hello and welcome to another episode of study this where we review various textbook chapters today we'll be going over chapter 10 of Gaytan and halls medical physiology where we essentially describe the circuit board of the heart and how it functions to allow the heart to contract in a rhythmic way and in a synchronous way as well if you're feeling generous please feel free to give the video a like and subscribe to the channel it will help us out greatly and allow us to continue to make these videos so a concept that we should talk about first is why do we actually need the circuit board within the heart and what we're trying to do the overall concept of the electrical activity of the heart is to actually stimulate the atrium to beat first so the top chambers to beat first fill the ventricles with blood priming them to pump and eject that blood out of the heart and then there needs to be a delay between that signal between the atrium and the ventricles to allow our blood to fill since the electrical activity moves quite fast and then after that delay we need to send that electricity through the heart muscle all simultaneously so then the heart all contracts as one rather than one portion contracting before another portion which will just result in a a poorly synchronized contraction and reduced force would be generated so our various electrical components of the heart include the sinus node which is our pacemaker that is what stimulates the heartbeat we have our internodal pathways and the atrium so these pathways thought of as highways so they help to send that electrical signal around the atrium so then the entire atrium can contract as one we then hit the AV node or the atrioventricular node and this is located at the junction between their atrium and the ventricles and that's function is to delay that signal from being sent to the ventricles to allow them to fill with blood and then we have the bundle branches of the pic energy fibers and these also act as highways but this time for the ventricles to send their signal around the entire heart muscle or the hot and tired ventricular muscle so then they can all contract this one now the sinus node is located in the HRM for the near the superior vena cava and that has a self excite-ation ability so it is able to spontaneously produce its own action potential resulting in a rhythmic impulse that stimulates a regular heartbeat and it does that through naturally leaky sodium and calcium ions and the reason why these calcium and sodium ions it naturally leaky is because the resting membrane potential never actually reaches the normal low value of negative ninety we're more sitting up here at negative 55 millivolts so not all of those so far sodium channels were actually closed and there is some if we get into more details there's some other sodium channels which remain open called the funny current channels but essentially there is a leak of sodium into the cell resulting in this very gradual increase in the resting membrane potential it's not a instant depolarization because it's just a slow leak but there's a very strong increase in resting remember membrane potential until we reach threshold once threshold is reached we then open up our calcium channels our l-type calcium channels which then results in the rapid influx of calcium and our action potential then the calcium channels close potassium channels open which leave the cell repolarizing the membrane for only getting to negative 55 millivolts so those are our main components else slow leaky sodium channels which are allowing sodium to enter the cells we reach threshold calcium channels open influx of calcium resulting in an action potential and in those clothes and our potassium channels open and we have a loss of potassium and a loss of positive ions out of the cell so repolarization and this is superimposed on top of our ventricular muscle fibers showing how the resting membrane potential is quite different from the sinus local tissue and then so once that sinus node actually sends off its signal so our sonís node over here in our right atrium it gets spread to the atrial muscle nearby but then also through these highways and the internodal pathways so if three of them our anterior middle and posterior which all seem that's the around the atrium so there now two atria are going to contract at the same time and then they all congregate into the AV node so they turn into this AV node which functions as we've already mentioned to slow that impulse so it's a nice kind of traffic jam here because there is a reduction in gap junctions so there is a higher resistance and we have a slowing of that impulse coming through this Junction here until we reach our bundle branches or Purkinje fibers and then it turns back into a highway so you can think of it as two highway systems separated by a area of traffic jams or traffic lights which prolongs the impulse so then the atrium can fill the ventricles with blood giving at that time and then the Purkinje fibers then function to actually send that impulse right around the left and right side of the heart so then entire ventricular muscle was able to contract as one so these becomes you fibers seem to rapid the loss of the impulse around to the different ventricular muscle and we can see that here these are all the time points at which the impulse reaches the heart now a feature of the AV node that I should briefly mention here is that it is a one-way track so you can't have that impulse going backwards through the AV node in some disease states we do have an anomalous pathway through the fibrous membrane between the atrium and ventricle so then we can have the ventricular impulse spreading through the ventricles and then it manages to spread back over that fibrous membrane and then restore mutilate the atrial tissue and that results in what's called an arrhythmia or an abnormal heart rhythm but that's an abnormal process that's a pathological process so that is the normal heart rate so we have the sinus node as our pacemaker sending that impulse through the atrium delay that AV node then sent through the ventricular muscles now we do have other ectopic pacemakers or other pacemakers cells within the body now the AV node can also have a self-excitation property and so do the Purkinje fibers but the AV node is a lot slower than the sinus node so the sinus node always rides it and then the Purkinje fibers are even slower still so if the SA node decides not to fire then the AV node which is its own self excite-ation process will be able to fire after a period of time and then if the AV node doesn't fire then the Purkinje fibers can fire after some time as well and these impulses created by these other pacemakers and called escape beats because they only occur when there is a delay and now normal sinoatrial impulse and the heart is escaping so they now Hawking continue to beat even if this side or HR on the node becomes dysfunctional now when this occurs if there is a sudden cessation of an impulse let's say through the AV node so the ventricular muscle never gets told to fire then the Purkinje fibers will kick in and do their own pacemaker but there is a bit of a delay when that's been suppressed for so long so then there may be a delay in the heartbeat for several seconds to even up to 20 seconds and during that time if you're a person then you're actually faint because you don't have oxygen delivered to your brain but after that 20 second timeframe hopefully that pacemaker will then kick itself into gear and then start to do its own firing it usually a pretty slow rate but at least it will be rhythmic and you won't actually collapse anymore but you won't feel good when you try to do any sort of activity and then we've got some other ways that we've already talked about in the previous chapter that the heart rhythm is controlled so our parasympathetic nervous supply is mainly innovating into the sinoatrial know than the AV nodes and when it sends off an impulse it releases acetylcholine and form the vagal nerve endings from the vagus nerve and that actually functions to slow the rhythm of the sinoatrial node and the AV node conduction it does that by increasing the permeability to potassium ions so now a resting membrane potential gets even lower so those leaky sodium channels now have to leak even more sodium in order to reach threshold so since we have a longer time until threshold has reached our heart rate slows down and then at the AV node since we have a lower resting membrane potential we just need a stronger impulse from the atrium to stimulate a beat through the AV node so we can get some blocks through the AV node with sympathetic innovation then which is mainly also innovating all the heart muscle itself but it releases norepinephrine which does or defects through the beta-1 adrenergic receptors and what it does is increase the permeability to sodium and calcium so two effects there so the sodium and calcium are involved with that it's low increase in ristic membrane potential we're going to reach threshold faster since we have more leaking and since we have increased calcium entering the cell we're going to have stronger contractions since calcium is directly related to cardiac muscle contraction and then that really summarizes our chapter for today please feel free to drop a comment otherwise we see in the next video