okay so we're going to continue our discussion on cardiac electrophysiology and today we're going to talk about conductivity and rhythmical excitation and again here are our unit objectives and before we really um get into the details of this lecture i just want to briefly mention that the heart tissue um it doesn't behave as these indiv the cardiomyocytes they don't behave as individual muscle fibers or anything like that they the heart the whole heart just works as a functional syncytium it's they're connected with these gap junctions that allow electric current to travel from one cardiomyocyte to the next and so they all really work together in a very coordinated fashion um the heart tissue contracts together relaxes together um and they're just very tightly connected the gap junctions allow for the electric current to travel smoothly and quickly and remember the differences between electrical synapses and chemical synapses which means that the current can move in both directions it can move in this direction but it can also move in the opposite direction and this may have some um consequences to to the heart tissue you may not learn about these consequences now and that may be later in your clinical courses but nonetheless it's important to realize this fact and know that this is one important feature of gap junctions is that they allow current to move in both directions but under normal conditions um the heart the current is going to move down the heart tissue and they're all going to contract more or less together looking at the conduction pathway we have an idea that it all starts at the sa node and then once the sa node fires and it starts to conduct that impulse it can travel it basically travels from the sa node to the av node here but we have a number of high conduction pathways that the impulse will move through from the sa node to the av node these are called your internodal pathways we also have a little branch here that stems from the right atrium or the sa node in the right atrium that stems into the left atrium that's called bachmann's bundle or the inter arterial tract once um the impulse reaches the av node it's going to crack to cross there's a fibrous tissue that we have that separates the atria from the ventricles so the av node in is going to then um extend out and cross this fibrous tissue until we get we we do this through the bundle of his and then this bundle of hiss right here is going to branch into the left branch and the right branch or the main stem left bundle branch left bundle branch and then the right bundle branch the left one is going to have an anterior left bundle branch and a posterior left bundle branch but they're both going to travel towards the direction of the apex of the heart before they turn around and go up again up to across both sides of the heart so the impulse travels down the septum and then it travels up both sides this way and and finally we're going to break into these purkinje fibers that are going to supply the the heart ventricle and they're going to play actually a pretty important role in distributing the electrical impulse from the av node down across to heart tissue when we look at the sequence of depolarization in cardiac muscle i'm going to try and expand this here so you can see the different steps so it really all starts at the sa node then this impulse travels through the internal pathways to the av node the depolarization is going to start in the septum it's going to move from left to right as you see by the arrow here okay and the the impulse continues down the septum all the way to the apex of the heart and then it travels up both sides just like the an anatomical configuration of the bundle branches the depolarization happens posterior portion of the base of the left ventricle happens slightly first what's important here that i think i skipped this one is that the depolarization of the ventricular myocardium happens from the endocardium to the epicardium meaning the inside portions contract first followed by the outside portion so the endocardium is the very innermost portion of the ventricle that's facing the cavity and the epicardium is the very outermost portion that faces outward so contraction is always going to happen at first from or depolarization and contraction are going to happen first from the endocardium and that's going to spread out to the epicardium remember that electrical activity always precedes mechanical activity so you're going to get an electrical activity first and then that's going to be followed by the mechanical activity when we're looking at conduction velocity the different parts of the conduction system they have different velocities and they don't conduct all at the same rates so if we're looking at atrial muscle for example it's going to be pretty slow and it's going to conduct at a velocity of 0.3 meters per second however the specialized internodal pathways that are present in the atria are going to be much quicker and they conduct at about one meter per second i mean this is what you see here right these internal pathways conduct at about one meter per second but once we reach the av node the av node is actually pretty slow and there's a benefit to that we briefly mentioned that before and the conduction velocity there is from 0.1 to 0.05 meters per second this conduction velocity increases as we go down the bundle of hiss and the bundled branches in in the purkinje fibers this reaches a velocity of two to four meters per second so this is the fastest um conducting tissue that we have in the heart the hiss and the purkinje fibers i also want you to remember this last bullet point here the conduction velocity does not depend on the action potential duration rather it depends on the time it takes to spread the action potential to neighboring tissues and then you can see the conduction velocities here so this is at time point zero this is at 60 milliseconds 170 200 and finally 220 excuse me 220 milliseconds the total time it takes for the impulse to spread from the sa node down the av node down the bundle of hiss and the bundle branches all the way to to the full heart when we take a deeper look at the conduction through the atria so the impulse is fired at point zero time and it reaches the av node at about 0.03 milliseconds but then it there's a delay of about .09 right milliseconds until this this action potential crosses the av node and then as it penetrates this is the penetrating portion of the av bundle as it penetrates there's another delay right of about 0.04 milliseconds and so if you start if the sa node fires at time 0 it's going by the to reach the bundle branches at time 16 seconds i'm sorry i was saying milliseconds i think and the correct it's seconds not milliseconds and so 0.03 seconds point 12 seconds and point 16 seconds so point 16 is that total delay from the sa node all the way to the bundle branches and this conduction delay is due to the just the nature of the slow response action potential but also because there's a decreased number of gap junctions in this component at the av node when we compare this to the different types of cardiac tissue the gap junctions here are at a much slower density and this also contributes to that slow conduction speed and this low conduction speed is very important as we mentioned it allows time for the atria to contract fully and empty the blood into the ventricles before the ventricles start contracting because again if they contract at the same time this is going to be counterproductive we want to allow optimal ventricular filling before the ventricles contract their blood and expel their blood out to the periphery but also if we have an abnormality happening in the atria and the atria start firing at rates that are much higher than what they normally should be these are conditions called atrial flutter or atrial fibrillation in which the contracting rates can reach 200 and 300 even 400 beats per second at the atria the av node because of that slow conduction velocity serves as a gatekeeper between the atrium the ventricles it will not allow every single beat to reach the ventricles and this is actually very beneficial because as you will learn later you know we can live without blood coming from without active participation of the atria but we can't live without active participation from the ventricles and so if ventricular contraction is not optimal that is going to lead to deficiencies in physiological function the same is not said about the atria per se although there are definitely consequences to that but having that gatekeeper between the atrium and the ventricles is actually very very important from a strictly physiological perspective and finally so we know that the sa node is your pacemaker is pacemaker of the heart it's what determines the firing rate and the intrinsic firing rate of the sa node as you see in this table is about 70 to 80. however a resting heart rate really is considered anywhere from 60 to 100 and that's considered to be normal and that's considered to be a normal sinus rhythm however the heart has this really cool feature if if something happens to the sa node right and and instead just say whatever happens and it's not working anymore then you have other tissue specialized tissue in the heart that can take over if the sa node is not working the av node can also fire and it although its firing rate is slower about 40 to 60. if something happens to the av node then the bundle of hiss can take over automaticity and it can control the firing rate of the heart but its rate is about around 40 beats per minute and then finally the purkinje fibers themselves can also initiate contraction but their rates are slower at about 15 to 20. and so the question is well why is it that it's the sa node that's the pacemaker and not the av node or the bundle of his or the purkinje fibers the answer to that is very simple it's because of this concept of overdrive suppression and this concept simply states that the the pacemaker with the fastest firing rate is going to be the one that dominates and controls heart rate and it happens to be under normal conditions that this should be your sa node and that's why your sa node is your pacemaker however again if anything happens we have this redundancy right if the sa node is ischemic and dies and it's not working av node can take over a bundle of his can take over purkinje fibers can take over but the law is and and the fundamental rule is whatever pacemaker with the highest firing rate is going to be the pacemaker that drives heart rate and so these latent pacemakers that are not active they can become active under different scenarios like for example the sa node is suppressed maybe strong vehicle stimulation reducing the sa node firing rate allowing say the av node to take over or maybe the intrinsic firing rate of one of these pacemakers right av node or bundle of his or king fibers can exceed that of the sa node due to some kind of pathology um and finally there could be a conduction block if the a if there's say ischemia to the av node and the av node dies now the sa node is working you know just fine but there's the av node is dead therefore the impulse that's fired from the sa node is no longer reaching the ventricles so now what can happen is that the bundle of hiss can take over firing you will have what's called a third degree heart block in which the atria are are beating at their own frequency and the ventricles are doing their own thing because every one of them now has an independent pacemaker this is a very serious condition but nonetheless this is can this is what would happen in this scenario so all of these three different possibilities are different reasons of why one of these latent pacemakers can take over the role of being the predominant um controller of heart rate in any individual case or scenario all right and with that we end this lecture thank you so much