Arrhythmias | Types, Pathophysiology, Diagnosis, Treatment

what's up ninja nerds in this video we're going to be talking about arrhythmias but before you guys have an arrhythmia looking at all the stuff on this board before we really dig into this stuff and start filling all this out please go down in the description box in the description box we've link to our patreon in patreon we're going to have notes comprehensive notes that we're going to cover in this whole lecture on arrhythmias we're also going to have a picture of this board before everything's drawn on it and a picture of everything after it's drawn so that you guys can follow along and benefit as much as possible from this lecture so please go check that out so the reason why i'm telling you guys this is that hopefully in the near future we're going to have a website where every video that we've covered on our youtube channel will have corresponding comprehensive notes pictures of the whiteboard with the diagrams beforehand and after the video so that we can help you guys in your learning process so ninja nerds please go check that out and let's get into this all right engineer so let's talk about arrhythmias right first thing we need to talk about is the definition of arrhythmias what is an arrhythmia if you were really basic and we ain't basic but we'll do basic first an arrhythmia is abnormal electrical activity within the heart simple as that but we're ninja nerds so we really should say that an arrhythmia is when there is an abnormality within either rate rhythm sequence of conduction or origin of conduction that is the definition of arrhythmias now the easiest way to really kind of define arrhythmias is based upon abnormalities and rate so the first thing we need to know is what is a normal rate and once we know what normal is we know what abnormal is so what's a normal heart rate a normal heart rate which is set by the sa node the sinoatrial node when it fires it sets a normal heart rate of anywhere between 60 to 100 beats per minute this is considered to be a normal heart rate if you go above 100 beats per minute that's abnormal you're going too fast how do we define that tachycardia so we can say a tachyarrhythmia is when there is an abnormal rate how high is that rate we're talking greater than 100 beats per minute as attack arrhythmia when we go too slow or we go lower than the 60 beats per minute we're going too so that's bradycardia so bradycardias are associated obviously in this case with bradyarrhythmias and this is whenever you're going less than 60 beats per minute now let's be clear here you can go way above 100 sometimes in situations of fibrillation close to 350 beats per minute or more so pretty scary stuff so that's the basic way we talk about arrhythmias now that we have the basic kind of definitions of our tacky brady arrhythmias let's talk about the two subtypes of tachyarrhythmias and it's really simple obviously everything above the ventricle any arrhythmia if i were to kind of draw a line here any arrhythmia that occurs above the ventricles is called supraventricular tachyarrhythmia there's one particular one that is usually due to the sa node firing too fast and that is called sinus tachycardia okay the next type is usually because let's actually draw this in green so it really sticks out here there's an irritable area in the atria that's firing it's generating abnormal electrical activities and that's going to the av node before the sa node fires and gets to the av node that's called an atrial tachyarrhythmia there's a couple different types of atrial tachyarrhythmias and what are they the first one i really need you to know is when there's just one of these little areas just one firing consistently that's one ectopic focus so we call it focal atrial tachycardia pretty straightforward right what happens if you have multiple maybe we have three little ectopic areas in the atria that are firing abnormally that's multifocal atrial tachycardia pretty straightforward what if i have a bunch of little areas that are firing as well but they also are similar to multifocal lateral tachycardia i have multiple little ectopic areas that are firing really really fast faster than this rate that could be atrial fibrillation okay so usually we're talking about atrial arrhythmias as usually vocal atrial tachycardia multifocalator tachycardia atrial fibrillation and one more there's an abnormal arrhythmia a superventricular tachyarrhythmia that occurs near the tricuspid valve that we'll talk about later and it creates a reentrant circuit and it's called atrial flutter and then the last two so we had two categories so far one is an arrhythmia due to sa node firing these other ones one two three four is due to an irritable atrial area firing before the sa node fires the last two here there's one that's a problem with the av node there's a re-entrant circuit within the av node and it's creating really fast rates and that's called atrioventricular nodal reentry and tachycardia there's another one where there's a re-entrant circuit a loop that's generated through an accessory pathway between the atria and the ventricles and we'll talk about that one later it's called a v rt important to remember you'll hear this term kind of thrown around a lot called svt or psvt and psvt also known as paroxysmal supraventricular tachycardia let's make that look like a better v there proximal superventricular tachycardia is a special kind of name that we give avnrt avrt and sometimes even focal atrial tachycardia but these are the two primary ones okay so we've talked about the supraventricular tachyrhythmias the types do a sa node problem due to multiple atrial arrhythmias all of these and due to a re-entrant circuit in the av node this one or a reentrant circuit via accessory pathway avrt let's now talk about the ventricular attack arrhythmias so ventricular attack arrhythmias is you have an irritable area within the ventricle again some irritable area within the ventricle that is firing and it's firing and generating an abnormal electrical activity within the ventricles and because of this this produces particular arrhythmias called ventricular tachycardia okay so ventricular tachycardia now here's the big thing i need to kind of preface really quick there's two different types of ventricular tachycardia one is you can have what's called monomorphic and this is usually the most common type and we're going to abbreviate this v-tach monomorphic v-tac and the other one is called polymorphic v-tac all this is really simply is if i have one little irritable area in the ventricle that's firing and creating this abnormal tachyrhythmia within the ventricle that is monomorphic but if i have multiple irritable areas within the ventricles that are firing this is polymorphic v-tac just like it was if it was focal atrotachycardia or multi-focal lateral cardiac same concept one other thing to add on with the polymorphic v-tac is there's two types this one right here we're going to kind of keep by itself this is what's called a polymorphic v-tac with a normal qt interval we'll talk about it later but there's another special type that always comes up in your usmld exams which is called polymorphic v-tac which is again is a type of vtac but it contains a prolonged qt interval and we give a very special name to this you know what they give it to points which means twisting of the points and again we'll get into this arrhythmia a little bit later really nasty when you see this you're probably going to poop your huggies the next one you'll also poop your huggies and this is a very abnormal rhythm very dangerous rhythm called ventricular fibrillation and again this is due to multiple ectopic foci within the ventricles that are firing and also they can have what's called reentrant circuits and we'll get into what all that stuff means later i'm just prefacing everything here for you okay we talked about the supraventricular ventricular tachyarrhythmias the next thing we have to talk about is bradyarrhythmias bradyarrhythmias is you're going too slow we already know that but again it could be a problem where the sa node isn't firing fast enough it's firing too slow if the sa node is firing too slow that's referred to as sinus bradycardia okay sinus bradycardia the other issue is there could be something wrong with the av node it's taking a dump it's not working today it says okay you send message messages to me sa node i'll receive them and maybe i'll send them but i'll send it slower than i need to or maybe i won't send any action potentials down and so there can be a block if you will in the av node which means that there's a loss of electrical activity connection between the atria and the ventricles there's a couple different types of conduction blocks or heart blocks and they're very easy you want to know why because they just have a number in front of them we just go in order so you have a first degree heart block okay so first degree heart block which isn't as severe believe it or not i have one and then a second degree heart block and a second degree heart block there's two types one is referred to as mobitz one and the other one is referred to as mobitz 2. now another name for mobitz one is they have like a we'll talk about later is they have what's called a winky back a dropped qrs so remember sometimes you may hear second degree heart block mobitz1 winky bach okay the next one is going to be the most deadly one can be very deadly if not treated quickly is a third degree heart block okay so these are due to conduction blocks within the av node this is due to the sa node not firing fast enough this covers our too fast too slow rhythms the next thing we have to talk about is there's an one that actually is fast and slow and it's a really odd one and let's talk about that called sick sinus syndrome sick sinus syndrome so remember i told you it's kind of a combination that's why you got like a nice little blue and red in there it's mixed so what happens is they have a tachyarrhythmia associated with this usually what happens is the sa node before we actually say the tachyrhythmia the sa node is usually dysfunctional so because they have some type of sa node dysfunction whether this be due to fibrosis of the sa node whether this be due to some type of myocardial scarring whether this be due to some type of just a problem with the sa node intrinsically as it starts to dysfunction it doesn't fire as fast and because it doesn't fire as fast it produces what it produces a sinus bradycardia so that's where you can get some bradycardia but then what happens is because of this underlying bradycardia and the sa node being dysfunctional some other area in the atria has to kind of take over to compensate for the sa node dysfunction and so sometimes as a result of this say no dysfunction these patients develop an associated supraventricular tachycardia whether this be atrial flutter whether this be atrial fibrillation or whether this even just be like a pac of some time kind like a premature atrial contraction and because of that they'll have intermittent bouts where they have sinus bradycardia with compensatory concomitant svt that produces a tachycardia so you know sometimes there's they call this tachy brady syndrome it's like a subset of six sinus syndrome so it's kind of an interesting one where you see kind of an intermingled mix of the two all right beautiful we talked about the types of arrhythmias we have kind of a nice basic intro into them now let's dig into the pathophysiology all right engineers so we talked about the types of arrhythmias we have our kind of our really good foundation down now what we need to do is talk about the pathophysiology what causes these arrhythmias to develop so we're going to go through each one of these we're going to have tachyrhythmias the most common causes or pathophysiological reasons is usually an increase in automaticity i'll talk about what that means or triggered activity okay and the last one is a re-entrant circuit and we'll go through all three of these and talk about what they mean in great detail but just again write that down so you have a little note that these are the three most common reasons for attack arrhythmia next one is brady arrhythmias this is usually due to decreased automaticity or a conduction block again write these down so that when we go through them you have everything ready to roll all right so now that we have our pretty much common reasons for these let's dig into automaticity first all right so first thing we need to talk about is we know that tachyrhythmias brady arrhythmias you see they're both the same color different colors they have the ability to increase or decrease automaticity associated with those arrhythmias and we'll talk about some of the underlying causes but first before we do that let's talk about what the heck automaticity is what is automaticity it's really simple you know whenever um the sa node it has those remember we talked about this in the cardiovascular system if you haven't watched our video go in watch the video on the intrinsic cardiac conduction system in our cardiovascular playlist we go into more detail here i'm going to breathe kind of cover the surface a little bit here but if you guys remember the sa node has special little channels called funny channels which allows for it to kind of intrinsically on its own depolarize send action potentials and cause the heart to contract on its own without any nervous system innervation on its own and how it does that is again the sa node fires goes down to the av node av node to the bundle of hist down your bundle branches and then through your purkinje system that's our normal kind of conduction pathway the normal automaticity rate is 60 to 100 beats per minute what if i have some modulation of that normal automaticity well zach that kind of makes sense right darn right it does because we're an engineers we make sense of stuff what if i have something like the parasympathetic nervous system you know cranial nerve 10 parasympathetic nervous system so your cranium nerve 10 is also known as what nerve i know you guys know this vagus nerve the vagus nerve or cranial nerve 10 releases a lot of what onto the sa node or the conduction system in general it releases a lot of acetylcholine and acetylcholine you guys know what that does right it causes the potassium ions to leave the cell hyperpolarizes it and relaxes it and then it does what it decreases the conduction from the sa node and decreases the movement of conduction from the av node down what does that do that drops the heart rate and if you drop the heart rate what is that called bradycardia if you drop it below 60 beats per minute that could be one of the reasons for a brady arrhythmia so again this is usually what system here with the cranial nerve 10 this is the parasympathetic nervous system but what if i have the sympathetic nervous system you know the sympathetic nervous system the normal sympathetic nervous system within the spinal cord is about t1 to l2 right but going to the heart out of that t1 to l2 output only t1 to about t5 of your sympathetic nervous system goes to innervate the heart now it does two things it can innervate not just the sa node but it can also innervate contractile myocardial cells but let's not focus on that one right now what i want you to know is that when the sympathetic nervous system releases what kind of neurotransmitters here it releases an increase in norepinephrine or an increase in epinephrine what do these things do they increase the conduction via the sa node and increase the conduction through the av node down that's going to increase heart rate that's going to increase automaticity and if it goes above 100 beats per minute it's considered to be attack arrhythmia wow we just made sense of this stuff so what would i say then if i have too much sympathetic nervous system outflow i'm going to drop the heart rate i'm going to increase that rate really high but if i have a lot of parasympathetic outflow i'm going to drop the heart rate really low so now we have to talk about what are the things that increase the sympathetic outflow and what are the things that increase the parasympathetic outflow because that's our underlying causes okay so first one we have up here let's just go and order the top one the parasympathetic nervous system we said is gonna drop the heart rate right and again what do we say if we drop the heart rate it's called a decrease in automaticity right so a decreased automatic and sometimes if we drop that kind of heart rate down enough it can lead to a brady arrhythmia which can become sometimes symptomatic we said one of the reasons because there is other reasons one of the reasons is due to increased vagal tone so there's an increased vagal tone or increased parasympathetic nervous system activity you know what's crazy is that sometimes this increased vagal tone can be completely physiological or normal you know whenever people are sleeping they're resting they're digesting you know they're doing all that stuff their vagal tone is a little bit higher because their parasympathetic nervous system is a little bit more active when we're sleeping so that may produce some brady arrhythmias while you're some sweater sleeping or bradycardia in general the other thing is it could be due to endurance athletes you know certain athletes endurance athletes their myocardium is so strong and so powerful that they can have a higher vagal tone associated with it so that could be another reason says endurance athletes with very powerful myocardiums have lower resting heart rates a pathological reason for an increased vagal tone is usually an associated inferior wall mi this can kind of create like a reflex vagal tone so inferior wall and mice are usually due to what coronary artery a right coronary artery occlusion so think about right coronary artery occlusion producing an inferior wall my that also can produce some increased vagal tone other things that can do this is think about what if i not just increase the parasympathetic tone what if i actually gave drugs that kind of like block the not block it but slow down conduction through the av node now there is certain drugs that can kind of slow down conduction through the av node what are those drugs that basically slow av conduction because if we slow av conduction we're also modulating the automaticity this would be things like beta blockers things like calcium channel blockers or things like digoxin so that's another thing to be thinking about okay so not only if we slow av conduction right but what else so we can either increase vagal tone that would decrease automaticity we can have slower av conduction but also another thing is what if i kind of really slow down the metabolic activity of these nodal cells right so if i slow down the metabolic activity that could also maybe slow down some of these depolarizations so certain things that can really kind of decrease metabolic activity is going to be uh like a low body temperature you know hypothermia so if somebody is out there you know hiking on some mount everest or something like that and they get too cold maybe they can decrea they can develop some decrease automaticity but other reasons is think about a hormone that really controls a lot of our metabolic activity thyroid hormone so sometimes if people are really severely hypothyroid like in a condition called mexidema coma where they can have really really low thyroid hormone levels this can also produce some severe bradycardias and decrease automaticity so that could be another reason another one is usually due to an electrolyte imbalance and the particular electrolyte here is if they have too much potassium okay so hyperkalemia could be a very powerful reason a big one that i really want you to remember that can cause decrease automaticity because it alters that resting membrane potential and that really affects the electrical activity within the heart the last one that is always coming up on your exams is due to high intracranial pressure someone has high intracranial pressure whether it was due to a stroke whether it's due to a tumor whether it's due to some type of hematoma or mass it causes a lot of pressure that can cause brain herniation and whenever it leads to this brain herniation this can lead to a very particular triad called cushing's triad and one of the components of cushing's triad is low heart rate they also have hypertension and they can have irregular ir respirations so they can have irregular respiration rate a low heart rate and hypertension due to high intracranial pressure so again this one will come up on your exams probably doesn't happen that often though in real life but again think about that decrease automaticity what reasons increase vagal tone slowing av conduction decreasing metabolic activity don't forget this one hyperkalemia and high intracranial pressure or leading to cushing's triad the other thing is what is going to increase the automaticity so now let's talk about those factors factors that increase the automaticity okay we already know the primary one the big one that i want you guys to take away is the sympathetic and parasympathetic tone right so automaticity so automaticity we said the big one main reason is increased sympathetic nervous system tone via the t1 t5 outflow big reason really need you guys to remember this one hypovolemia if someone is hypovolemic that can be a primary reflexive type of thing so whenever someone's low has low blood volume it leads to low blood pressure you guys remember our video on blood pressure regulation if not go watch our video a low blood volume low blood pressure creates a reflex which activates your sympathetic nervous system sympathetic comes in increases heart rate and does what vasoconstricts the blood vessels so that's one way that our sympathetic tone is kind of a reflexive thing the other reason here is usually due to hypoxia so some type of underlying hypoxia you know hypoxia is when there's low oxygen delivery to the tissues there could be many reasons if you guys haven't watched our video on hypoxia watch our videos on hypoxia as well but usually this could be due to low red blood cells so someone has anemia very severe anemia if they have maybe some type of underlying lung disease like copd or you know what else what if they have some issue where there's a clot in their pulmonary vessel like the pulmonary artery and blood's not getting to the lungs to oxygenate pulmonary embolism this is actually one of the most common arrhythmias associated with pulmonary embolisms people always say it's all that s1q3t3 no sinus tachycardia is the most common arrhythmia associated with pulmonary embolism so again don't forget pe is another potential cause all right so these are some of them another one don't forget about this one is what if someone is taking a drug that acts like epinephrine and or epinephrine it's kind of a sympathomimetic that could be another reason and the big thing you need to remember is usually certain types of drugs like what sympatho mimetic sometimes i gotta catch my brain up with writing sorry some pathomimetics this is usually things like cocaine methamphetamines or drugs that we use to increase people's heart rate okay the other thing is besides sympathetic so drugs that mimic the sympathetic nervous system is sometimes just remember your hypothalamus is a part of your limbic system so sometimes if people are experiencing pain or anxiety that can activate the hypothalamus activate the sympathetic nervous system and again increase heart rate so also be on the awareness of particular types of pain or anxiety as other causes of this the last thing is if you increase metabolic activity of your cells if you increase metabolic activity that may increase the electrical activity and this is associated with opposite of what was decreased so it's going to be seen with fever and it's also going to be seen with hyperthyroidism okay so hyperthyroidism now the last thing that i want to say before we move on here is that what type of arrhythmias are usually associated with a decreased automaticity and which ones are associated with a increase in automaticity so decrease automaticity i want you to be thinking about what type of arrhythmia i want you to be thinking about sinus bradycardia okay whereas in someone who is actually having what increased sympathetic tone which is causing increased vagal tone this is most commonly associated with sinus tachycardia you can see this with some atrial and ventricular arrhythmias but this is going to be the most common cause for these arrhythmias okay now that we've drilled that let's move into triggered activity all right so we finished up talking about automaticity now the next type of cause for underlying tacky arrhythmias is triggered activity really simple straightforward what happens is you guys know you have your normal conduction system sa node av node bundle of hiss bundle branches and burkinases and that's our normal conduction system let's say that you develop an irritable area right some irritable area within the ventricular myocardium or some irritable area within the atrial myocardium and because it becomes irritable due to these underlying causes which we will discuss it starts firing and because it starts firing it's not following what your normal sequence of conduction going sa node av node downwards it's going in at from an ectopic area an ectopic pathway because of that that's considered to be an arrhythmia that was the definition of arrhythmia what are the underlying causes for these areas becoming triggered that's important the first thing that you need to know is let's say we zoom in on either of these cells we'll just pick the ventricular one for this case let's say this irrita the cells become irritable when it becomes irritable it starts producing a particular type of abnormal depolarization called an early after depolarization again we'll talk about what this means whereas in this cell let's say it's also becoming irritable it's just another type of cell it becomes irritable and it produces what's called a delayed after depolarization and again we'll go over these in more detail with these graphs here but reason why i'm telling you this is that eads and dads have different underlying causes and produce different types of arrhythmias eads are most commonly associated with what it's most commonly associated with electrolyte imbalances like low potassium low calcium low magnesium or it also can be associated with particular drugs and this is super important we're going to create a little mnemonic for you a b c d e anti for all of them a rhythmics which once one a one c these are your sodium channel blockers and three potassium channel blockers anti biotics the most common ones are going to be your macrolides right so these are your myosins zithro erythroclarithomycin then your anti we're not spelling it right but it's going to help with the mnemonic psychotics and this is going to be like haloperidol another one is called zoprazodome okay or risperidone there's many different types of other antipsychotics and then the next one is anti-depressants and the big one here is going to be your tricyclic antidepressants but the other ones that you want to be taking consideration are also to a smaller degree your ssris so tcas tricyclic antidepressants these are another potential trigger and then the last one here is going to be your antiometics and this is going to be something like ondonzotron which is also known as zofran right let me talk about its brand name all right these are very strong triggers for eads so again i want you to remember that all of these particular things here are very strong triggers for these myocardial cells and then from that they produce an early after depolarization remember these causes the next thing is what are the underlying causes for delayed after depolarization they're less clear a little bit more ambiguous but the big one that i don't want you to forget the most common reason is going to be underlying ischemia so if someone has some underlying ischemia maybe they're having an active mi right so they're having an mi or they're having some type of coronary artery disease of some form and this is producing some irritation to these ventricular atrial cells other reasons is because you could have some type of underlying hypoxia and this hypoxia could be due to a lung disease of some form or maybe other reasons as well it also could be due to inflammation you know there's particular inflammation of the myocardium what's that disease called myocarditis that could be a very potential uh intense one as well another reason is because you're really stretching the myocardium and as you stretch the myocardium believe it or not it really alters the activity within those cells they're normal depolarization repolarization what are conditions that really stretch out the myocardium dilated cardiomyopathy and mitral regurgitation are two big ones so again ischemic causes hypoxic inflammation stretch associated with these two diseases the next one really important one is some increased sympathetic tone due to any of the underlying reasons we talked about over here with increased automaticity that could also trigger that and the last one that i want you to remember here is dig toxicity so digoxin toxicity can also precipitate some of these effects as well when these cells are irritated due to these underlying causes they generate a delayed after depolarization why am i stressing so much on this here let me explain why so why am i stressing so much on knowing these eads and dads the reason why is remember i told you eads and dads produce a special type of arrhythmia the really big one that i want you to remember is that eads are commonly associated with a particular type called a poly vtac with a long qt interval what do we call that guys torsodes de points okay really important to remember that so what in the heck is an ead believe it or not it's really simple okay let's say you take that normal contractile myocardial cell and when you look at this it has this normal kind of waveform where it has a depolarization due to sodium ion influx a plateau due to calcium influx and potassium leaving and then a repolarization due to potassium leaving this is kind of their normal depolarization and kind of like contractile waveform now let's say that at this point here as the cells in its plateau phase you agitate the living crap out of this cell and because of the low calcium potassium magnesium or drugs it becomes so agitated that it comes out of repolarization and starts firing that can produce that torsade points so that's really the underlying cause and the underlying kind of mechanism behind these eads is early depolarization that comes just after the previous depolarization from the normal contractile myocardial cells in the opposite situation here let's say that we talk about a dad a delayed after depolarizations these are commonly seen with multi-focal atrial tachycardia focal atrial tachycardia and also v-tac but not the polymorphic v-tac with prolonged qt monomorphic v-tac and polymorphic v-tac with normal qt intervals very important okay so once we have that the same mechanism but again i'm telling you guys it's so simple because it's literally within the name normal waveform we already talked about this but all that happens here is that instead this was early after depolarization so the normal depolarization is this up one and you're still depolarizing in this kind of like somewhat of a plateau phase so right here is you're still kind of depolarizing as you go down you're repolarizing so at this point it's a little bit later after depolarization has occurred at this point in this point so maybe about right here this ventricular myocardial cell or atrial myocardial cell is going to start causing some of these irritable depolarization waves and these are called your dads okay so again that gives us the underlying mechanism and the arrhythmias associated with these a particular pathophysiological mechanisms now let's go into re-entrant circuits all right so the next type of pathophysiological mechanism i want to go through is re-entry and again this is associated with the tachyarrhythmias what is re-entrant circuits before i start these i want to preface that re-entrant circuits are usually seen in a couple types of arrhythmias and we'll explain some of these in more details than others the ones that we'll talk about a lot is your av nrt and avrt which we said these were kind of your svts if you will right so we kind of call this your what your proxismal superventricular tachycardia or svt the other ones that are associated with re-entrant circuits a really interesting one is atrial flutter but another atrial rhythmic called atrial fibrillation remember we said vtac could also be associated with triggered activity v-tach and v-fib can also be seen in with re-entrant circuits so there's other reasons that they can also generate arrhythmias besides triggered activity it could be they have little reentrant circuits and we'll talk about what those are the one that i want to spend a little bit of time first discussing with is the avrt this is a really interesting one so let's talk about this one here and this is the avrt again what does that stand for atrioventricular reentry and tachycardia what happens in this first thing you need to know is that atrioventricular reentering tachycardia is due to an underlying accessory pathway that exists between the atria and the ventricles most common area is usually left atrium on between the left atrium left ventricle that's sometimes it's called avrt is usually seen with wolfe parkinson's white syndrome right that's one of the most common subtypes of avrt usually there's this accessory pathway in this between left atrium left ventricle and it's called the bundle of kent so what is this accessory pathway called so you have again you have what's called an accessory pathway and the most common type here is going to be the bundle of kent there is another one called the bundle of james you might see that also in your your studies and it's associated with longan levine syndrome but this one is the big one because the bundle of kent is seen with wolf parkinson's white syndrome now what the heck does this accessory pathway do well remember it's like an electrical window in other words if you have some electrical activity that's coming from the atria down through this it can pass information down to the ventricles if you have information coming from the ventricles it can pass information up to the atria so it's a bi-directional accessory pathway that's very important you wonder why because there's two different types of a wolf parkinson's white syndrome or again avrt the first type that i want us to talk about is the most common type and this is called orthodomic avrt orthodontic avrt is going to be the most common type of or particularly avrt and this right here is usually whenever you have electrical activity that can start at the sa node right it can even start somewhere else but sa node generally going to the av node but here's the important part it goes down the av node through the bundle of hiss down your bundle branches down your purkinjes depolarizes the ventricles right normally in a normal conduction pathway it stops there the ventricles depolarize then they repolarize and then the sa node fires again but guess what these individuals some underlying congenital cause they have this tissue guess what happens when the ventricular ventricles depolarize they can pass right back into the atria come back down stimulate the av node and go back down the circuit again and if they have fast atrial rates this can produce really high tacky arrhythmias pretty fast ones sometimes so this is called orthodomic avrt and the big thing i want you to remember is it goes down which way goes down the av node and comes up the bundle of kent that's important for another reason why if it goes down the av node and up the bundle of kent it's following your normal conduction pathway that means that the ventricles are going to depolarize at the same time right and left that produces a narrow qrs complex remember that orthodontic avrt narrow qrs what did i say orthodontic avrt narrow qrs why am i stressing that there's another type of avrt called antidromic avrt way less common but again a little bit more lethal reason why is this electrical activity goes the opposite direction if the atria is firing it'll go where through the atria instead of going through the av node it'll go through the bundle of kent come up through the ventricles depolarize the bundle branches depolarize the bundle of his av node come back into the atria and then move back down the bundle of kent again that is the dangerous one you want to know why because if someone's having like a-fib or something like associated with this anti-drama kvrt that means every atrial fibrillation kind of firing that they have will be able to go through this accessory pathway completely unregulated and the atrial rate and ventricular rate can almost equal one another big thing to remember bundle of kent is not as regulated as the av node av node conducts slower bundle of kent will conduct things really fast so that can be really dangerous also with antidramic avrt think about it is it following the normal conduction pathway sa node going through the atria going down the bundle of kent no it's not going down the av node and downwards so because of that because it's going which direction down the bundle of kent and up the av node it's not following the normal conduction pathway and that produces a wide qrs complex that's important to remember okay that's how we kind of differentiate these two really now that discusses our avrt the next thing i want to talk about is the av in rt remember i said we were going to focus on two of these primarily with av nrt there's a abnormal pathway that is developing within the av node all right we said avrt is usually like a congenital cause associated with this bundle of kent av node usually has some type of underlying cause which we have to talk about but there's an abnormal pathway so what i want to do is zoom in on the av node look at this abnormal pathway and talk about the underlying causes of it so again we're zooming in on this av node here right so here is going to be our av node and just to give you kind of some information let's say that this electrical activity coming here it's coming from the atrium maybe from the sa node and it's coming down into the av node and what it would leave what what's after the av node what would this structure here be we'll abbreviate it bundle of hiss what would it come after the bundle of hiss the right bundle branch or we'll come after this this side the left bundle branch so we kind of have our normal kind of flow here that we know about our normal conduction system let's say the atria fires when atria fires normally goes down through the av node moves through it completely and then to the bundle of hiss and the bundle branches but in people with av and rt they have an abnormal pathway and the reason why is usually there is some type of underlying fibrosis or scarring that is occurring within the av node what is the reason for this scarring or this fibrosis this could be due to again what is this associated with this avnrt this can be seen with myocardial scars maybe they had a history of myocardial infarction maybe they've had heart surgery before and that's the reason for the scarring that's occurring during the av node or maybe they have some type of fibrosis you know as people get older they can develop some idiopathic fibrosis that can occur within the av node as well so scarring fibrosis these could be some reasons because of that underlying scarring or fibrosis it produces an abnormal two abnormal pathways that occur within the av node let's talk about these this pathway here which we're going to talk about it's alpha pathway this pathway here is called the beta pathway big thing i want you to know alpha pathway versus the beta pathway really straightforward here with the alpha pathway big thing i want you to know is that they have slow conduction they don't conduct action potentials through that pathway very fast because of the underlying usually fibrosis of that area whereas in the beta pathway there's usually fast conduction so it's producing it really fast through this area the underlying thing here is that these have slow fast conduction but alpha pathway because it conducts slowly it kind of repolarizes and goes through its refractory period much quicker so it has a short refractory period whereas in the beta pathway this has a long refractory period because of its underlying fast conduction let's explain what the heck that even means atria fires moves down through the atria into the av node as it comes into the av node it can bifurcate into these two areas which way would it go well i can go into the alpha pathway and then go into the beta pathway remember alpha is going to move really slowly okay and the beta path that i think is going to fly like a [ __ ] it's going to fly through here and it's going to go down the bundle of hiss into the bundle branches and then down into the ventricles depolarizing the ventricles but it moves so fast that it goes up the beta pathway and as it approaches this kind of wave coming down here they both cancel each other out and then depolarization within the av node ceases after depolarization ends what has to happen repolarization so they start going through the refractory period now remember if we were to have the next stimulation here from the atria coming down into the av node think about this here which one is going to come out of refraction first the alpha pathway but what's going to happen to the beta pathway it's not going to be out of refraction so let's kind of highlight that here let's put like a kind of a dark green thing here saying that hey you can't stimulate me because i haven't come out of my actual refractory period because it's longer you can go down the alpha pathway though so what happens is next time the atria fires and it comes into the av node it'll bifurcate and go only this way through the alpha pathway go down the bundle of hiss to the bundle branches go down depolarize the ventricles here's the thing though and it's so cool because it moves so slow down this actual alpha pathway and gets down here to go to the ventricles by the time it gets down to this point guess what else happens this beta pathway starts coming out of refraction as it comes out of refraction watch what would happen let's imagine we kind of skip forward a second here it kind of comes down this pathway here we're already at this point here right this whole thing came out of refraction this sent this impulse down into the ventricles ventricles depolarized then what happens this has already come out of refraction so guess what these waves come up the beta pathway as they come up the beta pathway they send electrical activities up to the atria cause the atria to polarize then it moves back down the alpha pathway sends an action potential down to the ventricles and comes back up the beta pathway sends another electrical activity and goes back down do you guys see the whole point here it's creating a re-entrant circuit that's not going to stop and because of that re-entrant circuit every time it's going through the circuit it's spitting off these electrical kind of like vectors that are going into the atria and into the ventricles and causing them to polarize at fast rates that's why this can be problematic and that's the underlying mechanism big thing i need you to remember is there's two ways that this can happen the most common the most common type of av nrt is going to be when it goes alpha to beta or we say slow fast pathway okay so going this this which we just talked about is the most common really uncommon for it to go the other direction okay fast slow that discusses that let's finish up talking about these other really uh smaller ones atrial flutter afib vtec vfib so really quickly let's talk about atrial flutter the only reason i wanted to mention this one is because there is this abnormal re-entrant circuit that occurs right here at the tricuspid valve area at the tricuspid valve there's this really abnormal uh reentrant circuit and so atrial flutter has a large re-entrant circuit near the tricuspid valve or we call this the cavo tricuspid isthmus and this can produce some really fasty nas rates at nasty rates as well so again cable tricuspid isthmus can produce re-entrant circuits that are pretty pretty fast okay now the next thing we have to talk about is a-fib v-tac v-fib okay with atrial fibrillation you get multiple little irritable areas within the ventricles that create their own re-entrant circuits and then fire things down into the av node and down to the ventricles with vtac again one little irritable area that can generate re-insurance circuits as well v-fib multiple little areas that are generating re-entrant circuits so the whole thing that i want you to understand here is the underlying reason for avrt av nrt talk about this slow fast pathway and then talk about this large re-engine circuit with atrial flutter and multiple re-entrant circuits with afib and v-fib and a large re-entrance circuit associated with v-tac okay now that we understand this let's finish up with conduction block all right ninja so let's finish up with the last pathophysiological reason for these arrhythmias so we talked about how brainy arrhythmias are associated with decreased automaticity right we already talked about that and we finished up all the underlying reasons for tachyrhythmias the last reason for brady arrhythmias is a conduction block this is really easy it's pretty much just like the sinus brady it's just we really shut down that av node instead of slowing av conduction we really kind of shut down av conduction pretty hard so some of the reasons are actually going to be the same so what would be some reasons i shut down this av node what if i just completely kick the blood supply that's going to it what is that called am i so their right coronary artery generally supplies this av node so if someone develops what's called an inferior wall mi due to a right coronary artery occlusion that could be one potential reason for that av node being jacked up and not sending action potentials down to the ventricle the other reason is due to underlying fibrosis so what if somebody has some underlying fibrosis of this av node and because it's fibrotic it's not conducting electrical activity as well so it's slowing down or really not allowing electrical activity to move down through it and into the ventricles that could be another reason another really big one we talked about over there but don't forget it guys is hyperkalemia if someone has really high potassium it really alters the electrical activity within the resting membrane potential the next thing that you have to be thinking about is drugs what if i give drugs that really just shut down or block the conduction through the av node what if i give things like beta blockers or what if i give things like calcium channel blockers or what if i give things like digoxin these are all drugs that can really shut that down as well okay the next thing i need you to be thinking about is what if there's some type of infiltration i put deposits in the av node i really deposit that thing up what if i have certain infiltrative diseases so infiltrations from conditions that are rare but you should know them amyloidosis or sarcoidosis these are potential things that you want to be thinking about as well okay the next really really big one that you guys can't forget it comes up a lot is there's a nice little bacteria that really jacks up this av node and it comes from a tick it's called lyme's disease so lyme's disease is another potential reason that someone can develop this so again lyme's disease is usually due to a bacterial infection caused by the borrelia burgdorferi there can be other reasons like if someone is developing some type of underlying cardiomyopathy that's kind of really changing the overall structure of the myocardium but these are going to be some of the most common reasons for someone experiencing a conduction block if you guys remember the most important ones do not forget inferior wall am i lyme's disease beta blockers and high potassium these are going to be the big ones that you guys really need to remember for the conduction block boom roasted let's move on to talking about the ekg differences in treatment all right ninja so now let's talk about the ekg differences between these arrhythmias and then come up with a nice little treatment plan so how do we go about this nice little algorithm first thing determined too fast too slow if it's too fast it's attacking me too slow brady arrhythmia let's say we start with this too fast it's too fast we know it's a tachymeter it's one of these four categories how do i figure out which category it's in first thing i do is after i find out that it's too fast i check my qrs complex that's my first thing i do so i'm going to go ahead and i'm going to draw out here just a quick little diagram of a q r s complex first thing i need to know about my qrs complex is the width the normal kind of like what you would like it to be is if it's less than 0.12 seconds that's normal and so since it's going through your normal conduction pathway av node bundle of his bundle branches then we consider that to produce a nice little narrow qrs that's good okay it means we're following our normal conduction pathway if it's greater than 0.12 seconds that means we're not following the normal conduction pathway it's not going from av node down to the purkinje it's hitting a block or it's the the origin of the actual rate is coming or the origin of the conduction is coming from some other area so because of that that produces a wide qrs complex so too fast narrow wide now i have my narrows and i have my wides well what's the difference between these well now i can categorize these but now the next thing is is it regular or is it irregular how do i determine that the next thing is i'm just going to draw a couple qrs complexes here right if i draw a couple qrs complexes you have the upright wave the upright wave is your r wave right what i want to do is is i want to measure the distance from the r to r to r to r to r to r to r right so it's called your r to r interval the r tar interval what i want to do is is i want to measure the distance if the distance between each r wave is the exact same that is a normal kind of regular rdr interval so it's considered to be a regular rhythm so if the rdr interval is constant so we'll put normal r to r interval right then that is going to produce a regular rhythm if that is not a consistent or there is an abnormal r to r interval then that is an irregular rhythm okay so that's the first thing i do now let's take it just one extra step here when you're looking at these 12 lead ekgs you get these little boxes on the ekg how the heck do i know if it's greater than 0.12 seconds zach one little tiny box on the ekg is about 0.04 seconds so three little boxes .04 times three is going to be 0.12 seconds if it's greater than three little boxes that would be what a wide qrs complex okay and then the next thing is when you're looking at your ekg just take a piece of paper and put just put a little line on the piece of paper line it up with two rdr intervals put a line on that piece of paper line on that piece of paper and then just keep tracking at each point of the way to see if the r intervals match up with that little things you drew on the paper if it does it's normal if it's not it's irregular pretty simple trick right okay boom too fast we've now categorized it into narrow wide and we know if it's regular irregular now what are the differentials within these groups nice and nice i'm glad you guys asked i know you guys are asking right narrow qrs regular i want you to think of a couple first one i want you to think of we're going to abbreviate the sinus tac the next one is focal atrial tachycardia fat or it could also be av rt or av nrt what do we kind of group this as your svts right we kind of called this your psvt proximal supraventricular tachycardia and the last one is atrial flutter now that is our differential for narrow qrs with a regular rhythm what if it's a narrow qrs irregular rhythm the first one that i want you to be thinking about first one on the top of your differential should be atrial fibrillation after that the next one is atrial flutter with a variable block i'll talk about what that means and how to identify it and then the last one is multi-focal atrial tachycardia okay so narrow qrs regular we know the four in the differential neurocure is irregular we know the top three in the differential wide qrs regular rhythm first one no matter what you better think this right at the top of your head v tac right we'll put tac vtac and vtac when we're talking about this one is a particular type of vtec you see all the qrs waves that we're going to be talking about they're all the same morphology so because of that what did we say that was called monomorphic vtec the other types is going to be svt superventricular tachycardia so one of the avrt or avnrts with aberrancy which is called a bundle branch block so there's a block and we'll talk about what the heck that means in a second and the last one is going to be anti-dramic avrt okay this is the least common one probably the lowest on the differential the two big ones that i want you to remember is vtac and svt with the bundle branch block the last thing is if you have a wide qrs and an irregular rhythm then what do we have this is your polymorphic vtac remember there was two types of polymorphic vtac one is you had the normal qt and the other one is you had the long qt interval right and what do we call the long qt interval torsades to points so don't forget about what that one will put t d p towards the points the next one and again you see this one it's probably gonna poop your huggies afib with wolf parkinson's white syndrome and the last one which believe it or not is actually one of the most common types of wide irregular rhythms is afib with aberrancy meaning it has a bundle branch block and then there's one last one but it's usually a result of a breakdown from polymorphic vtac or afib with wolff-parkinson's white syndrome and this is called ventricular fibrillation you see this one not good you got to get immediate kind of cpr going all right so we now have categorized all of our tachyrhythmias beautifully we have our differential of which one it could be now what we got to do is we got to take a look at some of these ekgs and say okay which one would it be if i see this this and this here's the great thing here's what's nice about this some of these even if you can't identify the difference you can treat them empirically and see which one improves and that usually helps you to differentiate which rhythm it is so now let's go ahead and talk about the ekg differences let's talk about our differential let's get into a little bit more detail so we have our differential sinus tac focal atrotachocardia svt atrial flutter which one is it how do we identify it first thing let's look at this first ekg when i look at this ekg the first thing i want to know is is it sinus rhythm in other words how do i determine if it's sinus rhythm is there a p wave that i see visible before every qrs complex that's the first thing i want to know so let me write that down is it sinus tac how do i determine if it's sinus tac is there p waves present okay yes there is let's take it one step further when you're looking at a 12 liter kg the best way i've found to determine if it really is sinus is you find p waves and we're going to put an up arrow those p waves are upright in lead 2 but they are inverted we'll put a down arrow in a v r meaning that they're kind of look like a u that is one of the big identifiers that it's most likely sinus tax so i see p waves upright lead to inverted an avr this probably a sinus tag do one more thing to make sure make sure that after every p wave is a qrs complex and after every qs complex there is a t wave if it is it's normal sinus rhythm but there's some tachycardia occurring with it where you're actually going a little bit too fast that's the first thing now how fast do these usually go said sinus tack it usually doesn't get above 150 okay it can sometimes but usually doesn't get above 150. so that may be another small identifier all right we've knocked that one out the next thing is i'm going to look at the next ekg oh zach what is going on here these p waves are there but they don't look the same they're actually inverted huh but there is a after every p there's a qrs and then a t wave so it looks like sinus but the p wave isn't upright assume i'm talking about this as lead two so this arrhythmia here is focal atrial tachycardia usually one of the most common presentations of focal atrial tachycardia is an inverted p wave the reason why is remember your electrical depolarization from ekg basics video sa node down to av node creates a depolarization vector that kind of goes downwards towards the left pointing towards the positive electrode of lead 2. if the left atria let's say there's a little focal area that's firing from the left atrium and it's depolarizing the atria moving in this direction away from the positive electrode of lead ii what does that cause an inverted p wave that's usually the most common type of focal atria tachycardia so it's going to look opposite of sinus tack for the most part so they'll have p waves but guess what they will be inverted and lead to an upright in avr and there's a p a qrs and a t wave usually now one quick little tip for you is let's say that you see an ekg you see that there's an inverted p wave and lead to an upright and avr and you're like oh zach said this is focal at your tachycardia before you even assume that you better go back into the room make sure that the leads are actually put on properly and that they're not misplaced because that might be the reason why it's actually inverted okay so make sure that it's not misplaced and if it is it's most likely vocally at your tachycardia all right let's say that we have figured out that it's this one or this one now we go to the third one the next one is let's say that i say okay is there p waves oh man i'm looking at this i don't really see any p waves instead i see these jacked up sawtooth waves where are these things these don't even look like p waves whatsoever these sawtooth waves are usually identifiable as atrial flutter so this would be something that i want you guys to be thinking about with atrial flutter look for sawtooth waves and usually these sawtooth waves are most visible in leads 2 and leads 3 and an avf if you don't see it there i like to take one other lead that i take a look at and that's v1 so also take a look at v1 usually because of that re-entrant circuit it's going counter-clockwise it produces inverse sawtooth waves and two three avf so again take a look there see if you find it next thing one more thing to add on to atrial flutter what do you notice that these aren't p waves but they look like they're called flutter waves or solitude waves do you notice a pattern two flutter waves qrs two flutter waves qrs so there's a two to one ratio pretty much going throughout this and it's constituted one throughout the entire arrhythmia usually with atrial flutter if it's regular and narrow it has a constant ratio in this case this is a two to one ratio but maybe it could be in other scenarios a one to one a three to one a four to one so that's the important thing to remember is you need a constant ratio two to one the entire time okay we'll talk about why a little bit later last arrhythmia okay this one i look at and i'm like whoa exactly to look for p waves i don't even see any p waves i don't see any flutter waves i don't see any p waves so the p waves aren't even there the p waves in these scenarios guess what because of this last arrhythmia the p waves are actually usually hidden within the qrs complex if you get lucky maybe you might get a kind of a little inverted or retrograde p wave that comes after the qrs complex sometimes but this is most likely indicative of what if i don't see p waves it's most likely avrt or avnrt which is a type of svt alright so what do we say it could be it could be av rt or av nrt and again this was the way that we kind of describe svt again what do we say we should be looking for with this look for either no visible p waves because they're probably actually hidden within the qrs complex or if you can find some retrograde p waves and if you want to try to find those retrograde p waves usually they're best seen in the same things that you see for atrial flutter 2 3 and avf okay so that's the big thing that you guys want to be looking for when you're talking about narrow regular how do i figure it out go through these steps figure out which one it is but here's the thing let's say that you don't figure it out that's fine what i can do is the first one that i want to try to try to differentiate with is sinus tack i really want to try to figure that one out first try to find if there is p waves if not sometimes what i would do is give them fluids usually the fluids will improve and make it more visible with sinus attack but let's say that you figure out that it's sinus attack if it is first thing that you do is treat the underlying cause what did i tell you the underlying cause was primarily for sinus tachycardia increased automaticity which was most likely due to increased sympathetic activity what was the first thing i told you was a very strong stimulator of sympathetic nervous system activity hypovolemia what would you give them fluids that's why i said usually give the patient with sinus attack fluids they will improve usually whereas these other ones they won't really improve that much with fluids so that's the first thing i like to do is give fluids and then try to figure out the other cause maybe they have a fever give them tylenol maybe they have epoxy give them oxygen maybe have a pee i gotta give them heparin or tpa figure the underlying cause treat that it usually obliterates the sinus attack now if i find out that it's not sinus tack i got these other three that i got to deal with guess what treat them the same how do you treat them first thing you'll do is in the short term to stabilize them is start off with so we're going to say treating these start first with what's called a vagal maneuver sometimes these work sometimes they don't what you do with a bagel maneuver is you can do a couple things you can either have them kind of bear down like they're gonna you know poop or something like that you can either do that or you can take like a little syringe and have them breathe and kind of blow into the one and try to push the plungers back as far as they can that creates the same kind of effect increasing the intrathoracic pressure and increasing the vagal tone if you increase vagal tone what does that do to the av node it slows down the conduction and it helps to obliterate this supraventricular tachyrhythmia sometimes it doesn't work though so what's the next thing that you do you give a drug that actually blocks it hardcore but it's a short acting drug you can give like six milligrams of it and this is adenosine really blocks that av node pretty well usually will obliterate the svt or the avrt or avnrt sometimes it won't hit the atrial flutter in the focal atrial tachycardia so what's the next thing that you might have to do for atrial flutter or focal atrial tachycardia if the adenosine doesn't work you have a beta blocker or a calcium channel blocker so the next thing that you'll try is a beta blocker or you can try a calcium channel blocker the only reason you do one of these is depending upon contraindications now let's say that you try all of these things and it doesn't work and you haven't been able to obliterate this rhythm the next thing that you can do is you can electrically cardiovert them you hit them with electricity and this is called cardioversion okay electrical cardioversion in this situation the other thing reason you can cardiovert them is let's say that they're in this rhythm and all of a sudden they start becoming hypotensive remember these three causes hypotensive altered mental status or if they start having chest pain or any pulmonary edema if any of those reasons arise you cardiovert them before you do anything else because they're unstable at that point in time but if you tried all of these and it still doesn't work you can still do cardioversion but you cardiovert immediately before these if they're unstable okay after we've treated them stabilize them then what am i going to do long-term treatment i got to be thinking about right so what am i going to do to kind of fix this from happening again there's one particular treatment where you take some radio frequency waves and burn the re-entrant pathway in the avr tier the re-entrant evr pathway and the av nrt i'll burn the cable tricuspidism so it doesn't actually create re-entrant circuits i'll burn the ectopic focus with photoatrial cardiac tachycardia and they won't generate for the most part these abnormal rhythms so because of that that's another option is what's called radio frequency ablation of the abnormal tissue from the underlying pathophysiology we talked about it's all coming together right beautiful we've tried to figure out these causes we figured them out we treated it now let's figure out the next one which is narrow irregulars now let's go to the next one narrow irregular rhythm i have my differentials a-fib atrial flutter with a variable block are multi-focal atria tachycardia what do i do okay first thing is i look for p waves same thing do i see p waves no in these situations i don't really see any p waves oh wait i do i see one in this one we'll talk about that one in a second it does have a little bit of p waves but it's really weird one i don't really like this rhythm but we'll talk about it last first thing i do look for p waves are the upright lead to inverted navr and are we following the p qrst pathway let's look at this rhythm am i doing that no there's no p waves no visible p waves okay so there's no visible p waves what the heck is this little squiggly lines right here that are coming before the qrs complexes these are called your fibrillation waves and these fibrillation waves are due to these little multiple ectopic foci that are firing or those multiple re-insurance circuits that are firing and this is something that will tell you that this could be most likely atrial fibrillation so what am i looking for i'm looking for fibrillation waves so fibra umulation waves most visible in v1 that's the first thing i look for fibrillation waves present most likely in v1 the next thing i look for is after i've tried to determine if it's afib is i look for that classic this one is so classic remember you're looking at those rdr intervals it's so irregular it's insane your r intervals are all over the place so they love to give this i don't know it's a stupid term but they like to call this an irregularly irregular rhythm okay so sometimes you might see that come up on your exams because it's just so awkward of a rhythm all right you see the fibrillation waves you see this super abnormal irregular rhythm again this is the one that i want you to see is the most common type of narrow irregular remember these fibrillation waves we kind of put like a little a little f with it right so these little fibrillation waves that you're seeing here sometimes it's little f again if you see fibrillation waves most common of v1 and irregularly irregular rhythm it's afib next thing let's say that i go to the next type of arrhythmia here i don't see fibrillation waves but i don't see p waves but these look familiar don't they guys oh wow this had it's like flutter wave again those sawtooth waves that i was talking about before but i thought atrial flutter was a regular remember i told you it can also be irregular so with atrial flutter this is the next one that i want you to remember again you're seeing sawtooth waves you're seeing these nice little sawtooth waves and again where are they most visible test your knowledge two three avf you don't see it there take a look at v1 here's the thing that we got to talk about because we said atrial flow over there was a regular rhythm let's explain why why is it irregular here look at the flutter waves two flutter waves qrs complex one flutter wave one qrs complex two one one and two you keep going back and forth between a two to one ratio and a one to one ratio that should make sense if i have two flutter waves and then a qrs that's going to produce a different distance between the r and r intervals that's common sense right so because of that that's why we use that term variable block where they have in this case a two to one and a one to one type of ratio and that is where we get that term that variable av block okay all right beautiful next one we have no fibrillation waves we have no flutter waves but i do see p waves i see a couple of them but they don't look anything like they should if i see these and i see no like normal p waves oh wait i see one because i have to have something to compare to that's why i hate this rhythm if you don't have any kind of normal p waves to compare to it's kind of hard to identify as being abnormal let's say i have a normal sinus p wave in this situation and i look here at this p wave and try to compare it oh wait that's inverted that's not the same boom there's one that one's kind of pointed that one's more rounded that's a different one this one looks all kinds of jacked up it's like an m that looks nothing like that and this one does kind of look like it but i have three morphologically different p waves in this situation and again it's because they're different means that they're coming from different areas in the atria one area is firing another one is firing it's producing different p waves that's why they're different morphologies and some of them may be closer to the av node some may be farther from the av node and that's why the rdr intervals are different because it's depending upon where that ectopic focus is in the atria maybe a farther distance or shorter distance so what is this one here called so with multifocal atrial tachycardia multifocal atrial tachycardia what do you guys need to remember besides this being kind of a stupid arrhythmia it is three or more morphologically different p waves the next thing is that it has to be tacky the reason why it has to be tachyarrhythmic or greater than 100 beats per minute is because there's another rhythmia that looks just like multifocal her tachycardia but it's a normal rate that's called a wandering atrial pacemaker so don't confuse them the next thing i want you to remember with multi-focal atria tachycardia is that it's due to an underlying they have some underlying disease that's causing this and if you fix that it fixes the issue kind of like sinus tack in a way this is usually due to some type of lung disease like copd or maybe even a pulmonary embolism or due to an underlying heart failure these are two big conditions you guys want to remember with multifocal atrotachocardio okay boom we've determined which one of these arrhythmias it is based upon our algorithm and our differential the next thing we have to do is start treating it let's treat these the same way we would treat up here you can try a vagal maneuver on these ones but generally it's not going to improve so you can try it but generally it doesn't really work so most likely if you see a narrow irregular you can try adenosine adenosine usually doesn't work as well either so the next thing that you're going to go to here is you're going to go adenosine and you're going to probably go most likely first if you see narrow and irregular you're most likely going to reach first for a beta blocker or a calcium channel blocker because again which one that i say is the most common cause afib afib doesn't usually respond to adenosine you can give it a shot but most likely you're going to go to a beta blocker calcium channel blocker first after you've tried that let's say it doesn't work if that doesn't work the next thing you're going to do is the same process up here cardiovert them hit them with electricity to try to re-start that hard and to generate a whole new rhythm again big thing you guys can't forget here is that after if any of these arrhythmias at any point in time become unstable what do we define that as hypotension pulmonary edema chest pain or an altered mental status you hit them with electricity regardless you can also do it if this isn't working okay now after i've cardioverted them i have to have some long-term treatments that i can use to prevent these things from happening now we're going to have another electron atrial fibrillation because it's one of the most common arrhythmias so we'll have to talk about this one in more detail but for the just the basic part here long-term treatments of these arrhythmias again same thing burn the abnormal chemotricuspidismus burn the ectopic foci burn the multiple ectopic foci in these situations and that is called radio frequency ablation the other thing that you also want to consider especially for afib so if someone has atrial fibrillation okay sometimes atrial flutter but afib is the big one that you don't want to forget you have to do what's called a chad vasque score and that you can plug that into your little md calc it's like you know there's a particular thing that you're looking for in a point system here we're not going to go into too much detail on it but if you calculate this and it's greater than 2 that is telling you that they have a high need to be anticoagulated so what you'll do is you'll start them on anticoagulants okay to try to prevent these individuals from developing a deadly imbalance that can spread to multiple different areas the most deadly one or scary one is into the brain leading to a stroke so that's the big thing is radio frequency ablation and afib really got to try to anticoagulate them if there is need based upon that score okay and sometimes they may need long-term management with a beta blocker a calcium channel blocker same thing if someone has atrial flutter they may need a beta blocker long term okay so we talked about the narrow irregular now let's hit our wide and regulars let's talk about our wide regulars okay we got our vtac svt with aberrancy these are the two big ones again anti-dromic avrt it can happen but i want us to talk about it more with the wide irregular so let's focus on vtac and svt with aberrancy here's the thing when you look at this one you'll notice wait zach how do i know i thought there's supposed to be two rhythms because there's two things that you wanted to talk about primarily that's what's tough about this one with this wide regular weathermark what's called a wide complex tachycardia it can sometimes be very very difficult to differentiate is this rhythm here a v-tac or is it an svt with a bundle branch block how in the heck do i know the difference between them because they can look pretty much the same so here's a couple ways that you should remember them so let's say that we talk about vtac here and let's say that we talked about svt over here and we just kind of like make little comparisons between these two about how svt with a bundle branch block let's be more specific bundle branch block and how do we differentiate these all right first thing when you're looking at them they're both going to have wide regular rhythms but vtac these qrs's are even wider how wide we talking baby usually we're talking greater than 0.14 seconds for their qrs complex for svt with aberrancy it's usually less than 0.14 seconds so there's one identifier okay the next thing is you look at the p waves to see if you can see sometimes you may get lucky where you see a little inverted or retrograde p wave snuck within the qrs complex that's called av dissociation okay so with vtac this one has av dissociation okay with the svt with aberrancy there is no av disassociation okay that's important to remember okay the next thing here with vtac there's something we'll talk about in another ekg series where it's called extreme right axis deviation usually vtac has extreme right axis deviation whereas svt with aberrancy does not have extreme right access deviation and last but not least which i think is probably one of the most important ones because sometimes this can be really difficult to identify is usually vtac is a history of some type of cardiovascular disease okay usually cardiovascular diseases and older greater than 35 years of age svt with a bundle branch block is not very common in individuals with a history of underlying cardiovascular like structural heart diseases okay so usually it's no history no significant let's put significant past medical history of cardiovascular diseases that are usually structural in origin and usually less than 35 years of age so again these are not the same how do we differentiate them these factors but in real life who cares if it's this one or this one you want to know why here's why if i treat someone who has svt with a bundle branch block okay and they actually have v-tac i can kill them if i treat someone who has v-tac right but they actually have an svt with aberrancy it may actually improve their arrhythmia or it may not really affect it at all so what would you rather have right so that's why pretty much every time you see someone who has a wide regular tachycardia you should always be the first on your differential should be the most common is going to be vtec okay treat it empirically in that sense the reason why is if you treat again another reason if you give adenosine because that's the common treatment for a for svt if they have antidramic avrt it can also worsen the situation because you do not give av nodal blockers to people with antidramic avrt especially if they have some other pre-excitation like afib or afib associated with uh the antidramic avrt so again off my soapbox most common treat for v-tac just be careful unless you know it's svt with aberrancy you treat it as those v-tac so with that all being said let's assume that this is v-tac how do we treat it okay with v-tac okay the primary thing that you're going to do for treating this situation here is you're going to give them something called amiodarone amiodarone is an antiarrhythmic okay so it's going to help to try to regenerate and re-kind of set their normal rhythm another drug that can be considered instead of amiodarone is another drug called procainamide okay and there is other ones that you can try as well but these are usually the better options in these situations so let you try these first amiodarone or procainamide if these do not work then the next thing that you're going to go to here is you're going to put pads on the patient because vtac is very unstable okay we're treating this as so it's stable but it can quickly become unstable and break down into what's called v-fib so you should always have the pads on them and if you've tried the amiodarone or procainamine that didn't work you can cardiovert them but have them pads on them in case they become unstable because then you can still cardiovert them or worst case scenario defibrillate them the only difference really between synchronized cardioversion and defibrillation is what the word says synchronized is you're timing that electrical jolt that you're going to give them to line up with the r wave okay that can sometimes be difficult in irregular rhythms though so again if it's regular you can cardiovert them become unstable you can also cardiovert them if it's svt with aberrancy though okay so if it's svt with a bundle branch block they're gonna benefit from the adenosine okay so you can consider adenosine in this situation as well and here's why they say sometimes in the algorithms you'll see treat with adenosine first because if it is svt with bundle branch block it'll usually obliterate it if it doesn't then it's usually v-tac monomorphic v-tac but again you give adenosine to someone with v-tac it could worsen the scenario so if you give adenosine just be cautious okay and then the antidramic avrt that was the last one there you're going to treat it the kind of the same way that you would treat v-tac as well so anti-drum kvrt give them procainamide or amiodarone and then cardiovert them after you've done this and you've stabilized the patient one last thing i need you guys to be remembering here long term what do we do well we kind of already talked about it a little bit which you've seen kind of a pretty consistent basis with these radio frequency ablation burn the crap out of these abnormal ectopic areas with svt or with the v-tac or the antidramic avrt the other thing though is with vtac this is a very nasty arrhythmia and you got to be very careful okay usually vtac the most common cause do you guys remember go back and let's see triggered activity was one of the big reasons we said and it was related to the dads what was the most common one i told you for the dads ischemia so because of that you want to look for the underlying cause and that is most likely an mi so look after you've stabilized them generated their normal rhythm again look at those st segments look for elevation depression check the tropes and if there is send them to the cath lab to get a pci after you've figured that out though the next thing is do they need sometimes with vtac they may need an automatic like an implantable cardiac defibrillator because if they go into vtac again and they're not at the hospital what can happen they can die so you want that defibrillator to identify it and then hit them with the electricity to regenerate that rhythm there's a lot of indications for these that's that's past the scope of this lecture so let's just kind of assume aicd for recurrent or malignant v-pack okay boom roasted let's move on to the next thing which is the wide irregulars last one here for the tachyarrhythmias wide qrs irregular rhythms we have our differential polymorphic v-tac let's do this thing first let's hit it right out of the way this can sometimes be very difficult to identify okay if you have a polymorphic v-tac you want to look at the qt interval before they started going into this nasty little arrhythmia here so this is usually a polymorphic v-tech how can you tell if it's polymorphic you see the qrs waves they look different so they have different morphology so because they're different morphology different amplitude and stuff like that that's why it's said to be a wide irregular okay first thing i'd like to look at is was there a normal qt interval before they went into this deadly kind of arrhythmia so that's the first thing we got to address if it's polymorphic vtac polymorphic vtac with a long qt interval how do i determine that again usually you want beforehand before they even went into this type of rhythm they had some type of identifiable kind of of rhythm here that you could have looked at and what you're looking at is you're measuring that q t interval and seeing if it was prolonged beforehand what is considered to be a prolonged qt interval there's a lot of different numbers i like to just say if i see a qt interval that's approaching it's either greater than or equal to 500 milliseconds i'm going to start pooping my pants a little bit because this is most likely torsades to points okay polymorphic vtac with a prolonged qt interval so again which one are we thinking this could be torsades the points okay so that's the first thing i find this abnormal waves i check my qt i find that it's prolonged if it is not prolonged then it is polymorphic v-tac with a normal qt interval or there's one other condition so let's say that you have someone with a polymorphic vtac with a normal qt interval okay and the other scenario is you have someone with afib with wolf parkinson's white syndrome okay with parkinson's white cinder and these are your two that you're trying to figure out here usually if someone has a fib with a bundle branch block or aberrancy that's actually going to be kind of one of the slightly easier ones to identify and plus it's kind of one of the most common so we'll talk about that one last but i'm trying to look at the difference between these two it's sometimes very very difficult it really is with polymorphic vtec with a normal qt interval and versus afib with wolf parkinson's white syndrome sometimes it can be so difficult to differentiate them one of the things that may help is that afib with wolf parkinson's white syndrome has pretty high rates pretty high rates and remember why what kind of wolf parkinson's white syndrome is it most likely antidromic avrt which means the electrical activity from afib is going where right through the bundle of kenton to the ventricles so the atrial rate and ventricular rate can almost equal one another the problem with that is that afib and wolf parkinson's white syndrome is if you give this an av node blocker so let's say that you gave this person an av node blocker now all the electrical activity that's going from afib for coming from the afib it won't go to the av node which is highly regulated it'll only go through the bundle of kent and because of that if you do this this can quickly break down into v-fib okay can generate some really nasty rates so that's why the only thing that you want to just be aware of if you're trying to really kind of differentiate the treatment differences is that if they have afib and wolf parkinson's white syndrome don't give them any kind of av node blocker an alpha so what are those guys remember them abcd adenosine beta blocker calcium channel blocker digoxin stay away from those so that's why since that is the case it doesn't really matter if you determine if it's polymorphic v-tac with normal qt or a-fib with parkinson's white syndrome you want to know why as long as i avoid av node blockers and i treat these the same i should be okay so what is the treatment in this situation for a polymorphic vtac with normal qt and afib with wolf parkinson's white syndrome what i'd like to start off with first is treat this with amiodarone so i'm going to treat this with amiodarone or i can try procainamide and see which one of these you know see if they work if i've tried this amiodarone or procainamine and it doesn't work what do you think i do same thing i did with vtac cardiovert them so the next thing i'm going to do is i'm going to cardiovert the patient if at any point in time though here's the thing you got to be careful of with polymorphic v-tach you may cardiovert them synchronized that's what they'll say synchronize here's the problem though sometimes the machine has difficulty kind of syncing up with those r waves because of the irregularity and how fast it's going so sometimes cardioversion really this may be more defibrillation if you see this type here okay and again afib with wolfe parkinson's white syndrome the treatment is going to be the same as polymorphic v-tac with normal qt okay the only thing that is different is that you avoid av node blockers at all costs adenosine beta blockers calcium channel blockers and digoxin one more thing here with the polymorphic v-tac with prolonged qt before we go into a-fib with bundle branch block is that with this one this is the one that actually thankfully is kind of the most weird and different type of one with someone having polymorphic vtec with prolonged qt and suspecting its torsades to points do you guys remember the underlying pathophysiology behind torsos to points it was an ead right or the big causes for eads hypokalemia hypomagnesemia or hypocalcemia and the offending drugs the abcde drugs so what would i do here well you're probably saying oh give them potassium and magnesium you're so right give them mag empirically though first you get mag sulfate then check their potassium levels and make sure that it actually is low then replete the potassium levels so what would you do for torsades you're going to give them magnesium sulfate and then replete potassium levels these are the two ones if it's low okay then what else discontinue the offending medications or lower their dosages antiarrhythmic antibiotics antipsychotics antidepressants antiomedics now the other thing that you could do you just want to write this down just as a side sometimes you may stabilize them with the mag repleting their potassium and then getting rid of the offending medications sometimes though after you've stabilized them they still may have a prolonged qt interval and you want to prevent them from going into another torso points so what sometimes they may do is do what's called overdrive pacing or give another drug which is called isoproterenol and what these drugs do is is they kind of increase the heart rate a little bit if you increase the heart rate a little bit that shortens the qt interval which is going to decrease the incidence of them going back into another torsade points so you understand okay beautiful polymorphic vtec with prolonged qt greater than 500 mag replete potassium discontinue meds overdrive pace these two polymorphic v-tack would normal qt or a-fib with wolf parkinson's white amio procainamide cardiovert but just be aware you may have to de-fib them because the machine won't sink sometimes and then with afib with wolf parkinson's white for the love of goodness avoid the av note blockers a b c d right last thing here with the a fib and a bundle branch block a fib with a bundle branch block believe it or not or also called aberrancy is the most common type of wide irregular the way that you can differentiate this one from all these others is because usually the rates are not as fast so it's still fast but not as fast but here's the big thing the qrs morphology is usually the same but because the person has a-fib where there's multiple ectopic foci that are firing and it's going down that bundle branch system what did we say it was a common theme with afib the rdr intervals were never the same it was so irregular but because we hit a block it's not going down your normal conduction pathway so it widens that qrs complex so look for his qrs morphology to be relatively the same not different and then if you can find that or you've ruled out all the other causes then you treat them with a beta blocker or a calcium channel blocker if that doesn't work you cardiovert them if that happens okay now the last thing that you guys need to see here is again let's take a look over here at these rhythms if you look here at this one again we said this was the polymorphic right you could see the constant differences between this qrs and these qrs you see how this one it has different rdr intervals though different r here different rdr here different rdr here but all the qrs complexes are exactly the same pretty much the same morphology which one would this lead you more towards a fib with the bundle branch block what would this one lead you more to these other three how do we differentiate this from this qt interval prolonged not prolonged how do we differentiate these two sometimes you can't treat them empirically got it last thing is long-term treatment after you've figured this out how do you do their law what's the long-term treatment in this situation here so the long-term is going to be the same as we've talked about before radio frequency ablation of the abnormal pathway and in someone who's developing these abnormal rhythms like polymorphic v-tac with a with a normal qt or they have some other issue here like v-fib which we'll finish up with you want to consider an auto an implantable cardiac defibrillator if they have recurrent v-tac or v-fib okay so that leads us to the last thing to finish this up why are these so dangerous why are these so dangerous okay one of the reasons why is that sometimes these kinds of arrhythmias can quickly break down into what's called v-fib and v-fib usually produces no pulse and these can they can be very very dangerous so in these situations with v-fib you go with cpr chest compressions epi and defibrillate do it again and again and again so again that finishes up our tachyrhythmias let's hit it home with our brady arrhythmias all right brady arrhythmias so now we said okay is it too fast too slow it's too slow if it's too slow we have to kind of look at our ekgs a little carefully here the first one that i want us to talk about here that you guys think about right away is is it sinus bradycardia that's the first thing i need you guys to be thinking about is it sinus bradycardia how do i determine that i'm looking for my p waves right so here's my p wave here and here's my p wave here is after every p wave there is a qrs complex yes if after every p wave there's a qrs complex there's a normal p wave that is sinus bradycardia it's just moving slower than your normal rate okay you've determined that it's sinus bradycardia what's next next thing is let's take a look at this next arrhythmia this next arrhythmia same thing do you have p waves yes i do have a p wave after every p wave is there a qrs complex yes there is so what's the problem with this is this sinus bradycardia now this is the next step that you look at look at your pr interval so go before the p wave all the way up until you get to the q a that's our pr interval if the pr interval is greater than 200 milliseconds that is considered to be too long that's a prolonged pr interval so again pr interval greater than what 200 milliseconds what is this this is a first degree heart block okay now you determine that it's not sinus brady you determine that it's not a prolonged pr interval the next thing that you got to go to is okay let's take it next to this next rhythm here okay what's this one here do i have p waves at every point where's my p wave here's my p wave here's oh i got two p waves here okay so i got a couple p waves if at after every p wave is there a qrs one here one here i don't have one there i dropped a qrs okay so i know that there's not a qrs for every p wave okay that's interesting let me take a look at the pr interval let's see if there's anything abnormal with that so i'm looking at my pr interval from here to here that's that's long i know i'm making it up because i don't have my boxes there but again if i did it would be too long then i'm gonna look at this one that's even longer and then i dropped my qrs remember the little poem longer longer drop you have a winky bock that is a second degree heart block mobitz one remember i said the winky block was a drop qrs so if you see a pr interval that is getting longer and longer and longer and longer progressively and you drop a qrs complex then this is a second degree heart block mobitz one and that drop qrs is called a winky buck beautiful let's move on to the next one next situation here check my p waves do i have a p wave and after every p wave is there a qrs well there's my next p wave drop to qrs here's my p wave qrs here's my p wave qrs here's my p wave drop to qrs okay so if i'm kind of looking here i'm seeing something very interesting where not every p wave is followed with the qrs complex okay that's that's interesting what's the next thing i do check my pr interval you obviously can't tell here because i don't have the little boxes but my pr interval is normal i'm going to tell you guys that my pr interval in this situation is normal so i have a normal pr interval but i also have dropped qrs's out of nowhere if your pr interval is normal and you're dropping qrs out of nowhere this is a second degree heart block mobitz2 and there's another interesting second degree heart block that i want to talk about so now let's take a look at this next one here kind of similar here again take a look at the p wave is there a qrs yes p wave is there qrs no i dropped a qrs there p wave qrs and then again p wave drop to qrs p wave qrs p wave drop to qrs p wave qrs there's a pattern to this if you guys see it i have a normal pr interval in all of these okay i want you guys to remember that for this situation there's a normal pr interval and again i can tell that because it's not greater than 200 milliseconds and i'm dropping qrs's but i'm doing it in a very weird pattern where the p wave is being generated no qrs another p wave then a qrs so that means and it's happening every time you see these two that are always lumped together that means for every two p waves that i'm firing i'm only getting one qrs pattern so i have a two to one second degree heart block okay it's kind of like a kind of a variant of the second degree heart block mobitz too okay the last one here is looking here okay let's see i got my p wave here i drop a qrs or i don't even produce a qrs in this situation i got a p wave and then oh i produce a qrs but this qrs don't look nothing like that qrs why it's wider so now i'm having dropped i have a normal pr interval so let's put that down pr interval is normal and i'm dropping qrs's and my qrs complexes are super wide that's telling me that i'm not going through my normal conduction it's not going av node down it's stopping at the av node and then the ventricles are depolarizing on their own that means there's complete disassociation between the atria and the ventricles there's no connection between them anymore once that happens where you have a normal pr interval but you're dropping qrs's and the qrs's are wide and if you calculated the rate between this qrs complex and that it's probably going to be equal to the ventricular rate which is about 20 to 40 beats per minute if you calculated the rate between p wave to p wave that'll probably be around the actual sa node rate which is around 60 80 beats per minute so because of that they're usually going to beat at their own intrinsic rates because they're completely disassociated and that is a third degree heart block bad now in these situations here's the thing these arrhythmias are the ones that you got to watch out for all the other ones are pretty much benign you don't really have to deal with them they're usually pretty much asymptomatic but in these second degree mobitz 2 to 3rd degree heart block the problem with this is their heart rates can drop pretty low because that conduction through the av node is really jacked up remember the formula cardiac output equals heart rate times stroke volume if you increase heart rate what happens to the cardiac output it increases right if you decrease heart rate you decrease cardiac output if i'm really dropping my heart rate here what's going to happen to my cardiac output i'm going to drop my cardiac output then the next formula if you have your blood pressure is equal to cardiac output times the total peripheral resistance if you decrease cardiac output you decrease blood pressure so now from this situation i'm also going to have decreased blood pressure if i drop the blood pressure enough that the patient goes into hype starts having significant hypotension so their blood pressure is really dropping they start having an altered mental status or they start having chest pain or any types of like pulmonary edema this is considered to be unstable and you have to treat them if they don't have really any of these things you don't really have to treat them you can just kind of monitor them but if they experience any of these situations they're considered to be unstable we got to treat them so what do we do so first thing you got to do is we're going to give them atropine so i'm going to start off with atropine what the heck is atropine i just want you to remember atropine is going to decrease your parasympathetic nervous system effect on the av node in other words it's going to block acetylcholine from binding to the av node if you block acetylcholine what did acetylcholine do when we talked about decreased automaticity it slowed down conduction if i block acetylcholine now i have nothing inhibiting conduction it's going to increase conduction that should jack up the heart rate a little bit all right so sometimes atropine doesn't work so sometimes what we have to do is we have to kind of oppose not just oppose the parasympathetic but increase the sympathetic so if i give something like epinephrine right epi that's going to increase my sympathetic nervous system activity what did the sympathetic do increased av conduction increasing heart rate so i oppose this parasympathetic increase of sympathetic sometimes that may bring the heart rate up sometimes it doesn't so sometimes what you may have to do is do what's called pacing so you may actually have to pace the patient and there's a couple different types one is you can put it on their chest called transcutaneous the other one is you kind of float it down the venous circulation it's called transvenous and then sometimes in situations where it's a particularly a third degree heart block you may need what's called a permanent pacemaker to be put in place okay so this is the thing that you're going to go through once they have any of these instabilities atropine epi pace okay after you've stabilized them the next thing you have to do is you got to figure out what was the underlying cause for all of these dang issues here and it was most likely what do you guys remember conduction block i told you there was a couple things i needed you to remember that were the common causes of conduction block do you guys remember the first one i told you inferior wall am i so we have to treat underlying so treat the cause basically and what were some of these causes so the first one we said was an inferior wall mi what was that due to an rca occlusion right coronary artery occlusion what do you do for this look for any signs of stemi and stemi check maybe some positive troponins maybe they were positive what do you do once you determine that get them to the cath lab and then once you get into the cath lab they get a percutaneous coronary intervention we put a stent in there that may help it the next thing is after we've done that is we move on to the next step what was another particular cause another big one that i wanted you guys to remember was hyperkalemia remember hyperkalemia can really be a nasty condition it can really affect those electrical activities what do you do for this situation and hyperkalemia there's a particular protocol that we go by you first give them calcium in the form of calcium chloride or calcium gluconate that stabilizes their cardiac membranes after you do that you give stuff to shunt potassium into the cells and the things that you give to shunt potassium into the cells is insulin but you don't want to over crack them and drop their sugars so you give them a little bit of sugar with d50 and then insulin will push potassium into the cells and albuterol will also push potassium into their cells and so that'll kind of lower the circulating potassium levels the other thing is sometimes when high potassium occurs it can produce acidosis so sometimes you may have to give a little bit of bicarb to treat the acidosis and then finally you may need to give some lasix to pee some of that excess potassium out as well so these are going to be things that you'll go by to treat the underlying cause for those two issues so we said inferior mice we had hyperkalemia what was the other big thing that i needed you guys to remember the other big thing that i needed you guys to remember here is overdose from the calcium they have too much calcium channel blocker too much beta blocker right so if they took too much of a beta blocker or too much of a calcium channel blocker or too much of digoxin all those things was blocking the av node what do i give for a beta blocker i give glucagon what do i give for a calcium channel blocker i give them calcium what do i give if they have digoxin i give them digi bind okay we're almost done ninja nerds the next thing high yield big one lyme's disease was another one i told you don't forget about lyme's disease lyme's disease was caused by what type of infection it was a tick bite right that released the beryllia bergdorferin and really jacked up the av node in this situation you're probably like oh yeah limes you treated with doxy yeah you think it's actually ceftriaxone so in this stage of lyme disease it's more of a severe stage so you actually have to give them a drug called ceftriaxone in this situation and then the last thing that i want you to remember is that there could be other causes other than conduction blocked not as important but remember there was the ones that was like hypo thermia what would you do for hypothermia rewarm them and hypothyroidism what do you do for hypothyroidism you give them thyroid hormone right so you give them what's called a levo thyroxine if they have something called mexidemocomb which can produce some pretty severe bradycardia sometimes heart block so again these are the things that you have to remember treat the underlying cause because that may prevent these continuous brady arrhythmias from occurring ninja nerds we finished arrhythmias all right ninja nerds in this video we talk about arrhythmias i hope it helped i hope you guys did like it and as always until next time [Music] you

Channel: Ninja Nerd

Views: 231,877

Rating: 4.9710221 out of 5

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science, USMLE, USMLE Step 1, UWORLD, United States Medical Licensing Examination, high yield lecture, arrhythmias, HIGH YIELD, step 2, INTERNAL MEDICINE, MEDICINE, STUDY, REVIEW, Medical Specialty, USMLE Prep, type of arrhythmias, tachycardia, bradycardia, bradyarrhythmias, tachyarrhythmias, sick sinus syndrome, atrial flutter, atrial fibrillation, ventricular tachycardia

Id: UBUUQccYfZQ

Length: 108min 37sec (6517 seconds)

Published: Wed Mar 03 2021