conduction system of the heart your main goal on this page of your notes is to really understand how the electrical signal passes through the heart in such a way that the Atria end up Contracting first and the ventricles after Okay so let's start off in the right atrium of a frontal section of a heart for you here there are a group of cells in a portion of um the right atrium that are called the sinoatrial node and that's where the signal begins sometimes this is called the pacemaker of the heart and these cells are autorhythmic what that means is that they can generate an action potential without nervous input and left to their own devices they'll generate about 75 beats per minute now these cells then uh spread out around them or this they they send their Action potentials all around the right atrium and they pass through the wall between the right and the left atrium and cause the action potential to be propagated all the way through the right and left atrium and what that means then is all of the Atria are depolarized followed quickly by um a mechanical contraction so the Atria contract first and they squeeze their blood down into the ventricles but that is not the only autorhythmic group of cells there's another autorhythmic group of cells in the right atrium called The Av node or the atrio ventricular node and it gets its name because it's at the bottom of the Atria and at the start of the ventricles and these cells are also autorhythmic but they are Auto rythmic at a slower rate than 75 beats a minute so they usually just obey the SA node so you can see it's a backup measure if something were to happen to the SA node the AV node could keep the heart beating and so of course then the signal comes from the SA node to the AV node now the AV node passes its electrical signal to the middle muscle of the heart and there's another group of auto autorhythmic cells called The Av bundle at the top of the interventricular septum in the old days we called this the bundle of hiss named after the scientist that discovered this particular part of the pathway so the signal goes from the SA node to the AV node to the AV bundle now like I said the AV bundle is also Auto rythmic meaning it can generate its own Action potentials even if no one tells it to you can see that it's slower than the SA node if the AV node is damaged we call that heart block and what happens then is the signal can't get from the SA node to AV node and then to the AV bundle but the AV bundle keeps generating its own Action potentials so you still will have the ventricles Contracting at a very slow rate of 40 to 60 beats per minute so in a heart block if damaged and it prevents the signal from reaching the ventricles okay then the um bundle branches are the has the electrical signal goes down the sides of the Inver interventricular septum to deol ize the right and the left ventricles so this would be number four bundle branches and then number five purple the heri named after a famous anatomist heri fibers they send the signal up the sides of the right and left ventricles so the last area to depolarize and contract is going to be the top of the ventricles so you get the contraction first occurs through the Atria and squeezes blood down into the ventricles and then the contraction starts at the bottom of the ventricles and squeezes the blood up and out of um the pulmonary trunk and the aorta to go to the systemic and um pulmonary circulation so again the Tome is that um ultimately the Atria contract first and then that's followed by the ventrical which contract from the bottom up oops sorry you couldn't see all of that so you can modify the beat this is 75 beats a minute if the S if all of these nodes are working as they should then the heart would beat just at 75 beats a minute if the AV node is block then the ventricles would contract at 40 to 60 beats a minute if there was a heart attack for example but under uh in the case of a healthy heart you can modify the SA node with nervous input so we're going to use um a green pen or highlighter to represent parasympathetic input on the heart and this would be coming from a branch of the 10th cranial nerve hopefully you remember that that would be um a branch of the Vegas that's cranial nerve number 10 this would be the parasympathetic input on the heart that's why we did it in green and hopefully you'll also remember what neurotransmitter would be released onto the myocardial cells right there and that's acetyl choline and hopefully we'll also remember that it will be released and bind to colon ergic receptors and then the ultimate effect of that again a review from uh biology 241 is that by binding to the col energic receptors then um potassium is allowed to leave the cell and the hyperpolarization hyperpolarizes the myo cardial cells and if they are hyperpolarized or more negative than usual then they are going to be less likely to fire Action potentials and it will decrease heart rate but not only that it also decreases the strength or the force of the contraction or what we call contractility now you probably remember that sympathetic is going to have OPP opposite effects so let's use a pink highlighter to represent that kind of modulation and this is more likely to be coming from a branch of off of the spinal cord right so this would be a sympathetic neuron and that would be from coming from the spinal cord do you remember the cranial or the Thor thoracolumbar uh branch of the um peripheral nervous system or the autonomic nervous system is between T1 and L2 right so you have a a neuron there that then will synapse in the sympathetic chain ganglia and then send a fiber to the SA node and it will release not acetyl choline but norepinephrine which will bind to specifically a type of adrenergic receptor do you remember beta 1 adrenergic receptors on the myocardial cells and what that will do is allow more calcium to be available both at the axon terminal for the releasing of neur norepinephrine but also allowing more calcium into the myocardial cell so it increases calcium availability in the cell and you remember calcium is required for muscle contraction and so this will increase both the rate at which the heart beats by its effects on the axon terminal and and the um depolarization of the cell and it will also increase contractility or the force of contraction merely by having more calcium available for the meas and heads in muscle contraction okay now let's go down to the bottom of this page we're going to look at an EKG so in this EKG that stands for um a Electro cardiogram or e c g and what that literally means is the electrical writing of the heart like if you get a telegram it's a writing from far away tella means far so this is the electrical heart writing and used to be called an EKG is also a common way of seeing that because German spelling of cardio is like that cardio and the Germans um were instrumental in developing this procedure so on the x axis is time and on the Y AIS is uh voltage and this is looking at the whole heart so if they put electrodes let's say kind of at this angle across your chest then they're going to be able to read the electrical signal heading through the heart at that angle and then each of the traditional bumps that are seen is given a name so the first bump is called the p-wave and what is represented there is the depolarization of the Atria so this first part right here as they depolarize and then look at this really big electrical activity you see when you're looking at EKG don't worry so much about it going down it's the whole look of it is um just think more electrical activity if you see a bigger Spike so I'll use purple for this one this is called the QRS [Music] complex so the QRS complex and what that is what you're seeing is the ventricles are depolarizing so that's when the signal is passing down and up The ventricle walls so qrx sorry QRS complex is ventricular depolarization and then the last bump is the repolarizing of those ventricles we call that the t-wave this is um ventricles repolarizing so regaining their negative resting state the Atria also repolarize but they're repolarizing while the ventricles are depolarizing and so it's covered up or hidden then a couple of interesting things to put on here about disorders there's something called um wpw or wolf Parkinson's white Disorder so named after the three guys that work together and what this is is when um cells in the Atria are autorhythmic rather than obeying the SA node so what can happen is that you get these aberant Pathways um sort of like the Atria or just the signal is just hanging out in the Atria never going down to the ventricles can cause tacac cardia and what they do usually is they'll take um an Aion catheter and literally burn to death those cells that are being autorhythmic kill them off so that they are no longer blocking the signal from going down to the ventricles like it should so um causes atrial fibrillation and remember fibrillating is when the heart is a part of the heart is trying to beat so fast that it's not pumping it is an ineffective pump if it's fibrillating it's just like wiggling almost like Jell-O okay then the other a similar problem is an ectopic Focus or if you plural ectopic fosi and this is a similar kind of thing but usually um not dangerous it's when you have a few Renegade cells um myocardial cells try to set their own Rhythm and again this is going to disturb the normal depolarization and contraction of the heart and you can feel this if you've ever listened to your heart and you feel it Go bump bump bum bum bu bum bump bum bump and it you can feel it every once in a while you skip a beat or you have a few extra beats it's usually because Renegade cells are trying to set their own Rhythm a lot of people have this and it's not dangerous but the question is when does it when it does become dangerous which wpw is a disorder in which it is dangerous so it just depends um I guess it can be a spe spectum of purely harmless to life-threatening but if you have some of these cells you might notice that they are more active in their autorhythmicity if you're under stress you're fatigued if you've had too much caffeine which stimulates those nerve endings and makes the Renegade cells more active uh maybe if you are dehydrated so all of those um environmental things can cause those ectopic fosite to be more active