all right welcome folks my name is omelet matu i'm a faculty member at university of maryland school of medicine and we're going to spend a little time talking about syncope formal title for the faint of heart actually this is for all of you regardless of how your hearts feel we're going to spend some time talking about cardiogenic syncope there's a lot of different things that cause syncope we're going to focus on the cardiac causes now this actually is going to be a visual diagnosis lecture this is an ekg lecture i know many of you have probably heard a lot of lectures on syncope over the years and there's been a lot of literature and research has come out which has really taught us all that we especially in the united states we have a tendency to admit too many patients with syncope who get negative workups and we spend a lot of money and those patients can probably just get outpatient workups we know that we've come to realize that in terms of the workup in the emergency department if you do a good history and physical you really don't need in many cases to do much of a workup you should let your history and physical direct you to what you need to do with the work up if somebody for example is having a lot of vomiting and diarrhea then yeah check electrolytes if somebody has heavy periods or gi bleeding or anything like that or or severe weakness of course get a cbc and check the h but if they don't have things like that routine cbc routine electrolytes routine cardiac enzymes routine halter monitoring routine sending these patients for ep tests it turns out to have a very very low routine cat scan of the head incredibly low yield unless there's something on the history or physical physical especially neuroexam or heart exam unless you're somebody in the history of physical that tells you that you need to work them up in some way you don't need to do much of a work up there's no routine labs that you need to do but with one exception and that one exception that you should routinely do in everybody who comes in with syncope is the electrocardiogram and so that's what we're going to focus on what is it that you should be looking for on the electrocardiogram now these are kind of the no-brainers i put up here everyone knows that you're going to look for cardiac ischemia or an mi or a stamina yeah it's a no brainer you're also going to be looking for obvious arrhythmias and av blocks it's kind of a no-brainer also but there's a handful of other things that you should always be looking for they're not everyday but if you pick them up you're going to save a life and that's what this lecture is really going to be all about what are the other things that you need to look for every time you get an ekg on somebody with syncope and you should probably probably be doing ekgs on everybody who comes in with syncope now this is 100 but just about everybody all right so let's go through some cases and all of the cases i show you are real emergency department cases so put yourselves in the shoes of the emergency physicians that saw these patients when they come in and ask yourself what's the diagnosis of what would you do case number one this is a 29 year old man who comes in after a sinkable episode now he's sitting in front of you saying doc i feel fine that's the real history i feel fine he looks good he's got a pretty much normal exam his history is unremarkable no one else in the family died and he said that he was just doing some different things i think he actually in this case he was running to catch a bus and he got palpitations lightheaded and then he collapsed no trauma his exam right now is unremarkable and this is again a real case what ended up happening he got a bunch of labs he got cardiac enzymes sent on him everything's unremarkable he says doc is getting laid i want to go home so he ended up being discharged home and then he was exerting himself in some way a few days later and then collapsed and paramedics were called found him in v fib they shocked him they brought him into the emergency department and that is when i met him uh he was in cardiac arrest and i went back to the computer and found this ekg from his visit in the same emergency department a few days earlier and the ekg interpretation that we'll talk about in a moment was missed i pronounced him dead we were unable to resuscitate him real case and the diagnosis here is hypertrophic cardiomyopathy now one of the problems here with hypertrophic cardiomyopathy is most people don't learn how to diagnose hypertrophic cardiomyopathy on 1280kg even the cardiologists don't typically learn this unless you're talking about maybe a cardiologist who teaches the courses or writes the books on ekgs and the reason is most cardiologists learn to diagnose this on echo exactly on doppler echo they don't learn the ekg findings but you and i as emerging physicians we've got to know the ekg findings so what is it that you're looking for it's very simple when you see an ekg that shows high voltage big qrs complexes with deep narrow q waves right you look up there take a look at those key waves especially in the lateral leads one avl a little bit in v5 v6 the most common place that you see these deep narrow q waves sometimes referred to as dagger like q waves deep and narrow the most common place is going to be in the lateral leads sometimes inferior but most common in the lateral leads when you see that in the presence of high voltage send that patient for a doppler echo to make the diagnosis and you'll save a life all right so high voltage with deep narrow dagger-like q waves and and that's what this patient had hypertrophic cardiomyopathy the official read by cardiology later uh was lvh and possible old lateral mi well why would a 29 year old have an old lateral mi no these are not infraction q waves infraction q waves should be at least one box wide and usually at least a third the height of the entire qrs if we go back for a second these are pretty big keyways but they're not wide enough to call infarction qas these are not infarction q waves these are hypertrophic cardiomyopathy key waves because they're very narrow and deep with high voltage here's another case once again very simple visual diagnosis things to look for high voltage with deep narrow cues in the lateral leads in this case lead one lead avl lead v5 and v6 take a look at how narrow and deep those are with the high voltage here's another one high voltage in other words big qrs complexes and deep narrow cues one avl v5 and down there in v6 once again here's another example high voltage now sometimes when you get really high voltage you can get screwed up t waves that's the official term screwed up t waves in some of the leads you know everyone has seen lvh and that strain type of pattern high voltage produces abnormal repolarization so the t waves can sometimes look a little bit abnormal and a bit concerning but we've got high voltage and take a look at those q waves very deep very narrow not much in v5 or v6 but definitely in one an avl here's another example high voltage relatively high voltage and in this case there's not much in one or avl but when you look at v5 and v6 that's kind of bizarre looking but very deep q waves at the beginning of those qrs complexes and here's another example high voltage with deep narrow cues take a look at avl take a look at lead one take a look at how deep and narrow those are and sometimes you'll have flipped t waves just because the high voltage produces abnormal repolarization those are very non-specific but again high voltage with deep narrow q waves in especially in the lateral leads if you see it in the inferior leads you still worry but most commonly in the lateral is take a look at this case not much in one or avl but take a look at those q waves in v5 and v6 those are like those are more than daggers those are like swords there's just nothing else in emergency cardiology that's going to give you key waves that look like that so when you see the high voltage with deep neural qas send that patient for the diagnostic test of choice the doppler echo and if they pick up hypertrophic cardiomyopathy you get that patient off to a cardiologist as quickly as possible in the meantime you tell them no exertion and if there's any delay you put them on some beta blockers beta blockers or negative ionotropes no exertion and negative ion tropes beta blockers until they see the cardiologist and get a doppler echo and you know what you just save a young kid's life by knowing what to look for so again hypertrophic cardiomyopathy look for high voltage and deep narrow cues especially lateral leads the vast majority of these are males but we have seen some cases in women young women as well and your diagnostic test of choice is getting the doppler echo all right so we'll let that sink in just take a little mental break for a second so let's recap what is it that you're looking for on the 12 lead of a syncope patient you're looking for signs of ischemia you're looking for dysrhythmias in av blocks we've added hypertrophic cardiomyopathy to the list of things that you always look for okay what else are we looking for case number two thirty-year-old woman comes in after a sinkable episode and now she's sitting in front of you like most of these patients saying doc i feel fine now i had the syncope i had the passing out episode i fell out earlier and uh here is the 12-lead ekg and i think a lot of people will get this uh they're this is relatively new in the ekg literature just over the past 15 20 years or so and what that means is a lot of your older cardiologists may not have learned about this when they were in training but the key findings here are in v1 and v2 you see this kind of incomplete right bundlish type of pattern with this strange st elevation that's code oftentimes this st elevation like this convex upwards sometimes it's straight like what you see in this example every noun that is concave upwards but most concerning is if it's straight or convex upwards and that is as most of you said this is the the brugada pattern the brugada syndrome so what is bragata syndrome brigadis syndrome i'm not going to go into great detail but regatta syndrome is an electrical phenomenon that was first identified probably in the late 80s early 90s has become very popular in terms of the electrophysiology literature over in the recent years and this is something that has been associated with the sudden sometimes unexpected bouts of polymorphic v-tac patients can unexpectedly go into polymorph v-tac it's not necessarily associated with exertion in fact sometimes it's associated with uh with high vagal tone being asleep at night time or maybe after heavy meals when vagal tone is a little bit higher so it's not an exertional type of syncope but what happens is this is an electrical phenomenon that people believe is related to a sodium channelopathy where patients can suddenly go into polymorphic v-tac and if they're lucky it spontaneously converts back to sinus rhythm and they wake up right they go into polymorphy tech fall to the ground if they're lucky they convert they wake up if they're not lucky it degenerates from polymorphic into v-fib and asystole and we call that sudden death so you see sudden death and syncope oftentimes are the same disease along a spectrum of how lucky you are so when the patient comes into the emergency department after the sinkable episode you see this it's because they were lucky next time they may not be so lucky all right so again there's two types over the years people have talked about two different types of burgata syndrome the saddle type and the cove type on the right the cove type is much more concerning that's when there's that incomplete right bundle pattern with the convex or straight st segment elevation that you see on the right side the saddle type of elevation was first talked about 10 15 years ago but we now know that this is less sensitive and less specific so the electrophysiologists get really concerned about the cove type not as concerned about the saddle type if you see either of these in the right setting but especially the cove type you get on the phone with the electrophysiologist and i'm going to emphasize electrophysiologists because when you talk about all the different cardiologists that are out there you know they all have their special areas of expertise there's a general cardiologist and there's the lipid cardiologist the hypertension cardiologist and there's the interventional cardiologist there's the electrophysiology cardiologist the one group of cardiologists that live for this diagnosis is the electrophysiologist a lot of the others we've come to realize often don't know that much about this so if you have access to electrophysiologists make sure that they're the ones that you're getting on the phone with all right a few more examples here's a patient again similar to the other story this is a patient who came in after a sinkable episode and this ekg was obtained the formal interpretation by a general cardiologist was incomplete right bundle with st elevation possible mi possible septal stemi but the patient was totally asymptomatic so the emergency physician didn't know what to do with this it you know the computer's calling this a stemi con cell's cardiology cardiology comes down they say it looks like a stemi but the patient's asymptomatic so tell you what let's just admit the patient rule them out we'll do an echo so the patient gets admitted rules out gets an echo echoes normal this is purely an electrical problem it's not um an anatomic problem so the echo will be normal a stress test will be normal and mri would probably be normal it's only electrical is not anatomic all right it's a sodium channel problem uh that's the prevailing thought so anyway this patient is ruling out and is getting ready to be discharged and then someone else happened to see this ekg and said you know this this kind of looks like that forgotten thing that i've heard about and so again totally true story they went to google images and they pulled up google images for this brighter syndrome and they found ekgs that looked exactly like this and they said you know what i think this is brugada syndrome so they transfer this patient from the community hospital the university patient went right to the ep lab where in the ep lab they tested them confirmed the evidence of brigadis syndrome and then put an aicd in so that's the part i haven't talked about how do you confirm the diagnosis well the prevailing theory is that this is a sodium channelopathy and what happens is they'll take them to the ep lab and the electrophysiologists will infuse a potent sodium channel blocker typically something called agiline which is even more potent of a sodium channel blocker than procainamide or or fleck and eye things like that and when they infuse this medication one of three things happens number one nothing happens and that rules out burgata syndrome number two if the st elevation becomes more pronounced that rules in brugada syndrome or number three the patient just goes right into polymorph vtec at which point they just shocked the patient out of it you know it's it's not a big deal for the electrophysiologist to shock people out because they have they have electrodes inside the heart so if somebody lots of times they will provoke v-tac or polymorph v-tac and then just shock them out of it's not a big deal for them but that'll confirm the diagnosis of brigada also and and if the patient does have evidence of brugada syndrome then what they do is they'll give them the treatment of choice which is placement of an aicd that's the only proven effective therapy for this syndrome so they get an aicd and then they go on and hopefully live a happy normal life which is what happened in this case here's another case this is the patient that came to the emergency department that i and my colleagues took care of when the patient arrived in the emergency department the patient was in cardiac arrest we got the patient back returned spontaneous circulation and we looked up in some records and we found this ekg from a primary care doctor's office this ekg was obtained in the primary care doctor's office after the patient presented with syncope and it was read by the machine as incomplete right bundle that's it well when you look at this you'll notice that there's yeah there's an incomplete right bundle but st elevation is not normal for an incomplete right bundle a little bit of s television in v1 and v2 your money leads terminating in an inverted t wave that's very typical also and it was missed now i would never say that this is standard of care for a primary care doctor know about this but you can just imagine if they had known about this a week earlier when the patient visited them the outcome could have been very very different and unfortunately even though we got this patient back the patient ended up with severe hypoxic encephalopathy and last i heard lives in one of the nursing homes in baltimore with the peg and a trach and not much of a mental status all right here's another one take a look at this this is a bit more subtle and you see that incomplete right bundle pattern with a little bit of elevation this was picked up by the emergency physician and sent to the ep lab and they confirmed the presence of bragata this is definitely more subtle but again incomplete right bundle with s television is not normal terminating in an inverted t wave for comparison this is what a normal right bundle looks like right normally with the right bundle or an incomplete right bundle you'll have a little bit of st depression in v1 and v2 so if you ever see an incomplete or complete right bundle with st segment elevation in v1 or v2 especially in the right clinical scenario they came in because of syncope or near syncope you've got to think about brightest syndrome and get on the phone with electrophysiologists and this is another case where just by knowing about this diagnosis you might just end up saving life here's another example this is subtle again but there's an incomplete right bundle with st elevation terminating in an inverted t wave there's that saddle morphology in v2 and this turned out to be positive for bragata syndrome here's another one this one this is kind of limited to v1 but a very classic morphology in v1 this is a young person that was having intermittent near sinkable episodes and dr shepard here made the diagnosis here's another very classic looking v1 and v2 again incomplete right bundle with that convex upwards st elevation send that patient to an electrophysiologist and you're going to save a life and here's yet another example this patient was actually diagnosed at a community hospital and you see this the patient went there because of a syncopal episode v2 is a little bit unusual looking but again v1 is very classic for that regatta pattern the patient was transferred over to university to the electrophysiologists and the electrophysiologist looked at the ekg and said yep this begat until proven otherwise they took the patient to the ep lab and proved that it was pergotted the patient got a box aicd and ended up doing okay this ekg actually was overread by a general cardiologist the next day as well as just st elevation possible mi the general cardiologist did not know about burgata syndrome the electrophysiologist took one look at this and said this is bragata until proven otherwise so again i bring that up just to highlight the fact that there's a very different level of knowledge between your electrophysiologists and the other types of of cardiologists out there right so if you have an option try to get on the phone with the electrophysiologist here's another very classic example in in v1 now this was originally described by the brugada brothers back in the late 80s and and some other italians had described it around the same time also it was originally described in southeast asian adolescent males that's what where they first studied it in southeast asia but i'm not harping on that because it's now been identified in every ethnic group men and women the youngest age that's been identified that i've heard of is in infants and there's actually some people that believe that this may be a contributing factor to sids and the oldest patients i've heard about are all the way up to 75 or 80 years old and the oldest person in whom i have an ekg case is a 65 year old so even though this was first identified in you know teenage boys in southeast asia it's everywhere um and uh and they estimate that regatta may be responsible for about four to five percent of all medically related cardiac arrests put trauma aside think about that one out of every 20 to 25 cardiac arrests may be attributable to bragata syndrome this is not as rare as you may think all right so if you have in your career if you've seen 20 to 25 brugada cases statistically you've probably or i'm sorry if you've seen one out if you've seen 20 to 25 cardiac arrests in your career which is probably everybody here statistically you've seen brigada all right the computer will often miss this the computer will look at this and call this an acute mi i've never seen computers accurately diagnose this sometimes they over call it or under call it if the patient comes in with syncope and you see this then you've got to think about brigada which is what this was now on the other hand if you see this pattern and the patient comes in with chest pain yeah if they're coming with chest pain i'm going to call this an acute septal stemi so the history makes a difference if somebody comes in with syncope or near syncope or palpitations uh i'm gonna worry about brighter but if somebody's coming in with substernal chest pressure and you see us calivation then of course you're gonna call it a stemi all right okay so what are you looking for with brigada we're looking for a right bundle or an incomplete right bundle-ish looking pattern in v1 and v2 with st elevation if it's convex upwards that's the most concerning or straight terminating an inverted t wave that's the most concerning if it's if it's concave upwards that turns out to be less sensitive and less specific but if you've got a concerning history i would run with that and get on the phone with electrophysiologists either way all right another mental break here this is actually a restaurant in nashville where somebody sent me a sign of a restaurant called brugada i don't know if people go in there and collapse i'm not really sure but okay so mental break let's recap when you get an ekg on people who have just had syncope what are you looking for well everyone knows to look for ischemia and arrhythmias navy blocks we've added hypertrophic cardiomyopathy to list and we've added brigada to the list of things that you always look for all right what else what else can you be looking for well how about this here's a 26 year old nurse that i was working with one day in the emergency department healthy guy he plays basketball regularly he's not overweight no cardiac risk factors and he was popping these tums over and over he thought he was having a reflux i said what's going on he said i'm having palpitations i think it's just reflux so i said well why don't we get it in ekg and we got an ekg during one of these episodes and this was his ekg right he's got an irregularly irregular qrs pattern some complexes are narrow some are wide and i'm seeing some people are nailing the diagnosis this is atrial fibrillation with wolf parkinson white syndrome this is another one of those diagnoses that you've got to know now if you see the patient come in with this rhythm then it becomes kind of easy usually they're going to come in in normal sinus rhythm so let's talk briefly about wpw syndrome and for those people that are are going to do the ekg workshop we're going to go into this in a lot more detail but right now we'll just cover the basics of wpw remember what the classic triad is for wpw syndrome it's a short pr a wide qrs slightly wide qrs and then the delta wave that slurring of the upstroke at the beginning essentially you've got your p wave and then there's not much of a pr interval your p wave and then bam it goes right into the qrs and the initial upslope of the qrs is very inefficient and so it's slurred and then you'll notice that the back half of the qrs is very nice and normal because the back half of ventricular repo or depolarization is very efficient but the initiation of depolarization is inefficient so you get a slurring of the upstroke it's not rare 0.1 to 0.3 percent of the population so all of us will see it uh a few times a year probably and this is what you're looking for in the post-syncope patient you're looking for somebody with the short pr the delta wave there's a nice one short pr delta wave notice however that the short pr and the delta wave are not present in all of the leads and a lot of people just learn to look for delta waves you know if you look at the mid portion of this ekg you're going to miss it because the delta waves are present in only a few leads i've seen some cases of wpw where good delta waves are present in only one or two leads and if you're not looking everywhere carefully you're going to miss it so what i tell people is if you want to never miss wpw don't get in the habit of only looking for delta waves what you do is every time you read an ekg look at the intervals the pr the qrs and the qt if you always do that when you look at the pr and you see a short pr less than 120 milliseconds whenever you see a short pr and somebody who had syncope now that's your trigger to go looking everywhere for deltoids and then you'll pick it up and sometimes just one or two leads but if you're just trained or programmed to only look for delta waves you'll miss it but as long as you're looking at the prs your short pr will tip you off to go looking everywhere for delta waves and then you'll pick it up all right so this if you just glance at this you're going to miss wpw but when you look at this and you go through your stepwise approach to reading kgs rate rhythm intervals stop look for the pr and when the pr is short now you look everywhere and ah there's the delta wave in lead 2 and v5 and v6 and so on all right why do we worry about wpw well wpw patients are predisposed to have svts usually that's not a problem and they get treated pretty easily but wpw can also predispose to have a-fib and a-fib is the killer because what you end up with is irregularly irregular and you can get enormously rapid rates sometimes 250 300 beats per minute and patients often can't tolerate that for long eventually they're going to go down to the ground called syncope and they may not come back so you've got to pick up wpw when they are in this state before they end up going into this if you discharge them with this because you missed it next time they go out they may go into the afib and have a molly that have a terrible outcome so the key things here wpw with afib is irregularly regular morphologies vary some keroses are wide some are narrow and it can get extremely rapid what's happening here is that you've got remember think about what atrial fibrillation is you've got four or five 600 impulses or foci in the atrium that are all firing impulses down some are coming through the av node usually the av node will let about 150 plus or minus a little bit 150 per minute through and because they're utilizing his purkinje you get narrow keros complexes the av node also if it sees too many impulses it just squashes them it'll only wants to see about 150 it'll only let about 150 through all the rest of them it just kills them so that's a really useful function of the av node and then a lot of the impulses go down the accessory pathway which has no av node so it's all too happy to conduct everything and when it comes conducts down the accessory pathway you get myocytomyocyte conduction rather than efficient his purkinje conduction you get inefficient myocyte to myocyte conduction so you get wide complexes so impulses going down the av node are narrow impulses coming down the accessory pathway are wide so you'll see some narrow complexes some wide complexes some fusions between the two and because the accessory pathway has no av node it'll conduct everything it'll conduct at rates of 250 300 400 beats per minute if necessary so the av node only conducts about 150 per minute and it squashes all the rest of them all right so the resulting rhythm is irregularly irregular with morphologies that are changing narrow wide infusions and rates might be 200 250 or so all right once again take a look at this irregularly regular morphology is changing and in some places rates 250 300 beats per minute normal a-fib never goes that fast unless you have an accessory pathway all right irregularly regular morphology is changing some narrow some wide and in some places the rates can get really really fast because that accessory pathway is all too happy to conduct everything that you see now what happens if you give the patient an av nodal blocker right supposing you're not thinking about wpw supposing you're just thinking about afib with a bundle and you say yeah let's give them some av notable blocker let's give some calcium channel blocker dual tizen or a beta blocker or a dige or amiodarone which is an av nodal blocker well this patient got a got some amiodarone which is an av nodal blocker take a look what happens it's a very reliable kill some might call it a clean kill right if you give these patients any av no blockers adenosine calcium channel blockers beta blockers dig amiodarone you can induce and often will induce ventricular fibrillation why would that be well think about what your av nodal blocker does it takes out the av node it blocks at the av node now what was our av node doing our av node was conducting some impulses but it was it was squashing a whole bunch of others right so if you if you block the av node where do those five or 600 impulses decide to go they all just go down the accessory pathway so now which is all too happy to conduct everything so now instead of a rate of 250 or 300 beats per minute now you've got a rate of five or 600 beats per minute and that's called v-fib and you're called defendant right so you cannot use av nodal blockers with these patients if you see a patient with afib wpw probably the best thing to do for them is to just shock them or you can use procainamide but no calcium channel blockers beta blockers adenosine dig no amiodarone either all right take a look at this this is a-fib with the right bundle there's no accessory pathway here so you could give this patient any drug you want give them calcium channel blockers beta blockers because there's no accessory pathway how do i know there's no accessory pathway here very simple because the morphologies of the qrs complexes are pretty much all the same all the way across if there were an accessory pathway conducting the morphologies would have to be changing you'd have some narrow some wide some fusions the morphologies are all the same so i know there's no accessory pathway here's another one take a look at this i know there's no accessory pathway here either how do i know because the morphologies are staying the same if there's an accessory pathway the morphologies have to be changing and it'll probably be a lot more rapid so this patient has no accessory pathway i'm going to give them anything i want i'm going to give them diltiazem or beta blocker whatever doesn't matter all right so the key thing here is afib wpw it's irregularly irregular and the morphologies are changing appearance if the morphologies stay the same all the way across it can be pretty sure it's not an accessory pathway that's conducting anything all right so again wpw is one of the things that you always look for check the pr intervals don't just look for delta waves check the pr interval and every time you see a short pr then go searching in all 12 leads for deltas and that's when you'll pick up wpw all right okay so let's take another mental break here let's go back to the beginning when you get an ekg and a post-sync patient what are you looking for well you're looking for arrhythmias you're looking for ischemia you're also looking for hypertrophic cardiomyopathy you're looking for brugada and you're looking for wpw all right anything else well let's add one more thing all right this one this is one that your computer usually will pick up but you've got to know the significance of it here's a 40 year old woman who comes in after having some type of spell you know she fell to the ground she shook a little bit whenever bystanders are there and they see a person fall to the ground and shake what do they say all right exactly they say it's a seizure what do they tell the paramedics paramedics arrive and they tell the paramedics oh she got a seizure paramedics show up in the emergency department and they say we're bringing this patient here for a first time seizure you always check an ekg on anyone with a first time seizure and the reason is that sometimes the so-called seizure is not actually a brain problem sometimes it's actually a heart problem which made them have syncope and fall sometimes people with syncope fall to the ground and shake for 5 10 15 seconds or so that's not a seizure that's just some myoclonic jerks that are associated with syncope you know i remember the neurologists used to always teach not everything that falls and shakes is a seizure right sometimes syncope will fall to the ground and shake a little bit so you check an ekg and when you look at this ekg i think hopefully most everybody can see that this patient has a very prolonged qt interval you especially see it out there in v2 very prolonged qt interval prolonged qt why do we worry about prolonged qt in the first place well prolonged qt can lead to torsod well next question then of course how you know how long is too long for the the prolonged qt well when you use the bazette formula which is not perfect but it's the most commonly used formula it's probably what your computer uses when the qtc the corrected qt is over 500 that is when you start worrying about the market increase risk for torsod and the higher that qtc goes the more at risk the patient is for developing torsades so i really worry when i see the qtc the corrected qt the qtc over 500. if the qt sees 470 480 yeah your computer might call it prolonged but i don't worry too much about it until that qtc is over 500. and then when i see the qtc is over 500 then i start looking for the underlying cause is it hypoka hypomag hypocalcemia drugs you know what's the underlying cause but that's when the patients are at risk for torsot here's a nice case this was uh it was probably about 10 minutes before the end of my shift i was doing a 3 to 11 shift and i'm i'm cleaning things up and i think you know for once i'm going to get out on time uh maybe 11 30 right after sign out usually i'm there till at least 12 or 12 30 or so trying to clean up loose ends and i was really on top of stuff so i thought you know i'm going to be able to get out right after sign up and then they come and drop the chart right in the rack in front of me and i'm thinking uh you know do i really need to see this patient well it turned out that this was a psychiatry patient who had recently started having who had recently started some new medications and the triage note had a little bit of a red flag it said patient is somnolent and suicidal no big deal and then it said patient is faking syncope so i thought you know that's a little bit unusual well we probably ought to get an ekg since this patient's on some psych med so i said to the ekg tech do you think you can get me an ekg um take your time take at least 10 minutes no rush so honestly it comes back in two minutes and he shows me the ekg here it is so you're looking at it and there's the ekg it says doctor but you've got an ekg and i'm thinking oh you know look at this ekg it kind of looks like there's a prolonged qt in there she's on psych meds but you know what there's some artifact in there also so it's like five minutes before the end of my shift so i say the tech you know what do you think you could get there's some artifact here do you think you can get me a better baseline take your time take at least 10 or 15 minutes he comes back two minutes later and says doctor matu i've got a better baseline ekg for you here it is so i'm thinking oh my god she's going in and out of torsade so i said to i actually said to the tech what was she doing when you got the ckg he said she was faking syncope no she wasn't faking syncope she was trying to die she she was on these new psych meds that prolong the qt and she was going in and out of torsade and that was producing these intermittent episodes of syncope and we happened to capture it on one of these ekgs in and out of torson so that's really again what you worry about so thank god i got the ekg because if i had cleared her and sent her off to psych and she had a cardiac arrest back there that would have been a real disaster but this was related to her medications there's a lot of different things that can prolong the qt and set off torsade um here's a 51 year old who came in with acute gastroenteritis she was severely hypokay and hypomag from multiple episodes of vomiting and diarrhea and when you look at her 12 lead you can see a very prolonged qt up there you know you wouldn't normally think that a gastroenteritis patient is going to potentially die but on the monitor she went into torsade from severe hype okay so i've really learned to respect bad gastroenteritis i've really learned to respect severe dehydration and any patient who's at high risk for electrolyte abnormalities i get an ekg of those patients early here's an alcoholic who visits us probably every friday and saturday friday usually he's intoxicated saturday he's usually withdrawing on this particular day he came in with alcohol withdrawal he was wretching vomiting he looked really dehydrated and so i thought well he looks really bad he's at high risk for electrolyte problems let's get an ekg on him early and here's the ekg now it turns out these t-wave inversions are old but what's new is this very prolonged qt so instead of putting him in the hallway where we normally put the alcoholics when beds are filled just to get fluids and and some thiamin and magnesium and everything else we we put them on a monitor because his qt is long he's at high risk and while he was on the cardiac monitor he started going in and out of torsade so instead of just dripping in the magnesium we started pushing it in and it turned out he was hypokay and hypomag also which is typical for alcoholics and and then his ectopy went away but he very he could very easily have died laying in the stretcher in the hallway if we hadn't gotten that ekg right up front here's an interesting case this is a 39 year old guy who got brought in for presumed first time seizure and what did we say earlier if you look up in any review article or any textbook chapter the work up for first time seizure always includes check and ekg have you ever wondered why you need to check an ekg it's for this reason because sometimes people that are thought to have seizures from the brain are actually having just my clinic jerks and seizures because of a heart problem they're having arrhythmias if you have an arrhythmia that hyper profuses the brain you're going to fall to the ground and you might shake a little bit and everyone's going to think it's a seizure and it's not a seizure it's not a brain problem they don't need phenytoin or levitaracetam or valpro gas no what they need is an ekg to figure out what caused the syncope and if you look up here this patient got brought in because of first time seizure we got an ekg and this patient has a prolonged qt of 563. so we put him on a monitor and while he was there being monitored he had another seizure and it was preceded by a run of torsade he was having torsade that was hyper perfusing the brain he'd fall to the ground shake a little bit everyone thought his seizure he doesn't need any problem or any meds for his brain he needs something to he needs some evaluation to reverse the prolonged qt all right so again one of the things you've got to look for is the prolonged qt when do you worry about it you worry about it when the qt is to is too long over 500 to qtc and what should you do check the electrolytes take a look at their medication list and stay away from any qt prolonging medications all right all right well let's uh let's sum up what we've talked about what is it that you're looking for on the ekg of a patient who comes in after a syncopal episode everyone knows these top two are the no brainers everyone knows to look for cardiac ischemia and to look for dysrhythmias what else did we add to the list high voltage with deep narrow key waves send them for a doppler echo to look for hypertrophic cardiomyopathy v1 and v2 if they show an incomplete right bundle type of pattern with that coved st elevation terminating an inverted t wave send them to an electrophysiologist to look for a brightness intro make sure to look at the pr interval and anytime the pr is short think about wpw look for those delta waves everywhere and also pay attention to the prolonged qt if the qt is over 500 milliseconds then start looking for the underlying cause of potential prolonged qt hypoka hypomag hypocalcemia there's a lot of medications that can do it as well those are the things that you've really got to look for with that i will conclude if you have any questions please just shoot me an email at amlema2 comcast.net and thank you all for your attention