 Hi, welcome to Physiology Open. In this video, we are going to learn about the fundamental ways in which tachy arrhythmias may develop. To understand the topic, it is must that you know about how action potential is generated in pacemaker cells as well as in cardiac contractile cells. So, if you don't know about them, I will request you to go through the playlist given in the description section below. The word arrhythmia means that heart is deviating from a normal cardiac rhythm. Normal heart rate is 6200 beats per minute, which occurs due to generation of impulses from sinoatrial node. These impulses then excite the entire myocardium in a sequential manner. So, for normal heart rate and rhythm, it is important that the impulses should be generated from SC node, pass through the normal conduction pathway and that too with normal velocity. Now, remember arrhythmias may arise either due to abnormality of impulse generation or conduction or both. They are called brady arrhythmias when heart rate is less than 60 beats per minute and tachy arrhythmias when heart rate is more than 100 beats per minute. In this video, we will restrict to tachy arrhythmias. There are three major mechanisms by which tachy arrhythmias may develop. First is enhanced automaticity, then triggered automaticity and the third one is re-entry, also known as circus movement. We will deal with each of them one by one. So, first let us see how tachy arrhythmias may occur due to enhanced automaticity. The word enhanced automaticity itself suggests that for this type of arrhythmias to happen, there should be existence of automaticity and which this automaticity will be enhanced. The automaticity that is the capability of generating action potentials without any external stimulus exists in pacemaker cells. That means this type of arrhythmias will occur due to abnormality in the action potential of pacemaker cells. See, this is a diagram showing action potential of pacemaker cells. The phase four in this diagram you see slowly drips towards threshold and this leads to action potential. This phase four is also known as diastolic depolarization or pacemaker potential. So, if this drift enhances the slope of this drift will increase and it will cause enhanced automaticity. Also, if this maximum magnetic potential is less, that means it is little towards positive, it will cause the slope to reach to the threshold faster causing increase in the frequency of action potentials. Now, this slope can increase due to stimulation of the sympathetic system. Well, this occurs normally also, this is the mechanism to increase heart rate. But if it increases too much, it will lead to arrhythmias. Now, in little hyperkalemia, not too much hyperkalemia, in little hyperkalemia there is increase in RMP. That means towards a negative potential is less. This causes the slope to reach to the threshold faster because the potential change which it has to cover is lesser. Okay, sometimes ventricle cells can also have automaticity. Normally, it does not exist. However, in case of ischemia or injury, these cells assume automaticity. So, that may also lead to arrhythmias. Let's talk about second cause now. Second cause of arrhythmias is triggered automaticity. So, that means something is triggering the automaticity. These kind of arrhythmias occur due to something known as after depolarizations. After depolarizations are depolarizations which occur during or immediately after the repolarization phase. So, here is a diagram showing action potential of contractile cells and this phase three is the phase of repolarization. So, after depolarizations can occur either in phase three or in phase four of action potential. So, there are two types of after depolarizations. The ones that occur during the phase three of action potential that is during the repolarization phase. These are known as early after depolarizations EADs and that which occur in phase four that is after the repolarization phase are known as delayed after depolarization that is TATs. Early after depolarizations EADs can occur when there is prolongation of action potential duration. See phase two of action potential in contractile cells occurs because potassium exists from the cell is balanced by calcium entry. Now, these calcium channels inactivate after opening and can open again once they return to closed state from inactivated state. But to go from inactivated to closed state they do not need a change in potential this is very unlike sodium channels rather they do so with time. So, if the action potential prolongs these channels will close with time they will have enough time to close and they will be available to open again right. Since the membrane is still above resting membrane potential the channels open since they can open when the potential is above RMP that is the stimulus for their opening. So, then it causes calcium entry during phase three of action potential hence more depolarization. So, since this depolarization is occurring after normal depolarization it is known as after depolarization. So, that means it is an early action potential generation than usual thus it can cause tacky arrhythmias. So, EAD triggered arrhythmias mostly occur when action potential is prolonged in duration you might have heard the term QT interval prolongation and that it predisposes a person to arrhythmias. Well, if you see QT interval in ECG it includes ventricular depolarization as well as repolarization. So, prolonged QT interval is suggesting prolongation of time between depolarization and repolarization. Second type of after depolarization are delayed after depolarization which occur after the phase of repolarization. These can occur whenever there is intracellular calcium overload. This causes resting membrane potential to become less negative. Whenever intracellular calcium becomes more resting membrane potential becomes less negative. So, there is a chance of this potential to reach to the threshold before normal impulse arrives and this can trigger the automaticity. This can occur in myocardial infarction where damage cells are spontaneously release calcium from sarcoplasmic reticulum or in case of adrenergic stress because there is a full mechanism by which sympathetic stimulation can lead to increase in calcium entry inside the cells that we are not going to discuss in this video. Anyways, so till now we have discussed tachyrhythmias which may occur due to enhanced automaticity and due to triggered automaticity. Finally, let's talk about third type of arrhythmias which may occur due to re-entry. Re-entry arrhythmias can occur when there are two parts through which impulses can travel. See, normally impulse travels along the conduction pathway only that is from SA node to AV node to bundle of his and then to perpendicular fibers and via this conduction system it then depolarizes atria and ventricles also. Suppose another connection is established between atria and ventricles say by a defect in this fibrous ring which keeps the atria and ventricles normally electrically isolated from each other. Now there develops another pathway through which impulse can travel but these pathways differ in certain ways electrically. See, action potential in conduction pathway occurs due to influx of calcium while in contractile cells that is atria and ventricles it occurs due to influx of sodium. So electrically there are two different types of tissues atria and ventricles are fast response tissue and the cells in the conducting system are slow response tissue because the repolarizing case is not fast enough as that of contractile cells. Also the conduction is slower in this pathway. So what happens is that suppose there is a normal bead it travels via conducting system and depolarizes atria and ventricles. Now if there is an abnormal premature impulse which arises in atria it can pass via any of these pathways either via conducting system or directly from atria to the ventricle through the accessory pathway. Now see via this accessory pathway the bead will find the ventricles refractory because there is already in action potential due to previous impulse and there is still refractory. However the impulse will travel via slow pathway because due to slow conduction these cells of conducting system would have got enough time to recover. So once it passes via slow conduction pathway by the time it reaches ventricles ventricle cells would have recovered from the original impulse and would be excitable again. So now the impulse will pass from the ventricles to the atria and thus beginning the cycle again. So again it will pass from atria to the conducting system and this cycle will continue. Thus the reentry of the impulse has occurred basically from the ventricle to the atria which is continuing in a cycle. For this reentry to occur total time taken for the impulse to move around this circle has to be longer than the time for the cells to recover from previous refractory period. That is by the time impulse reaches ventricles ventricles should have recovered. So if the impulse say suppose takes time of t1 to reach the ventricles and ventricles are refractory for time period say t2 t1 should be greater than t2 otherwise the impulse will find the ventricles refractory. Similarly again by the time it reaches to the conducting pathway the cells of conducting pathway should have recovered. So say suppose they are refractory for time t3 so again t1 should be greater than t3. Otherwise if the impulse reaches faster they will find the cells refractory and the impulse will not be conducted further. So arrhythmia cannot occur. Okay so till now what we discussed in example of anatomical reentry we have seen a defect in the fibrous ring which is causing this reentry. Now there can be functional reentry. We cannot locate any anatomical defect in the structure sometimes then also there can be reentry of impulse. So sometimes tissue injury like infarction changes the characteristics of the tissue electrically and that part becomes slow conducting part. So if there is an area of sufficiently slow conduction in the ventricles impulses exiting that area may find the rest of the myocardium excitable and thus it will excite them. So it will no more need any impulse from a synod rather same impulse will keep on exciting the ventricles again and again. So in this video we discussed the mechanisms for how tachy arrhythmias can be generated. In the next part of this video we will see the physiological basis of how these arrhythmias can be treated that is we are going to discuss the actual logic of treating these arrhythmias. Thank you for watching the video if you liked it do not forget to subscribe to the channel Physiology Open. Thank you.