 Hi and welcome to Nursing School Explained. This video will go into basic cardiology as well as electrophysiology and will be the basic foundation of a series of videos to come that will go into cardiac rhythms and cardiac dysrhythmias as well as EKG interpretation. But in order to really understand where the dysrhythmias come from, we need to understand the basic electrophysiology and how things happen in the conduction system of the heart so that we then know how to interpret the dysrhythmias. So first of all, let's go back to reviewing the basic principle of cardiac output which equals heart rate multiplied by stroke volume. And cardiac output is always something that we worry about because the cardiac output is the contraction of the left ventricle that supplies the rest of the body with blood flow and is therefore super important to understand these electrical conduction problems when they occur. And then stroke volume can be broken down into preload, afterload and contractility. So preload is the ventricular filling of diastole, in diastole. So when the ventricles are not contracting when they're at rest, they get passively filled by the blood that flows into the heart. So depending on how much blood volume they get filled with depends on how strong that cardiac output will be. So for example, if the patient is dehydrated or has anemia, then that preload will be less and therefore the cardiac output will be less. Afterload is another important principle and that is the pressure that that left ventricle has to pump against to get the blood out of that left ventricle and into the body. And there are two determining factors that determine the afterload. And that is first the arterial blood pressure. The higher the pressure in the blood vessels are that go away from the heart, the more of a pressure or of a force the left ventricle is going to have to overcome to pump the blood into the body. And then the second factor is the arterial distensibility. So remember that as we age, our blood vessels get calcified. That means that they become less pliable, less stretchable, and they kind of harden. And so when the blood vessels, they usually are able to kind of expand and contract, they are very elastic, but as they harden, they are not able to expand so much. So now when the pressure comes through, when the blood comes through is ejected from the left ventricle and the arteries only distend so much because they've become hardened, then the left ventricle again has to overcome or has to pump harder to overcome that pressure and pump the blood out into the body. And the third principle here is contractility. And this is really what all relates to the cardiac conduction system. So contractility refers to the ability of the heart of that muscle fibers to lengthen and to shorten in order to produce that cardiac output, just like you would a skeletal muscle. So the ability to contract and then produce that cardiac output. So all these three times the hard way to produce that cardiac output. And when we talk about contractility, we have to talk about action potential. You might remember that from basic physiology class that there are three different stages which are polarization, depolarization and repolarization. And starting with polarization is also known as the resting membrane potential. So there is no electrical activity at all. This is a cardiac muscle cell here and inside we have positive charge and outside there is a negative charge, but there is no electrical activity. The plus remains within the cell. The negative remains outside of the cell and nothing is happening. No electrical activity is taking place while during depolarization. The cardiac muscle cells get stimulated by sodium flowing into the cell. And then this action potential kind of goes down like a wave. So sodium kind of flows in and causes that cardiac muscle contraction. And but this is only the electrical event. So this is the electrical event from the positive and negative charges that are expected to cause a mechanical event and the mechanical event being the contraction here. Now there are certain dysrhythmias where there is an electrical event, but it's not causing the contraction. And that would be PEA, also known as pulseless electrical activity, which is why we learn in basic CPR class that we always have to check the patient's pulse when they become unresponsive. Because on the EKG monitor, we might see a waveform. We might see this electrical activity, but because no contraction is happening, we are not able to fill a pulse. So this pulseless electrical activity, electricity is flowing through the heart, but it's not stimulating these muscle cells. And therefore the patient doesn't have a pulse, there's no circulation, and then certain measures will have to be taken. And this depolarization here on an EKG, the P wave represents atrial depolarization and the QRS complex represents ventricular depolarization. So the contraction of the atria comes first, followed by the contraction of the ventricles. And of course the ventricles are going to have a stronger and longer contraction because they are much bigger and they are the ones that produce the cardiac output. Now repolarization is when the influx of sodium into the cell stops and the potassium flows out. Remember whenever something goes in, something else has to come out in order to maintain balance between the positively and negatively charged ions. And the membrane potential returns to a negative resting level, which is the polarization also known as that resting membrane potential. So there is no activity, then every then the sodium flows in, eventually potassium flows out and then we're back to square one until the next beat hits. Where repolarization on an EKG strip is represented by the T wave, and that is ventricular repolarization, and we'll go into that a little bit more when we look at the actual wave forms. And then other important principles here are the refractory period. So a refractory period is the cell's ability to respond to a stimulus. And we have to distinguish between absolute and relative. So the absolute refractory period happens from the onset of the QRS to the peak of the T, so right between ventricular depolarization and repolarization, where the myocardium cannot respond to a further stimulus because it is currently in this depolarization phase and it hasn't quite repolarized yet. Now in the relative refractory period is when the downslope of the T wave hits and some cells may have repolarized, so they might have returned to the resting membrane potential, and they are therefore able to respond. And when another beat hits at that time in the relative refractory period, there is a high risk for dysrhythmias. So that's when it becomes really, really dangerous. Okay, so let's look over this here on the graph. So we have here, this is a normal EKG with our P, QRS, and T waves. And then here represented we have atrial depolarization represented by the P waves, ventricular depolarization represented by the QRS complex is what it's called. And then ventricular repolarization is the T wave. And then remember I said that atrial repolarization happens, but the atria are smaller chambers and they repolarize right after they depolarize. But on an EKG strip, we're not really able to see that because the ventricular depolarization has so much more strength in the conduction system that the atrial repolarization is kind of hidden behind this QRS complex. So we can't really see that. But remember the atria are not as important as the ventricles when it comes to dysrhythmias and production of the cardiac output. And then here we have the absolute and relative refractory periods that we talked about over here. So the absolute refractory period is from the onset of the QRS to the peak of the T wave. And then the relative refractory period is from the peak of the T wave to the end to the downslope, the entire length of the downslope of the T wave. So what that means is that when electrical impulse hits during the absolute refractory period, that means the ventricle is still depolarizing and we can't really expect the ventricle to be contracting again. However, if there's an additional impulse coming in through the relative refractory period, through this very short period of time, through this downward slope of the T wave here, then that's why dysrhythmias can occur. And then these properties of cardiac cells are super important to understand and that will really help you in understanding the different dysrhythmias that we're dealing with. So first of all, we have automaticity. And that means that cardiac pacemaker cells' ability to initiate an electrical impulse without a stimulus by a nerve. So all the cardiac cells are specialized cells. They are all pacemaker cells. We typically just think of the heart pacemaker as the SA node, the sinoatrial node. But every cardiac cell has the ability to take over as the pacemaker. And that can be without a stimulus by a nerve because we're thinking usually stimulation has to occur from a nerve. So whether that is moving your arms or your legs, we have to stimulate the nerve first in order to get the contraction going. But the automaticity, all the cells of the cardiac muscle have the ability to stimulate that impulse without a nerve being present. Now next, we have excitability and that goes hand in hand with irritability. And the way I like to remember that is we all know the excitable friend that we have, but sometimes we cannot get irritated with them because they're so hyper excitable. So think about this in terms of cardiac physiology. All cardiac cells have the ability to respond to an external stimulus that can be chemical, electrical or mechanical. So this relates back to the membrane potential. So chemical and electrical might be an imbalance that's due to potassium or magnesium imbalances or even sodium and calcium. If the level is abnormal, that can be the cause of dysrhythmias. And we have to have a certain level so that the cells are excitable, but not quite irritable. And we'll look into that a little bit in more detail after here. And then conductivity. So the cardiac pacemaker cells can receive an impulse and conduct to the adjacent cell, which means that an impulse anywhere in the myocardium can spread. And we'll go into that when we look at this graph up here. And then contractility is the ability to shorten causing a contraction in response to an electrical stimulus. So remember, when the cardiac cells get stimulated, they shorten, which then causes the muscle fibers to shorten and then lengthen. And actually that shortening causes the contraction and then produces that cardiac output. And the contractility can be enhanced by certain medications. And those are, or examples of those are digoxin, epinephrine, and dopamine. And those are very important medications when it comes to dysrhythmias. And we'll talk about that in the following videos. Now this graph over here is basically just the four chambers of the heart, the two atria and the two ventricles. And then in green, we have the conduction system. So typically we have the SA node, sinoatrial node as our inherent pacemaker. Then the impulse travels down through the atria to the atria ventricular node, which is between the atria and the ventricles, the AV node. Then we have the bundle of his that travels down through the left and right bundle branches and then up the ventricles to the prokinjee fibers. Now all these different systems, the SA, AV and prokinjee fibers, they have an intrinsic heart rate. So the SA node usually conducts the electricity at 60 to 100 beats per minute, which is the normal heart rate for an adult. Whereas the AV node or the bundle of his that comes a little bit further down in the conduction system have an intrinsic heart rate of 40 to 60. And even the prokinjee fibers, the last part here of the conduction system, they have an intrinsic heart rate of 20 to 40. Now when we see a patient with a heart rate in the 50s, for example, we have to think, did something happen with their SA node where the impulse is not coming from the SA node, but the AV node now has taken over and the heart rate is 50. Now certainly there are a lot of other factors that can determine the heart rate being 50. Then we have to look at the underlying rhythm. Do we have a PQRS and T wave that represents the atria and ventricular depolarizations in order to determine where the breakdown is in the conduction system? And then coming back to the principles that we talked about over here. So the conductivity, any cardiac cell can get excitable and then conduct an impulse. That means that a cardiac cell, for example, up here in the left atrium, can become irritable for whatever reason. Electrolyte imbalances, problems with circulation to the coronary arteries, whatever it might be, any cell in the heart can become irritable and then they want to take over as the pacemaker because of this intrinsic ability of every cardiac cell to have the pacemaker ability. And that then will show as a dysrhythmia. So that would be, let's say, a premature atrial contraction, for example, because now we might still have the conduction going through as normal, but now we have an extra beat or an early beat that comes from somewhere from an irritable cell in that atrium. Now, this can also happen in the ventricles. Of course, ventricular dysrhythmias, as you can imagine, are more dangerous than atrial dysrhythmias because when the ventricles are not pumping efficiently, then we're having a true problem. So even a cell down here in the ventricle can become irritable, but because it has the principle of automaticity, excitability with irritability and conductivity, so it can initiate an impulse. So now if this cell here in the ventricle is irritable, then it will conduct an impulse to the adjacent cells that then might travel down to the pockinji fibers and up here again. So we might not have an impulse that starts all the way starting from the SA node represented in that P wave, but it might be showing up somewhere later on in the prolongation of the QRS or the T wave because now we have this extracellular that's become irritable. So remember, these intrinsic heart rates are very important, as well as these four principles to really know where the cardiac dysrhythmias come from to understand how the heart functions and the innate ability of the cardiac cells to be a cardiac pacemaker cell. So this is the first video of this new series that I was mentioning in the beginning of the series. I will have some additional videos that go into sinus rhythms, atrial rhythms, AV blocks, atrial ventricular blocks, as well as ventricular dysrhythmias. So we're basically gonna cover all the different parts of the conduction system where something can go wrong. And remember that in nursing school, you're not expected to know the details of every single dysrhythmia. This is more advanced, which you will learn in your ACLS or Advanced Cardiac Life Support once you take these classes. And then you also learn, of course, how to treat these dysrhythmias. This is a very basic overview and also on NCLEX, you're not expected to know the depths and details of all of the different dysrhythmias. And my videos will show the most important ones. And if you understand these very basic principles, you should be able to really understand and how to interpret the dysrhythmias. I hope this video has helped you get a better understanding of the very basic electrophysiology and how it applies to the heart and dysrhythmias. Please also watch out for the following videos on the different types of dysrhythmias. Please subscribe to my channel if you find it helpful. Leave some comments below and share with your friends. Thanks for watching Nursing School Explained. We'll see you soon.