inactivation gate is closed, and the activation gate is still open. Can we excite this channel at this stage? Absolutely not. The inactivation gate doesn t respond to stimulus, so we re still on the absolute refractory period. When the membrane potential reaches about -40 mV, then the inactivation gate of the voltage gated
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channel starts opening, and the activation gate starts closing. And since it s starting to open, the gate becomes gradually excitable, going from 0% gradually up to 100% as the gate is opening. This phase is called Relative Refractory Period. So it can react to a stimulus at this point. After the relative refractory periode, we go back to having the inactivation gate open, and the activation gate closed, ready to receive another stimulus.
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The refractory periods make so much more sense when you understand the concept around these gates on the voltage gated sodium channels. Now, because the myocardium has these long lasting calcium channels which prolong the time of repolarization, the absolute refractory period in myocardium will last about 0.25-0.3 seconds in the ventricles, while in the atria it s half, approx. 0.15 seconds. Relative refractory phases are approximately half of the absolute
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refractory phase, so about 0.15 sec in ventricles, and 0.7 seconds in atria. Sometimes, and this is just pure theory, to characterize the excitability, we have a term called effective refractory period, which is basically the whole absolute refractory period, and also the beginning part of the relative refractory period. Because in the absolute refractory period you just cant generate an impulse here,
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it won t react at all. While in the beginning part, the cells are so low excitable that they just can t really respond to the impulse generated in the previous working myocardial cell. Alright awesome. Now let s do the lasts segment of this video. The cardiomyocytes have certain properties that s special. The first one is that the cardiomyocytes has the intrinsic ability to depolarize itself and cause a contraction. This is called automaticity.
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Now, why are the cells able to have this property? Because of the funny sodium channels. Awesome. Next, is that cardiomyocytes contract following the all or none law. Meaning if contraction happens, it s always maximal. If it doesn t happen then it doesn t happen at all. So for example in skeletal muscles if gradually give it stronger contraction, you ll see that the force of contraction follow the strength of stimuli, and the force will gradually increase until all the
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motor units have responded to the simuli. In the heart however, it won t respond to a subthreshold stimuli. But when it receives a threshold stimuli, it ll give a full contraction all the time. And remember this is primarily due to the electrical synapses between the cells which make the cells function as a syncytium. The third property for the cardiac muscles are the long refractory periods. Remembr we said earlier that the ARP is significantly longer than
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in other types of muscle, lasting around 0.25-0.3 seconds because of the plateau phase. I can t express how important this is for our heart. One good thing about it is that it prevents tetanus. Meaning, the long ARP ensures that cardiac muscle cells cannot be re-excited until the previous contraction is nearly complete. This prevents the possibility of something called tetanic contractions. What would happen if the heart could undergo tetanic
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contractions under normal conditions? It would prevent the heart chambers from filling with enough blood between the beats. This refractory period also help maintain a regular heart rhythm by preventing premature contractions, called extrasystoles and re-entrant arrhythmias. We ll talk more about that when we get to arrythmias, but this stability is essential for consistent and effective cardiac output. Let s visualize it just for a second. Here we
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see continuous stimulation with continuous depolarization and repolarization of the heart muscles. Within this area is the absolute refractory period, meaning if the heart would get an artificial stimulus within this period, nothing will happen, but if we give an artificial stimulus to the heart during the last 2/3 of the diastole, we can trigger additional systole called extrasystole, which is followed by a compensatory pause, which is longer than
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the pauses between regular heart contractions. And why is it longer? It s longer because the heart has now skipped one normal contraction because we received this signal during the refractory periode of the extrasystolic beat. Now the heart has to wait for the next normal stimulus to trigger the next normal contraction. This pause is so important because it allows the heart to fill up before it contracts again. Alright so that was everything I had for the
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cardiac muscles. We covered the different cell types, the action potentials of pace maker cells, the action potentials of contractile myocardium, as well as refractory periods and the different properties of cardiac muscles. The next video is going to be about the cardiac cycle. Thank you all for watching! If you found this information helpful and want a little extra practice on the cardiomyocytes, I've created a quick follow-up video with quizzes and questions.
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