>> Greetings. Today, we're going to talk about the heart and specifically we want to talk about the electrical activity within the heart. This is our first of the series of lectures on the Cardiovascular System. The heart Is divided, actually it's two pumps that are divided in series. We have a right heart which is getting blood from the, from the systemic circulation. It's coming into the right side of the heart, which then delivers the blood to the lung. And then the blood will return from the lung to the left side of the heart, which is then going to pump it out to the rest of the systemic circulation, this is a closed system, the heart is going to generate the pressured gradients and then the blood is going to be delivered through, through these different vessels and then return to the heart itself. On the right side and the left side we have two chambers, so we have the atrium And these are on the right and the left, and we have the ventricles. The atria are going to receive the blood and then the blood will move from the atria to the ventricles. And then from the ventricles, either to the lung or to the systemic circulation. In order to have the blood moving through the heart in a proper unidirectional manner, we are going to have to have specific control over the flow of the blood. And is, is going to be done by controlling the contraction of the muscle, which is the walls of the heart. This coordination of both the right and the left and of the atria to the ventricle to their contracted states, is going to be coordinated by an electrical system, and this electrical system is inherent to the heart itself. This is done by the pacemakers of the heart. So, within the right atria we have a pacemaker, which is called the SA node atrial node. This SA node atrial node fires rhythmically at a 60 to 100. 100 beats per minute. We have a second pacemaker which is located towards the septum which is dividing the atria and the ventricles and this is still located within the right atrium but near the septum. This atrialventricular node, or the AV node will have a pause in the electical signal and then it will release, it will fire off at about 40 to 60 beats per minute. There's also a, nodes which are present within the semptum that's dividing the two ventricle of both the right and the left heart. And, this, this, these pacemakers are called the Bundle of HIS and the Purkinje fibers. The Bundle of HIS is dir-, directly below the AV node and the Purkinje fibers then will take the electrical information. Both to the right and to the left ventricles. When these nodes fire, they are electrically coupled. This, the, the cells that are within the nodes are electrically coupled to contractile cardiac myocytes. And so, all of the contractile myocytes are going to depolarize to the beat of these, of these pacemakers. When the SA node fires, the atria then will undergo a depolarization. It will the, the conducting system will then fire off at the AV node, and the AV node then sends it's signal down through the septum, and the entire contractile fibers of the ventricles will then depolarize. The entire, the entire system takes about 400 milliseconds. From the firing of the a, SA node to the, to the end of the depolarization state of the ventricles. Then the ventricles are going to repolarize, and repolarization is going to occur in the opposite direction. So, we're going to repolarize from the In exterior of the walls of the ventricles and then from the, the apex of the heart, which is here, towards the base which is here, which is dividing the atria from the ventricles. So, repolarization is going to be in the opposite direction. The pacemaker action potential is called a slow action potential, and that's what's shown here. And as all, all pacemakers action potentials, it has an unsteady resting membrane potential. It starts at about a minus 55 milivolts, and then it slowly drifts toward threshold. And when it hit threshold at about a minus 35 milivolts, and there is a very sharp upswing, or a rapid depolarization. This rapid depolarization is due to the opening of the voltage gated calcium channels. We then have a closing of the calcium channels and opening of the potassium, voltage gated potassium channels which then allow us to repolarize the cells. As the cells repolarize, they then We'll come back then to a minus 55 millivolts. And again it starts to have a slow drift towards threshold. The slow drifts towards threshold is called Phase 4. The rapid upswing is called Phase 2. And the, and the, the repolarization of the cells is called Phase 3. Phase 4 has a very unusual, channel within it and that is called the sodium funny channel. This is a voltage gated channel which when it's open it will allow sodium to enter into the cells and some potassium to leave. The dominant, current, though, is carried by sodium entering into the cells. So the cells slowly repolarize. And are coming up to, depolarize. And are coming up to threshold. So these sodium funny channels, then, are opened in Phase 4. And we also have an opening of the calciu-, voltage gated calcium channels in Phase 4. What's unusual about the slow pacemaker potential is that it can be regulated. And this we all, you, you all are perfectly aware of and that is that your heart rate can change depending upon your daily activites. If youstart to run your heart rate is going to increaae. And that increase is going to be due to stimulation by the sympathetic nervous system. And through the beta-1 adrenergic receptors which are present on the heart. So if we look at how the beta adrenergic receptors are actually regulating the heart rate. We can we, that's what's shown in this particular figure. So the control is here. This is the green. And that's the same figure that we had seen previously. But in B, we now have added a, the norepinephrine or the stimulation through the beta-1 adrenergic receptors. If you notice the, that the cells are able to, to repolar-, depolarize much more rapidly in, after beta adrenergic receptor activation. And that they reach threshold at a much more rapid rate. Once they reach threshold, we again open the voltage gate. The calcium channels, this is an L type calcium channel. Just has we had, had before, and this is Phase 2. And then in Phase 3, we have the repolarization of the cells by opening the voltage gate or potassium channels and closing the voltage gated calcium channels. The difference in the slope In a phase four, with the beta adrenergic stimulation is that we have allowed some the sodi-, the, the cyclic AMP within the cells to rise. And that's in re-, in response to this, the stimulation by the ner-, by the sympathetic nervous sytem. This rise in cyclic AMP is actually affecting the opening of the sodium, the voltage gated sodium channel which is the funny channel so the channel is opening more rapidly and we are closing the voltage gated potassium channels more rapidly. That brings us then to threshold at, at a more rapid rate. Now the converse of this is that we have parasympathetic stimulation and the parasympathetics are through the muscle and its receptors. The muscarinicreceptors are going to actually slow the ability of the cells to reach threshold. And that's what's shown here in graph C. We two, two effects are a happening from the muscarinic receptor activation. One is, is that we're hyperpolarizing these cells. And that is, is that we're letting voltage gate potassium channels stay open longer. And so instead of stopping at a minus 55 millivolts it actually reaches minus 60 to 65 millivolts. So the sounds are now hyper-polarized, and then secondly that the sound, the opening of the sodium funny channel is slowed. And by having a slow rate for opening of that channel, we have a slow depolarization rate. And then we reach threshold, and once we reach threshold, again the action potential is set off and we open the voltage-gated calcium channels. And, and eventually, in phase two and then, in phase three we will open the Potassium channels and repolarize the cells. So, when we have a heart rate, normal heart rates are about 60 to 70 beats per minute, but if we have a heart rate that's greater than 100 beats per minute, which would be the same as if we had a high stimulation from the sympathetic nervous system, then this is called a tac- Tachycardia. And when we have a heart rate which is less than 50 beats per minute, then this is called bradycardia. So tachycardia is pretty easy to understand. We, we have tachycardia when we start running. We're going to increase our heart rates in order to be able to increase our cardiac output and to deliver oxygen and nutrients to this, to the working muscles quickly. When do we use bradycardia? So bradycardia, for instance an example of bradycardia is that there was an 18-year-old college student who showed up to have his wisdom teeth extracted at 8 o'clock in the morning. And the nurse comes in and she takes his heart rate and his heart rate is 55. And she then goes in to the oral surgeon and says this, this, this individual's heart rate is 55. Should I put him under. Anesthetics. And, and the anesthesia. And the oral surgeon comes out. He takes one look at the, at the young at the young man. And he, and he says so what team do you play for? And he says soccer. And the oral surgeon said, put him under. What is that? What it is, is that an athlete has a very high parasympathetic drive and that high parasympathetic drive actually moves their heart rate to the low 50, but this is not a pathological condition. This is from training. This is going to allow them, the athlete to have a much longer rise in heart rate as they are starting to exercise. This is actually an advantage to them when they are actually exercising and it is aerobic exercise that will increase the parasympathetic drive. So that's a perfectly normal individual. What would happen if we had a woman who's 80 years old and all of a sudden she, she, she has normally a heart rate that's 80. That all of a sudden her heart rate is 35. Is that normal? Now, something's happened to the pacemakers in her heart. And now, instead of having the heart rate driven by the SA node. She has her heart rate driven by the Purkinje's. Or the, or the, HIS bundle, in Purkinje system. So there are both pathological conditions that can give us bradycardia. And there's also normal conditions that can give us bradycardia within the. Within our system. Okay, but what about the entire heart. So when we, the individuals that are presenting themselves to medical doctors. And, the medical doctors want to find out whether or not the electrical system of the heart is working correctly. Those individuals can be tested and, they are tested by putting electrodes onto the surfaces of their body. And, then they record the signals, the electrical signals that are coming from the heart, the total heart This is called an electrocardiogram and these electrocardiograms what's de, designed here is what's shown here. So first we have the firing of the SA node and the, and the firing of the SA node on the electrocardiogram is too small to really detect. But then very rapidly we have a depolarization of the entire atria on both the right side and the left side of the heart. And do not occurs we can actually see the deflection, and this deflection now is going to be called a P wave. So we have a P wave which is showing the entire depolarization of the atrium. There's then a pause in the signals, and then the AV node will fire. And when the AV fires, there's a small deflection within the electrocardiogram. And then, veyr rapidly, we have a signal will pass down through the septum and the entire ventricle, then, will de-polarize. And under this condition. At this state we then have what's know as the QRS complex. So the QRS complex then reflects the entire depolarization of the ventricles and then following this we're going to have a period where we have repolarization, and the repolarization is shown here as a T wave So the electrocardiogram then can tell us how the electrical signal is moving from the nodes, across the atria and then into the AV node and then from the AV node through the ventricles and then whether or not we're repolarizing and what the time sequence is for these different events. So again the P wave is going to be our atrial depolarization and the QRS is going to be the ventricular depolarization and the T wave is going to be the ventricular repolarization. The isoelectric interval which is between S and T Is corresponds to phase two, of the fast action potential of the contractile cardiac myocyte. And as you recall, the Phase 2, is the time when we have, this is one. Two and three and this is four, Phase 2 is when we have calcium just entering into the cells, so during this period of time then when we have been calcium entering and this is going to trigger contraction of the, the ventricular cardiac myocytes, so its during this segment then that the cardiac myocytes contractions are going to be initiated. Heart rate will be between R and R. So heart rate is R and R. And the S-tTsegment then, this isoelectric segment is going correspond to Phase 2. And is also corresponding to the initiation of contraction. The intervals are telling us how long it takes to go from one node to the next node, or for, for the entire depolarization of the atria, and the entire depolarization of the ventricles. If we have a situation where we increase heart rate, then we have to shorten the time that, that the, that the cells are actually going to be contracting. And we have to get them to relax faster so that they're, that the cells, the beats are able to keep up with the filling of the heart. It's able to keep, keep up with need. So the part of the, the action potential which must shorten is then going to be Phase 2. And if phase two shortens, the period then that's going to shorten on the ECG is going to be The ST segment, or the QT segment. So the entire QT segment will shorten, when we have a sympathetic drive or when we are increasing our heart rate. The other, the other times that are going to shorten are going to be R to R. So our heart rate is going to be faster so the, the time intervals between the T, the, the R peaks is going to be shorter. We're going to have a faster heart rate, there is one other interval that's going to be shortened. You'll think about it and see what you come up with. So cardiac rhythm that's initiated by the SA node is said to be a sinus rhythm regardless of the heart rate. And the sinus rhythm means that there is a P wave that is followed by QRS and a T. So the P, every P wave will have a QRS. And the p wave simply means that the sinus the, the sinoatrial node is actually the pacemaker for the system. In certain disease conditions, we can have a faux side that starts to, to contract or to fire off independently of this, of the. The sinus, the sinus node. The sinus node is usually the dominant pacemaker because it's the fastest of the entire system, but this particular instance we may have a firing off where they're totally ignoring the sinus the sinus node. Under these conditions we can get an arrhythmia. And this arrhythmia can lead to fibrillation where the heart, the atria, if it's in the atria the atria start to, to contract at a very rapid rate. This can effect filling of the heart because the atria are having trouble filling, if it occurs in the ventricle it's an emergency because the ventricle So have a problem in filling. The electrochemical events that accompany the signal generation and the conduction that are observable on the ECG, can then tell us whether or not we have problems that within the electrical conducting system. So let's take a case. So, first of all, in their first ECG this is going to be a normal sinus rhythm in a. In the second one, in b, we have a p wave and then we have a second p wave. The first P wave has the QRS associated with it, but the second P wave does not. And we have a third P wave and again, we have a QRS associated with it. But then, the fourth P wave does not. So, in this particular case then, the sinus, the SA node is firing and it's firing at. At its normal rhythms. These are equally distant apart, so it's not an arrhythmia. It's a normal sinus rhythm, but not every SA firing is going to give us an AV firing. So that means that there's a problem with the AV node. It's not passing information down through the ventricles and Depolarizing the ventricles. So, this is a partial AV block. Only some of the signal is getting through. In C we have a situation where we have our P waves and they are equally spaced. So, we have the P waves are functioning correctly but that the P waves do not have and associated QRS. The QRS are actually functioning. A completely different, different rate. Much slower and independent of the P-wave. This says that what's happening in the atria is in, independent of what's happening in the ventricles. So the AV-node then is not conducting the signal from the sinus the, from the atria to the ventricles. And that means that we have an AV Block. And is the total AV block. So let's consider a case. We have Mrs. R. She's 80 years old. Her normal resting heart rate is 85 beats per minute. On Friday, she was unable to do her, her morning exercises and her resting heart rate was 35 beats per minute. So happened? The heart rate is being sent by the Purkinje fibers or the his bundle Purkinje fibers. So that means that she's not getting the information from the atria is not being transduced to the ventricles. So which ECG then represents her condition? On Friday. And it's going to be C, because she has a total lock of the AV node. See how easy that was? All right so what's our key concepts? So each heartbeat that is a contact, a cardiac cycle is going to involve an electrical activation of the atria and the ventricles. In both the right and the left chamber and they're going to e synchronous in their, in their active In their activity. Secondly, the action potentials of the pacemaker and the contractile cells differ. The pacemaker cells have an unstable resting membrane potential. The SA node is the fastest pacemaker. And it sets the rate of beating. Third our heart rate is determined by the autonomic nervous system. We have sympathetic innovation it's going to increase heart rate. Parasympathetic is going to decrease heart rate. Fourth the ECG is the sum of the electrical activity of the entire heart. P waves correspond to atrial depolarization and QRS complex depicts the ventricular depolarization. The T waves or the ventricular repolarization and repolarization is going in the opposite direction. It goes from apex towards the base, while depolarization is going from the base towards the apex. And five, the disease of the electrical conduction system is manifested by changes in the ECG. We either are missing specific waves or we have changes within the intervals explain it, which then depict a problem within that particular region. Of the heart. So the next time we come in here we're going to talk about how the contraction of the heart actually can generate pressure, and how the electrical system is actually, leading the contraction within the heart. See you then.
