Cardiac dysrhythmias (arrhythmias) (common)

so let's have a look at cardiac dysrhythmias now you may find it in your textbook or online your rhythm with arrhythmia now arrhythmia is a little bit of a misnomer because it means a lack of cardiac rhythm or no cardiac rhythm at all so the terms this rhythm is what we'll be using within this particular presentation and within your lecture notes and it's talking about at this functional cardiac rhythm so we're going to look at some of the most common dysfunctional cardiac rhythms know that this rhythm is so before we start going into this particular lecture make sure you watch the previous lecture on normal ECGs and normal cardiac rhythms and a couple things you should be aware of is the normal conduction pathway of the heart that's one prerequisite for this lecture and the other thing is that you understand what the criteria are in order to have a normal cardiac rhythm so I'm going to bring that back up right now because it's quite important for this lecture what boxes do we need to tick you don't have a normal cardiac rhythm so the first point is that our heart needs to contract between 60 to 100 times a minute so we need between 60 to 100 beats per minute it also has one of the boxes ticked for a normal cardiac rhythm what's the next like next point is now our conduction system okay so this is the electrical system of the heart that allows for an action potential to pass through the heart or contracts appropriately it should begin at the sinoatrial node so the sinoatrial node is where the conduction should begin the next point is that the signal should propagate along the normal conduction pathway which means it needs to start a death I know like we just stated and then go through the normal conduction pathway which means goes from the SA node to the atrium from the atria to the AV node from the AV node to the bundle of His and then through the very few G fibers and then from the Purkinje fibers through to the myocardium of the ventricles so this is the normal conduction pathway this is the way that the action potential should propagate in order for the muscle to contract appropriately and the fourth and final point is that depolarization or conduction should occur at a normal velocity now what does that mean a lot of these not speed but it's good to do with speed per time so distance per time I should say which is in this case I'm going to say meters per second so that means that the action potential or the polarization events should actually propagate throughout these particular components of the conduction system at their normal velocity and their normal velocity is actually quite different from each one for example the normal velocity of the action potential for the atria is 1,000 meters per second and the normal velocity for the AV node is only 200 meters per second but that's the normal velocity for those particular aspects or components of the conduction system so what that means is we need to tick all these boxes in order for us having normal cardiac rhythm if any of them are not tipped off then we've had some sort of dysfunction and this can result in a dish with here now what are the causes or mechanisms of the box is not being ticked what could actually be the cause of this well there's three major causes that we like to classify these into and if we have a look so these are the major mechanisms of dysrhythmias and they include number one they include increased auto municipal so what's happening well automaticity automatic you know that the heart spontaneously or certain cells within are spontaneously depolarize to send that action potential down and resolving depolarization events throughout the normal conduction pathway so that's called automaticity spontaneous depolarization is usually per gather the SA node as we just stated so what you can have is increased automaticity so this means that those cells increase the spontaneous depolarization so it happens more often or it could actually happen to cells that are not usually spontaneously depolarize so this could be other cells within the heart so that's one mechanism in which this rhythm is could it could occur like the other one can be re-entry issues so what are we talking about reentry now reentry is basically when you have a particular if we look at an area of the heart and let's just say this is just an area of the heart which has been scarred over or just doesn't conduct any electrical impulses when you have a signal traveling down when it hits when this electrical signal travels down hits this area where a signal cannot be sent it has to travel around right and then what it does is it moved up at the other end and continues down this is what normally happens but if you have an area of the heart in which some scarring has occurred for example what's going to happen is that as this signal comes down and splits into two one's going to stop and you ever want to go to keep going down and usually they meet in carefully each other out but what's happening here is that as this signal continue down is it also continues to move up around like that and what happens is it creates this really cycle where the signal continues to depolarize the same area and that's what we call reentry okay that's right the third mechanism of disturbance we can have a look at is what we call triggered activity now triggered activity is where particular myocardial contract certainly taught ourselves can track twice after the moaning being activated or stimulated will be polarized once okay now the most common of these and the mechanism of disturbance for cardiac arrhythmias tends to be the reentry mechanisms and that's probably going to be the one that we tend to focus on the most throughout this lecture so the way I want to look at all the different types of or most common types of catechist rhythm ears is broken down according to their location so as you know if we want to take a quick look at the heart and look at the conduction system you know that you go if we highlight all the various chambers so the H at the top medical down the bottom that the conduction system propagated signal up at the sinoatrial node and then this then propagated signal through the atria then the signal moves through the atrioventricular node which then sends it down the bundle of His and then after the Purkinje fibers to innovate the ventricles so I thought that the best way for us to break this down and look at all the different types of dysrhythmias is to start at the SA node so will first look at dysrhythmias of the SA node then we'll look at this rhythm is of the atrium then we'll look at dysrhythmias of the AV node then we'll look at dis riddim ears of the ventricles okay so that's how we're going to break up so let's first start with the sinoatrial node and have a look at some dysrhythmias comma dysrhythmias associated with the sinoatrial node now the first thing we need to talk about is if we look at the sinoatrial node that is usually the beginning point of the conduction system so when that gets triggered by the polarization event and propagates to the normal conduction system and results in a normal heart rate between 60 to 100 beats per minute that's just what we call our sinus rhythm so our sinus rhythm with our normal cardiac conduction and heart rate so a sinus rhythm if we were to look at it on an ECG the sinus rhythm looks a little bit like this so you have your P waves your QRS complex and your T waves you know that the P wave results or is actual depolarization your QRS complex represents ventricular depolarization and your T wave represents ventricular repolarization so this is your normal sinus rhythm and this is the normal ECG that is basically capturing all those electrical effects of depolarization repolarization events it's subtle we've had some common dysrhythmias for SA node well there's two major types those which increase the rate of the sinus rhythm and those that decrease the rate of the sinus rhythm so let's first look at those that decrease the rate of the sinus rhythm these are known as sinus Brady cards so bradycardia tells you that's slowing down okay so because again it's the sinoatrial node all telling you is that the spontaneous depolarization events of that sinoatrial node are happening more slowly over time which means your heart rate is slowing down that's all some sinus bradycardia is it's this normal ECG pattern it's a normal cardiac rhythm except it slowed down which means the p2p intervals along our or 1 so what you find with fast bradycardia is you have your p q r s t p q r s t and you can see that that piece of thing is it all is a lot longer than in the normal sinus rhythm in actual fact what you'll find is that if we look at these hardly sinus bradycardia our definition is less than 60 beats per minute now what could cause sinus bradycardia when actual facts are many carriers facts quite commonly in young healthy individuals and also well-conditioned athletes think about why well-conditioned athletes mean that they exercise hard the heart is strong and it doesn't take as many contraction the heart to provide the body or the tissues with the oxygen or blood that it needs so well conditioned athletes can actually have sinus bradycardia now these are normal conditions non pathological conditions in which people can science product area but what are some of the pathological conditions well somebody could increase the vagal tone you know the vagus nerves that wandering nerve it comes down when the cranial nerves come down innovates the heart tells it to slow down to give increased label tone that means it's stimulating the heart too much telling it to slow down it could also be the effect of hypoxia hypothermia it could potentially be the effect of some drugs that the individual may be taking and these may be common anti derivative drugs such as beta blockers or calcium channel blockers for example and it could be the drug effects of those so they could be some particular pathological cases now what do you do in cases of science great time well if it's a symptomatic no symptoms then the treatment option is doing nothing okay nothing needs to be done what happens in individuals who are symptomatic from bradycardia you know it could be particularly like headedness for example they may be noticing some of these symptoms may be syncope or near syncope potentially fighting what could be the results look a biga treatment option well basically if they're symptomatic atropine is quite common so symptomatic symptomatic keep on your head of spell and systemic atropine why at your pain what does atropine do at your pain blocks the palaces of Vedic nervous system hopefully that makes sense them because it's a small heart right and you know if you activate the parasympathetic nervous system you activate the vagus nerve anyhow they slowed down so entertain blocks that so blocking the slogan of the heart key resolve unit increase heart rate so atropine can be used in cases of systemic signs great academy okay let's talk about and increased heart rate that we've given at the sinoatrial node so it's depolarizing to quickly an actual fact it's depolarizing greater than 100 beats per minute this is known as sinus tachycardia meaning five heart rate originating at the sinoatrial node like I said by definition this is greater than 100 beats per minute and because it's originating at the sinoatrial node it's going through the normal conduction system just more quickly which means again you get a normal ECG pattern it just means that you're Peter Piot of all the shorter this time so in sinus tachycardia we'll give your p q r s t and then another PQRS t very soon after and again this will happen a hundred times per minute in regards to beat per minute now in what cases will we have sinus tachycardia well most commonly sinus tachycardia is a result of physiological stress so that means anytime somebody gets stressed out it can result in science tachycardia there that could be many different things that could be fear for example that could be pain or anxiety so in order to treat some tachycardia the best option is to treat the underlying cause of the physiological stress so tree me anxiety the fear pain for example okay so this is the sinoatrial node originating dysrhythmias you've got a normal sinus rhythm not a destroyed me that's normal cardiac rhythm that you've got sinus bradycardia which is a slow heart rate less than 60 beats per minute and sinus tachycardia which is a fast heart rate faster than 100 beats per minute and this is what they roughly look like on an ECG strip the next one we get next low dysrhythmias we're going to look at are those that are originated from the atria so it's going to draw the heart up again here we spoke about sinoatrial node the originating dysrhythmias but let's say where the river with me is originating now at the atria so if I'll inaudible tones again very roughly we're now skipping the SA node and we have the polarization events now originating somewhere within the atria okay that's the first point so atrial originating dysrhythmias originate outside of SA node now what that means is once this depolarization event occurred let's say it was to start here for example it's going to propagate its signal in many different directions until it makes it to the AV that AV node and then the AV node sends the signal through the rest of the normal conduction pathway so what that means is what type of differences should you see any cg4 atrial originating dysrhythmias well first thing is it bypasses the SA node which means you have absent or very abnormal looking T waves because we know the P waves are representative of atrial depolarization originating from the sinoatrial node and because it's originating at some different point so with atrial dysrhythmias that usually recognizes those in which are greater than 100 beats per minute so what does that tell you so it means that atrial dysrhythmias are usually atrial happy colonies and like I said that's greater than a hundred bits per minute but because it's not focusing on the P way that's 100 beats per minute looking at QRS complexes just five so atrial tachycardia 100 min great are greater than 100 beats per minute now if this action potential of depolarization that originates at one focal point such as I've drawn here if unsurprisingly called a focal atrial tachycardia which means beginning at one point or one area but you can have atrial tachycardia which originates from many different areas and this is called multifocal tachycardias and what that means is that originate here as well and here as well and here as well at here as well and so you get all this very strange-looking depolarization events we should see the P wave so you see some very strength sometimes it looks inverted sometimes it's up sometimes down and let me get normal QRS complex and then again you get this strange looking T waves okay now multifocal like I said is originating at many points begins at many many points in the atria okay now that's atrial tachycardia greater than 100 beats per minute however you can have atrial tachycardia which are a lot faster in actual fact ancient tachycardias which are known as atrial flutter and these actual flowers are actually between 250 to 350 beats per minute that is a shil flows between 250-350 beats per minute again originating at the atria and what you find is that this is usually due to what we call and I spoke about it at the end of this lecture reentry mechanisms so that means that you have your chambers if it were to start a depolarization event here remember I said if there's an area in which does not conduct the electrical impulse they usually meet on the other end and they cancel each other out and then they keep propagating but I said if there is some damaged area some areas is steaming of some of the tissue dies off a little bit what that means is when the signal gets sent down through an area that's scarred for example it results there so that is a scarred area we start sending a signal down one gets blocked the other one continues to cycle around and that's called a rare tree and it just keeps propagating a signal over and over and over again keeps sending it out now this is a rare tree mechanism and that's usually what causes atrial flutter and that's between 250 350 feet per minute now if you would have a look at an ECG of an atrial flutter it has what we call a sawtooth look to it so you have these really weird-looking P waves the QRS complex and again we're looking P waves in the QRS complex okay so it's this sort of like look that you see where the P wave should be which tells you that it's an actual flower sort of looking ECG so what could cause this well structural abnormality is probably one of the most common it could also be some sort of toxic drug effect can sometimes be due to digitalis toxicity as well what type of treatment options could be used for atrial flutter well we could use some of the common cardiac anti-discrimination that includes beta blockers and that also includes calcium channel blockers as well now if this lasts too long this could reduce the cardiac output of an individual why well because if the heart beating so quickly that it doesn't give it enough time in diastole relaxation to fill up with enough blood to down to push out to the rest of the body so if it's contracting too quickly or correct output could be reduced now a very interesting point you should be aware of is because what's happening here in the HL with this atrial based dis remains as the thing regardless of what type of signals being propagated here at the atria it is the rate limiting step in the AV node okay remember atria I told you about normal conduction normal velocity usually around about a thousand meters per second but then we have AV node which is about 200 meters a second which is basically point two seconds so what can happen is even though that's contracting and depolarize very quickly AV node will slow it down and so usually the fastest you'll get with atrial flutter the fastest conduction you'll get to the ventricles will be around about 170 beats per minute kind of slows down the nation flow now you can have atrial dysrhythmias that actually faster than 250 to 350 beats per minute these are called atrial fibrillation an atrial fibrillation is greater than 350 beats per minute now again it's due to these reentry multifocal reentry mechanisms so it's reentering happening at different parts of the heart that's why it's contracting so much and it looks like a bag of oils really and when you look at the ECG you don't really see much in regard for where the P wave should be you see this chaotic mess and then QRS complex and then get a chaotic mess and then the QRS complex okay so that's what we see for atrial fibrillation and the type of treatment option you can have again could be some of those anti dysrhythmias beta blockers calcium channel blockers but also electrical cardioversion okay electrical cardioversion so atrial fibrillation again because the angry mode is the light leading except the ventricles would be polarized at a slower rate that's still quite fast like I said around about 170 it's permit for the ventricular depolarization so that's atrial fibrillation now again you can have reduced cardiac output atrial fibrillation but these atrial events that are happening Angell takis atrial flutter atrial kids and you can see it's greater than 100 that it goes to the next stage 25350 then the next stage greater than 350 they're not necessarily life-threatening they can increase your likelihood of developing clots why is that because if it's just doing this like a bag of worms it increases the pull time for the blood and can increase the likelihood of clots developing up here in the atrium and then be pushed out to the rest of the body that's one point the other point is that it's not necessarily life-threatening these atrial tachycardia speeds because we're not blinded in the atrium you know that you get contraction they actually your first blog gets pushed down to the vegetables and the vegetables contract pushes blood out to the rest of the body either lungs or the rest of the body if the atria are contracting like a bag of worms which is seen in these cases it's not a big issue because blood will just fall via gravity through the atrioventricular capsule flaps or valves down into the ventricles so do you do even though it's not contracted probably enough blood will go down into the ventricles to be contracted out the problem you get is when the ventricles start to shake but that's when we move on to ventricular based dysrhythmias now the next point we're going to look at we've done sino you'll know we're going to HR we're now going to look at atrioventricular node based disrobe miss okay now again we'll draw the harder n so node AV node down the bundle appears in the Purkinje fibers okay so we spoke about SA node spoke about a chart now we're at AV node so what happens in these AV node based dysrhythmias well what we're going to focus on a stop and call AV node block which is actually also known as heart block and what this anything a block or Harbach is referring to is the fact that the signal that's coming from the sinoatrial node through to the atria okay so the signal propagating down through to ultimately go to the AV node don't be from the SA node through the atria to the AV node and then subsequently going down and obvious here at the AV though there's some sort of delay or with some sort of abnormal change or the some sort of blockage okay so what it is is a delayed or absence of atrial depolarization propagating to the ventricles effect that again is the delay or absence of all this hm depolarization propagating through to the vegetables so either a delay of some sort or it's not happening you can break this AV node block or heart block down into three different types you've got first degree heart block second-degree heart block and third-degree heart block so and they sort of progressed on in severity in a way first the green heart block basically this there is a delay in which this P wave because you know that this atrial depolarization is the P wave which then moves to this ventricular depolarization the QRS complex the P wave is delayed you know that the normal delay happening at the AV node right in point two seconds in actual fact in first degree heart block is greater than 0.2 seconds okay but delay the AV node which means on the ECG what do you get first degree heart block you get a p-wave usually the break is 0.2 seconds but it's great another point to actually get this big break between the T waves and the QRS complex okay that's what it is and then happens again P wave big break QRS complex and so forth now what you find here is this because that's p q r s t you're getting this big break from the p to the arc okay again i'm beat break from the P to the ass longer than normal but what you find is that the p2p usable stays the same so it's always going to be P 2 P 2 P 2 P it's always going to stay at the same length from each other what you get though is a widened P to R interval this is 1st degree heart block what do you do to first degree heart block nothing we don't treat okay all right what now let's look at the second-degree heart block second-degree heart block can actually be broken down into two types you can have what we call mobitz one and moments to I what's the difference between motorist 1 and motives - so what happens again is that there's some sort of delay that's occurring and you have your p-wave then you're going to have your delay then you're going to add your QRS complex and T then you have your paper then the delay gets longer QRS complex clearway greater than what you'll find is as these T to R P to R gets longer and longer which you don't see it have block 1 as the Peter R gets longer and longer at some some particular point the QRS complex disappears it just drops out and then from this P what are you going to get next with another P and then it goes back to the normal leg Peter ah this is mobitz 1 and then you don't do any trigger some of its 1 welcome some moments to well there's none of this lengthening so this sequential length in between P to R for motives - you just have I'll run this out for moments - you have p q r s t then you have p q r s t and what ends up happening here is that at some point the QRS complex just disappears and so - and then P nothing P joyous complex so the PDP interval remains the same when you get a dropping of the QRS complex at a particular point this doesn't require treatment and a treatment for moments - is a pacemaker ok so certain degree moments one moment - but some of it third degree have one third degree half-life of the difference well I've stated in first in the second degree heart block that there is a delay from the atrial depolarization to the ventricular depolarization which means you get a longer break between the PNR interval that's the first degree second degree only get this whole thing but sometimes some of these H of depolarizations don't ever even propagated for QRS complex to your depolarization then again is brave to RS complex depolarization break to our complex and then actual depolarization break no QRS complex that's second-degree heart block the QRS complex intermittently sort of drops off third-degree heart block what happens here is that that H of depolarization events are not related in any way shape or form to the QRS complexes so that means that the ventricles depolarize and contract independently of the atria so regardless of when this is be polarizing this will be polarizing on time and it will be polarizing accordance with a spontaneous firing of the AV node and the AV node unlikely remember the SA node spontaneously depolarize at 6,500 times a minute d let's SA node AV nodal spontaneously depolarize between 30 to 55 bits per minute which means in third-degree heart block P waves are not related to QRS complex and therefore ventricles depolarize depolarize between 30 to 55 beats per minute that's third-degree heart block and what do you need here takes my car okay so these are the AV node box pop up on a block 2003 you can see that has to do with p-waves turning into QRS complexes because it just take a little longer preload is turning into QRS complexes except some of those QRS complexes don't propagate and then P waves not associated at all with QRS complexes and their front full heart block that's no degree heart block the next and life I'm going to look at is ventricular based distributors yes so again drive the heart hrl atria ventricle ventricle spoke about those that originate the SA node spoke about moment originate the atria spoke about those originate at the AV node now we're talking about when we look at cardiac dysrhythmias of the ventricles so ventricular dysrhythmias ventricular dysrhythmias those that originate in ventricular myocardium or the hips Purkinje system that's what we're referring to ventricular dysrhythmias are those originating the ventricular myocardium sort of muscle electrical the hips or the Purkinje system two major types I want to look at you have ventricular tachycardia and what ventricular tachycardia is again it's a heart rate or ventricular contraction it's happening greater than a hundred times to a minute mr. Taylor construction that's happening a greater than 100 times per minute ventricular tachycardia the tubular tachycardia can move on into something that's more dangerous which is known as ventricular fibrillation now ventricular fibrillation is don't happen greater well actually what you should first look at is where we look at the ECG of ventricular tachycardia what you find is that you have these very strange their regular ECGs again hot greater than 100 beats per minute if you move on to ventricular fibrillation it just looks like a mess and that's because with the tricular fibrillation you've got to lose multi focal points that are depolarizing and it's resulting in similar to atrial fibrillation like that bag of ones you're getting that apathetically they're both ventricular tachycardia ventricular fibrillation well that they both results in a decreased cardiac output why because when the heart can track the ventricles in that nice sensation manner so all at once contracts pushes that blood out to the rest of the body that can deliver that blood in the appropriate way that's normal cardiac output about 5 liters remember 5 liters per minute now if it's contraction like a bag of worms why doesn't squirt out properly kind of output these drops patient can result let's just fill out headedness and syncope which is fainting but the patient can ultimately die which means the tricular tachycardia especially ventricular fibrillation are the most deadly or dangerous types of dysrhythmias that an individual can have and the only treatment for ventricular fibrillation is using AD fibrillation machine so deep fibrillating the patient remember that machine of those paddles and they were so clear or don't want those times we down a bus when you use that machine that D big delay that your defibrillator place putting through a jolts of electricity Reis trying to reset the conduction system of the heart and so these CGS with a little bit more radios to tacky still quite electrical college mess and ventricular fibrillation just look like a total utter electrical mess when you look at it on an ECG the loss or reduction in cardiac output can result in death sort of patient so it will just go through the common or most common types of cardiac dysrhythmias please feel free watch it again make sure you understand all the various causes some treatment options manifestations and so forth

Channel: Dr Matt & Dr Mike

Views: 48,974

Rating: 4.9315896 out of 5

Keywords: cardiac, heart, cardiac dysrhythmia, atril fibrillation, fibrillation, sinus rhythym, bradycardia, tachycardia

Id: 2GnjgTRybq8

Length: 40min 49sec (2449 seconds)

Published: Sun Jul 09 2017