where i'm going to talk about syncope evaluative modalities and therapy um i'd like to give you an overview of the definition and background of syncope initial workup uh evaluative modalities which include kind of all of these ecg carotid sinus massage tilt testing um [Music] you know prolonged uh ecg monitoring ep study stress testing and i'm not going to talk about atp tests because that's been kind of thrown out and potential treatments for um syncope so first uh definition syncope is defined as transient loss of consciousness due to cerebral hypoperfusion and it's usually associated with inability to maintain postural tone it has a rapid onset short duration and spontaneous recovery and it's usually in the absence of any clinical features that are specific to another form of transient loss of consciousness like epilepsy or some other condition uh this is a nice algorithm that you can kind of follow this is from uh the or the european heart um association uh guidelines from 2009 those guidelines have been updated in 2018 but i still think this is a very valid diagram so the first question that you have to ask and i i think it's the hallmark of syncope is whether or not the patient had loss of consciousness um so because patients are presented to you in the er somebody had syncope or near syncope so the difference is near syncope means that you didn't really lose consciousness you you came near loss of consciousness but you didn't actually have loss of consciousness the hallmark of syncope is you actually have loss of consciousness and you do not recall anything so the patient should say yeah there was a period there where it was just blank i i don't remember what happened and then i just woke up and you know people were around me uh trying to you know help me recover um so if there is loss of consciousness then you go down this algorithm was it transient was it was a rapid onset short duration was there a spontaneous recovery if the you know the answer is no so somebody has prolonged uh unconsciousness or had to be resuscitated then we're talking about either a coma or a or aborted sudden cardiac death if the answer is yes to all of these questions uh then we're really truly talking about transient loss of consciousness and then the question is was it traumatic or atraumatic so traumatic would be you know somebody hit you you got you got hit by a baseball in the head and and and you lost consciousness okay so that's basically a concussion uh or or if you got you know punched really hard same thing uh if it's if it's a non-traumatic transient loss of consciousness then you know most often that's syncope uh but you know you it could be an epileptic seizure it could be psychogenic and there are other rare causes one thing i want to point out is that when you hypoperfuse your brain initially people tend to have some seizure-like activity but the difference between syncope and an epileptic seizure is that the scissor is going to last for seconds to minutes and you're going to continue to see the pace and seize for a while um with with syncope or or you know and i see this sometimes when pacing is inhibited on a pacemaker and you get sort of abrupt hypoperfusion of the brain um the patient will do will have some seizure-like activity for like maybe five seconds like they'll shake their hands and then pass out okay but but an epileptic seizure should last longer than five or ten seconds okay um in terms of issues regarding syncope it is common it is costly it can be very disabling right so this poor guy here standing as a guard he may not be able to do this job for too long if he keeps losing consciousness right so people can lose their job because of you know recurrent uh abrupt syncope it can cause physical injury people often present in the emergency room with trauma i took care of a patient about six or seven years ago who was working on a scaffold uh doing you know construction work it was a hot day he experienced what we think was vasovagal syncope he fell off the scaffold and snapped his broke his neck and became paralyzed so that's an extreme um you know outcome of something that's common and usually doesn't lead to as much injury but sometimes if you have a bad fall you can really injure yourself and you know to the point that you could be paralyzed uh some people are very fearful that this can happen at any point so they lose their independence and there's some concern that if it's cardiac syncope you know it can lead to sudden death in terms of the breakdown ethiologist for uh for syncope about 60 of syncope is neural mediated vasovagal syncope the most common term is vasovagal but carotid sinus uh sensitivity falls under the same neural mediated syncope and there can be other similar triggers like call for swallowing or post-mixture reason all of these four fall under neurally mediated syncope or reflex syncope there are many names but they essentially mean the same and about 60 of the time that's um kind of the etiology of syncope about 15 of the time you have orthostasis so either drug induced somebody who's on multiple medications for blood pressure volume depletion somebody is dehydrated and all of a sudden they stand and they lose consciousness or um you know autonomic nervous system failure either primary or secondary we see this a lot in like parkinson's disease and other con conditions and this constitutes about 15 of syncope uh cardiac arrhythmias so bradycardia whether sick sinus or av block or attacking mediated syncopal episode a fast vt or svt or some other channelopathy those all fall under cardiac arrhythmias and they make up about 10 um and in terms of structural cardiovascular issues you know am i a prior myocardial infarct leaving you with a significant scar or pump failure aortic stent severe aortic stenosis can cause syncope you can have syncope in hypertrophic cardiomyopathy in pulmonary embolism in pulmonary hypertension and obviously also in aortic dissection these conditions make up about five percent and then despite all that we have about ten percent of undetermined etiologies uh for syncope in terms of the physiology of vasovagal syncope um the upright posture leads to pulling of blood about uh about 500 to 800 ml of blood can end up in the splenic circulation uh or in the pelvic circulation and lower extremities and that leads to decreased return to the right atrium and ventricle decreased cardiac output and blood pressure that is sensed by the arterial and cardiopulmonary baroreceptors trigger a sympathetic activity vasoconstriction vino constriction and a rising heart rate um that excess contractility is then sensed by c fibers in the ventricle and a signal is sent to the um the brain and sometimes you either have an in a ineffective reflex response meaning you get you know vasoconstrict enough and you pass out or you can have a paradoxical vasodilation which leads to further hypotension and ultimately loss of consciousness and you can have either a pure vasodepressor response which is purely hypotension you can have purely a cardio inhibitory response profound bradycardia or asystole and most often it's a mixed response and we're also dealing with reduced norepinephrine spillover uh to the to the plasma and that can be in the form of either reduced norepinephrine synthesis or increased norepinephrine reuptake this is a schematic of what we think happens this is not clearly defined um i don't think you're going to be tested specifically on the mechanism of at least in you know in terms of when i studied for my internal medicine boards cardiology boards ep boards i don't think there were very many questions specific on this topic um on this particular diagram but i just want to mention this is the general sort of understanding that we have and i don't think it's clearly defined but we tend to have triggers whether they're emotional triggers somatic triggers or some hemodynamic trigger that essentially go to the brain and you know the brain either causes vaso sends a signal back via different nerve fibers and you can get vasodilation of the splenic circulation or the lower extremities or bradycardia and asystole okay or you can have pure sort of autonomic dysfunction like we do in parkinson's disease and you know those patients tend to have the inability to you know chronotropic incompetence they inability to bring up their heart rate or they have inadequate vasoconstriction that leads to you know higher incidence of syncope they cannot react as fast to like this hemodynamic changes uh as a normal uh physiologic uh scenario you know person okay this is a very similar this is another diagram of basically what we talked about you know if you look at the very top it's you know a person leaning on a tilt table test that's what we're trying to induce during a tilt table test right we try to cause this decreasing venous return by the upright posture to leading to decreased left ventricular filling you know increasing pathetic tone but we're trying with the tilt table test to recreate what we think happens in uh in normal circumstances and leads to or abnormal circumstances that lead to a syncope this slide is from a study that was published in 2002 it's part of a farmingham study and they looked at patients for nearly 17 years of follow-up and the incidence of syncope is pretty equivalent between men and women there is some variation depending on aids but i guess the greatest message of this slide is that as we progress through life the incidence of syncope increases and uh the overall you know in this study out of 7 800 patients 10 822 experienced syncope at least one episode in 17 years so that it was about 10.5 percent of the population they started had syncope and the incidence was 6.2 per 1000 person years also from the same study i i find this slide to be very important i think that if you deem that the syncope was purely vasovagal that's the yellow line well that's a good prognostic indicator that because essentially it tracks patients who had no syncope which is the black line so basically if it's vasovagal syncope the prognosis is really good you're not gonna die suddenly you know you're gonna live just as long as people who had no syncope however if there's a if you find a cardiac etiology that's the red line then your prognosis is much poorer and same if you find a neurologic cause for syncope but as you can see here the risk of death increased by 31 among subjects all subjects with syncope but again when you break it down vasovagal syncope has a benign prognosis but the risk of death doubles with cardiac syncope this slide shows the breakdown of causes of syncope by aids so in young folks less than 40 years of age predominantly you have neurally mediated syncope less orthostasis less arrhythmias as you progress through life in this 20 years between 40 and 60 years of age orthostatic hypotension becomes more prominent arrhythmias and also all of a sudden you start building up cardiac structural heart disease when you're over 60 years of age you can see that you know half of it is a little more than half this neural immediate syncope the rest of it has to do with either an arrhythmia a structural heart problem or worsening orthostatic hypotension so the initial workup should include a detailed history and physical exam that is a class one recommendation i'm just gonna go over it once so class one means you should be doing it class three recommendation means you should not be doing it you're doing harm and then two a and two b um those mean two a's based on randomized data and most experts agree that you should be doing something and class two b is a softer indication okay for the most part you should be practicing based on class one and class 2a recommendations sometimes i dip into class 2b recommendations and obviously i try to never use a class 3 recommendation because that's contraindicated so phys detailed history and physical exam is a class 1 recommendation you should do that you should do a 12-lead ect on somebody who had syncope okay that's based on uh the american guidelines um and the european guidelines from 2018 gave you know tell us that we should also check for orthostatic blood pressure up front uh the initial evaluation should answer three key questions was it a single episode or not okay the story that you get sometimes from the er you know you really have to go down there and interrogate the pacing yourself you need to ask some specific questions did you lose consciousness do you remember the entire event you know did somebody have to resuscitate you or do you know if somebody you know you have to talk to the patient uh has the etiology of the syncope been determined you know was there an ecg tracing showing ventricular tachycardia or fibrillation or do we have you know do we know what caused it you know uh is there evidence suggestive of high risk features for potentially future cardiovascular events or even death what are the high risk features so bifasicular block okay defined as either left or right bundle branch block combined with a left anterior or left posterior fascicular block okay so that tells you that there's some conduction abnormality there so you may see right bundle branch block and you know you ignore it many times because the patient is asymptomatic but for the patient who presents with syncope even a right bundle branch block can be significant uh because that may be just an early sign of some infrahexian conduction abnormality that can lead to abrupt high grade av block and syncope um you should look at the qrs okay and narrow qrs you know 90 milliseconds you rarely have infrahissian disease when you have a very narrow qrs but if the qrs is wide irrespective of what type of bundle brands block you have uh it's just a sign that you know the electrical impulse is not getting down to the purkinje fibers the way it's supposed to you know it's not physiologic um you know you should obviously look for second degree av block whether it's mobitz one or more bits two more bits two is definitely worse prognosis than mobitz one but you know people can be symptomatic sometimes even with mobility one av block are they having some baseline um sinus bradycardia or even atrial fibrillation or atrial flutter with a very slow ventricular response because that might tell you that okay the patient right now has a heart rate of 40 they're asymptomatic they're sitting comfortably smiling at me but you know i don't know if the heart rate dips down in the 20s and they pass out you know so some baseline sinus bradycardia or slow ventricular response could be a sign of you know you know even worsening bradycardia at times if you're noticing episodes of non-sustained vt on telemetry if you've seen preex if you're seeing pre-excitation if you're seeing a long or circuit t interval if you have early repolarization if you have a brugada pattern you know those are the things you want to look for on the ekg and telemetry if you have negative t waves in the precordial leads and potentially an epsilon wave that can be suggestive of arvc another condition that can cause abrupt syncope loss of consciousness if you notice left ventricular hypertrophy on an ect that can suggest hypertrophic cardiomyopathy cardiomyopathy so these things matter the ekg matters and normal and totally normal ekg is a great prognosticator right normal intervals narrow qrs none of these high risk features you're you're good for the most part so this is what long qt might look like this is what brugada syndrome might look like this is cpvt you have bi-directional vt here okay short qt interval or early repolarization are high risk features in terms of carotid sinus massage uh so carotid sinus massage can be performed in patients more than 40 years of age they say you know to auscultate the carotids first make sure you're not dealing with some brewery before you apply and it's not really a massage it's more like pressure on the carotid bulb you hold the carotid bowl for about 10 to 20 seconds obviously make sure that there's perfusion from both carotids and no bruise before you do that uh but if the patient has some abrupt pause or profound bradycardia associated with that maneuver but and we've seen people even pass out with caroline sinus massage then you know that's a you know prognosticator that and sometimes we recommend pacemakers if these the the symptoms are are severe uh this is what a response a positive response might look like for carotid sinus massage you get this abrupt in this case 7.3 second pause an orthostatic challenge so you can have the measure the patient's blood pressure and the supine the seated position and the standing position if you notice a drop in the blood pressure the systolic blood pressure of greater than 20 millimeters of mercury or diastolic drop more than 10 millimeters of mercury and that happens within three minutes of standing uh that's a positive orthostatic challenge or if you have a decrease in the blood pressure to less than systolic blood pressure to less than 90. um if you have that drop irrespective of whether the patient passes out or not you know you can i usually report it as you know mild orthostatic intolerance or mild orthostatic hypotension you know without symptoms so you know you you can have orthostatic hypotension and the patient can be completely asymptomatic or you can have you know orthostatic hypotension and the patient loses consciousness so depending on those findings is how i kind of tailor my report of a tilt test till testing has been around since 1986 it's a safe test there have never been any reported tests during tilt table testing this is more or less what it looks like initially we have the paste and lay flat for about 10 minutes then we tilt them to 45 degrees for about two minutes and then we go to 70 degrees and and the patient is strapped on their lower extremities their torso so it's a safe environment if they were to pass out they're not going to fall and hurt themselves usually the nurse is present throughout the duration of the tilt test the physician often walks in and out kind of keeps we keep checking on the patient to make sure that nothing abrupt happens um if the patient passes out the table is lowered they're given intravenous fluids and they usually almost always recover um the end point of tilt table testing is induction of reflex hypotension and bradycardia uh sometimes you have a delayed orthostatic hypotension and you know sometimes that's associated with syncope and other times it's not um and again the responses i usually try to break it down was this purely cardio inhibitory did i see a long pause was it purely vasodepressor or was it a mixed response indications for tilt testing uh one is for the diagnosis of vasovagal syncope with a 2a recommendation a one is for delayed orthostatic hypotension also you know 2a recommendation to discriminate convulsive syncope from epilepsy to a recommendation for that and for the diagnosis of pseudo syncope so if somebody's on a tilt test and all of a sudden they just drop and there's no drop in their blood pressure there's no change in their heart rate it's probably psychogenic syncope okay i've seen that um twice not that often but uh tilt testing should be considered in patients with suspected reflex syncope um orthostatic hypotension or paws oh yeah and in gold here these were the american guidelines from 2017 and in in white uh were the european guidelines so they both give it a 2a recommendation it's a bit controversial some doctors they don't like tilt testing but i i do think that it gives us gives us some useful information but i guess my recommendation is don't stop at the tilt test because sometimes you can miss more important and more bothersome conditions with worse prognosis um limitations of tilt testing and negative tilt test does not exclude the diagnosis of reflex syncope and the sometimes correlation of the type of response during tilt test and spontaneous syncope is questionable so what i'm saying is that if somebody can has can have hypotension even passed out during the test but it doesn't necessarily mean that that's exactly what happens and that exactly is what caused the spontaneous syncope at home it just gives us some clues of what the patient may have i recently had a patient who had uh you know a clear vasovagal syncope on a tilt test but when i brought her in for electrophysiology studies he also had infrahysian block so if i had just stopped at the till table test i would have concluded that it's clearly vasovagal i should stop here and give her middle drain and fluids and you know but i would have completely missed uh in for his block the reason why i did an ep study on that patient is because she also had write bundle brands blog on her ecg which gave me a clue plus her history she was kind of standing you know washing dishes and all of a sudden she just had abrupt loss of consciousness there was no pro drone uh she was it wasn't hot he wasn't standing for a long time it just wasn't the classic presentation so i decided to do a tilt and an ep study the tilt was positive but so was the ep study so we ended up giving her a pacemaker cardiac monitoring so we use a lot of these in electrophysiology for multiple reasons but when somebody passes out that's kind of one of our go-to uh systems to use this is called the zeo patch uh many companies uh make them we use preventus there's another company called biotel but they're very simple we used to do holders with cables and you know based on how to go home with a little box but uh the past decade now we be we've been using more and more of these they're very convenient they're very discreet they're easy to apply they go on the chest on the left side if you can as you can see here there's a button in the middle we tell patients to press the button when their symptoms are most severe if they feel their heart racing if they feel like they're extremely dizzy and about to lose consciousness the importance is to have symptom rhythm correlation that's the gold standard so i want to know what the rhythm was at the time of the event okay so and zeos are helpful because they help us accomplish that you know have some sort of correlation that you know when the patient pressed the button they were in two to one av block or they had a profound pause or nothing happened and maybe it was blood pressure related or they had chest pain i don't know i just uh symptom rhythm correlation is very important and this is one way to achieve that other modalities telemetry if the patient is in the hospital you can give him a 24-48 higher halter i almost never do this anymore i've kind of either give him a zeo or go to something you know so event monitors are xeo preventive and and like i said biotel or we can go to an implantable loop recorder that stays under the skin for about three years the duration of monitoring should be selected based on the risk and the predicted recurrence rate so if the patient says oh yeah i pass out every day you know so then you probably don't need a loop recorder right but if the patient says i had an episode two years ago and i had an episode six months ago you may not capture anything uh you know in a 24-hour holder or even a two-week monitor so if the patient says you know the episodes are very infrequent you might go straight to a loop recorder so this is what what they look like when you apply them on the chest you know this is what a halter kind of more or less looks like um you know the in terms of uh the usefulness of external loop recorders there's some in terms of the diagnostic yield there's some mixed reports you know study from 1990 so the diagnostic guilt yield of 25 percent this study so the diagnostic yield of 63 other studies so that they're not useful i think they're fairly useful if they're used appropriately the implantable loop recorders the old generation of loop recorders looked like this about this size we had to make a cut on the chest dissect down to the back muscle and suture them on the pectoralis muscle and close the skin the more recent loop recorders the link and there are several other ones are much smaller and they can be inserted without a significant surgical incision it's a tiny little cut and it's injected under the skin these days we do this in our office you don't have to go to the hospital it's kind of like going to the dentist we give some local lidocaine with epinephrine tiny little cut it takes five minutes to put one of these in one sits under the skin and some surgical glue on the top of the of the skin and that's it the basin is set up with a home monitoring system that that's at their bedside and it communicates with a device the battery lasts up to three to four years the device is pre-programmed for significant bradycardias less than 30 beats per minute significant tachycardias we set that as we as we please and also the patient has is provided with a clicker that they can put on their key chain so if they have an episode they can press the clicker and it basically takes a snapshot and it saves that snapshot of the event otherwise the device continuously records things so the looping means that you you're continuously recording things and deleting you know rhythm strips throughout the day uh and it only saves those predetermined tacky brady episodes or anything that the patient presses as an as an event this study looked at um you know whether or not you should wait to put a loop recorder and as you can see the two pie graphs look just about the same right so whether you go straight to a loop recorder after the first episode of syncope or wait and have an extensive workup echo stress test you know maybe a full neurologic exam maybe a head ct and if you don't find anything then go to a loop recorder there's not that much difference the diagnostic yield if you use a loop recorder early it's just a little bit lower than if you do the extensive workup but they're very similar 27 versus 35 and the breakdown of what we find on loop recorders is also very similar so about 50 more than half the time you find some asystole or bradycardia eight to ten percent of the time you find some tachycardia mediated episode that causes syncopia or near syncope this is mainly syncope true syncope here or no arrhythmia in about a third of the patients if you if we if you look at patients who have pre-syncope um the diagnostic yield there is a little bit lower okay you know you get uh so with pre-syncope you only get brady or taiki episodes about 19 of the time each and the rest of the time you find nothing so you know ilrs are good for true syncope less useful for pre-syncope so here are the guidelines ilr is indicated in an early phase of evaluation in patients with recurrent syncope uncertain origin the absence of high risk criteria so you should look at the ekg and make sure you're not missing something you know like long qt you know and and then just give them a loop recorder when they may benefit from a defibrillator and a high likelihood of recurrence within the battery life of the device and ilr is indicated in patients with high risk criteria in whom a comprehensive evaluation did not demonstrate a cause of syncope so as an example let's say somebody has an ejection fraction of 40 percent and they had syncope and you brought them in and you've done everything they had a cath they had an ep study and you have you couldn't find anything you should consider a loop recorder you know that's a risky to you know it puts you in a difficult situation as a physician because you know who knows if the next event that you might capture on a loop recorder might be a catastrophic event but if you don't meet any criteria for pacemaker or defibrillator and your workup has been negative this is what you're left with unfortunately and you know the worst thing you want to see as an electrophysiologist is you know you give somebody a loop recorder for syncope and then they call you from the morgue to interrogate it and you find ventricular fibrillation and death okay that has happened you know and it's uh very very very rare infrequent but it can happen but again if you don't have if you don't meet any criteria for a defibrillator or a pacer you know this is what you're left with electrophysiology study that the diagnostic efficacy of ep study depends on the pretest probability so if you have a hunch that there is you know i'm seeing something here i'm seeing left bundle brands blog i'm seeing uh you know there's a prolonged pr interval here uh there's a there's some high risk feature there's hypertrophic cardiomyopathy here then the ap study is likely to be positive but if you take a bunch of people with syncope and normal ekgs and you do a bunch of ep studies on them then your diagnostic yield will be very very low so i don't recommend an ep study for everybody i kind of you know look at all the data and if i see features that are suggestive of a conduction abnormality or an arrhythmia then i recommend them in this study and as you can see here positive results occur predominantly in patients with structural heart disease so if you know that somebody has had a heart attack even if the ejection fraction is you know fifty percent if they have scar you might find scar-mediated vtec so the ap study has a utility there but in general sensitivity and specificity are not that great a lot of times ep studies are negative so uh indications for ap study if you have ischemic cardiomyopathy and you suspect an a rhythmic cause of syncope just like i i just said a v-tag on a patient who has even a small area of scar and preserve the ejection fraction otherwise by spicicular bundle branch block when when non-invasive tests have failed to make the diagnosis so you have a monitor you give them an event monitor they have left bundle brands blocked you don't see any anything during the event monitor but the patient has passed out once or twice you should do an ep study because there are clues during ep study that can tell you whether or not this patient is at risk for abrupt uh high grade av block in patients with asymptomatic bradycardia okay that's that's a softer indication and syncope patience preceded by a sudden and brief palpitation so um in asymptomatic bradycardia what you're looking for a lot of times is you know you're doing snares to see if they have uh sinus no dysfunction so if you can't prove it by an event monitor you're trying to kind of uh assess it during an ep study and and syncope with palpitations you're looking for an svt mechanism there or vtac mechanism so uh i was just alluding to uh sinus node recovery time which is the test that we do for sinus node dysfunction uh during an ep study and and what we do is we overdrive pace the right atrium and then you abruptly come off and you measure to see how long it takes for the sinus node to recover um so they found that in patients with uh sinus node recovery time of more than 800 milliseconds so in electrophysiology we measure everything in milliseconds they are eight times more likely to have syncope than in patients with a normal snare below this value if you suspect av block in a patient with a bundle branch block and you have a prolonged hv interval and i'll show you what an hv interval looks like uh if the hv interval is more than 70 milliseconds so the normal hv interval is 35 to 55 milliseconds if it's more than 70 milliseconds it's really bad and if it's more than 100 milliseconds it's really really bad you know those patients are very likely to have abrupt high grade or complete av block and syncope and sometimes sudden death okay uh we also use this uh procainamide infusion one gram intravenous over 20 minutes so if you have a marginal hv interval of you know 65 say milliseconds we give procainamide to see if we can push that out to over 100 and if it if it prolongs to over 100 that's also positive and you should consider a pacemaker or if you see induction of infra his block either spontaneously once you put catheters up or by pacing in terms of suspected tachyarrhythmias as i mentioned we we look for induction of svt with associated hypotension with patients with previous mi you look for sustained monomorphic ventricular tachycardia that's strongly predictive of syncope all right so now look at my last point here induction of vf is non-specific okay you can induce vf even in normal subjects but if somebody has had a heart attack and you either have a wall motion abnormality on an echo or you have an area that there is no blood perfusion on its on a nuclear stress test or an mri and that patient loses consciousness what you're trying to induce during ep study is sustained and monomorphic ventricular tachycardia okay that patient even if the ejection fraction is 50 should get an icd okay this is what sinus node recovery time looks like so just to orient you here um this is these are the surface leads uh here we're pacing in the high right atrium this little did so here is this his signal in this patient okay so a his v a you can't see that his v you come off this is your last paste beat and you wait to see how long it takes before the return sinus bit comes in okay so that's sinus node recovery time this is infra hessian block again surface leads p wave qrs t wave this is what it looks like on the ep pruca uh we call it the pruca that was the engineer who designed the system that we use um but this is a signal from the high right atrium and this is a catheter that's sitting across the tricuspid valve with a distal tip of the catheter in the ventricle the middle part in the hiss and kind of the proximal part in the atrium so you get this nice signal of an a a his and a v okay now look here so you have an a a hiss and a v and a a hiss and no v so that means that you got through the av node you got to the bundle of his and then you blocked so we call that infrahissian block and that has a worse prognosis if than if you had a know his nov that would be that would mean blocking the av node and that's what you see with mobitz type one uh that's more physiologic meaning that you know you'll most most people have a went back periodicity you block at some point it's just a matter of when you block and you know if the block is in the av node or below this case was somewhat controversial in my opinion it was a 45 year old male had mild depression he presented with syncope the story goes that he was caring for his core for his horse it was somewhere in maryland uh the horse accidentally stepped on his foot broke his foot shortly after and while he was trying to calm the horse and with his wife yelling at him he collapsed he fell on his face his astute cardiologist uh in maryland so that there was this st elevation it doesn't look like your typical you know what i'm about to show you but when this when we gave him procainamide he had it you know he had this which looks very much like brugada so you know she ended up getting an icd okay even though the controversial part here is that you know [Music] this episode of syncope was probably vague all right i mean his horse broke his foot and he lost consciousness however you know you also have this and you know when you put the two together syncope and brugada pattern you know anyhow this this gentleman it's a 2a indication you know but if you look at the fine print down here it says patients with syncope consistent with consistent with a reflex mediated mechanism should not undergo the implantation of icd um you know we brought this up to this pair with this space and sometimes you just have to have a discussion with the patient and say well we think you have this but you know it doesn't necessarily add up and it could it could have been reflex mediated if the patient says you know i absolutely want it or i absolutely don't want it sometimes you just have to kind of go with it 50 year old female with syncope okay what's the striking feature here okay she has a lot of lvhs right and this is these deep t-wave inversions right so syncope on a person with left ventricular hypertrophy is a little more significant right because if you die if you do an echo and you truly diagnose this patient with significant hypertrophic cardiomyopathy and they have syncope that's a high risk feature okay and icd implantation is reasonable in patients with hypertrophic cardiomyopathy presenting with more more than one recent episode of syncope suspected to be of a rhythmic nature a lot of times we just don't know uh in terms of echocardiography it is a class 1 recommendation for diagnosis and risk stratification in patients with suspected structural heart disease 2-dimensional and doppler echo during exercise in the standing or semi-supine position to detect provocable left ventricular outflow track obstruction so they're saying that if you have a patient with hypertrophic cardiomyopathy sometimes you want to put them on a treadmill test to see if they obstruct further with peak exercise uh and you know uh so that's when the or or if the gradient the left ventricular outflow track gradient the pressure gradient uh is you know less than 50. also you want to look for aortic stenosis obstructive cardiac tumors pericardial effusion and tamponade aortic dissection other etiologies so echo is a very useful tool it's benign ultrasound waves exercise stress tests should be offered to patients who experience syncope during or shortly after exertion okay specifically there you're looking for catecholaminergic polymorphic vt though that's a condition where people describe as you know i pass out when i pick exercise it's really bad right i mean anytime somebody passes out a big exercise not during the recovery period but at pick exercise that's that's bad uh you know you want to assess for long qt and if they can shorten their qt with exercise um if you have a type 1 brugada sd elevation during exercise or in recovery or if you develop a abrupt heart block second or third degree that get gets worse with exercise in terms of the diagnostic yield of all these modalities that we just discussed uh in this study they found that tilt testing gave us a diagnostic yield of 58 and then everything else ep study carotid sinus massage were lower so you unfortunately have to use multiple of this to get somewhere because often you know the individual tests have a low diagnostic yield so if you diagnose somebody with vasovagal syncope uh you educate them you tell them that their prognosis is fairly good uh we recommend counter pressure maneuvers so teach the patient to brace down if they feel a pro drum sit down to prevent trauma brace and it usually resolves uh increased salt and food intake sometimes i recommend low low carb gatorade as you know the gatorade was developed in florida uh for the university of florida gators in the 1960s i think and it was basically water with electrolytes and what they found was that water with electrolytes rehydrates you better than just water alone so you need salt and water uh to rehydrate appropriately and what they found was that less athletes were passing out they end up using winning the national championship that year and everybody thought that gatorade was the magic drink and anyhow that's the story about gatorade and if you look at all the medicines that we can potentially use for vasovagal syncope the only one that has a class 2a recommendation is miradrine and everything else has a software recommendation uh so flood record is on beta blockers orthostatic training all this stuff selective ssris or a pacemaker the kind of soft indications if you suspect syncope due to orthostatic hypotension which we previously defined it you know if it's due to dehydration rehydrate if it's due to drugs reduce or withdraw some of the medications if we think it's neurogenic orthostatic hypotension you know give them water and then you can use some of these recommendations compression garments counter pressure maneuvers meter drain droxy dopa this is a recently kind of recent medication that came out in the market it's called north terra sometimes it works sometimes it's ineffective after so many years of usage if you're gonna give somebody a pacemaker and i'll go into more details the pacemaker of choice is something with uh is a dual chamber device with closed loop stimulation which is a very specific algorithm it senses a drop in the impedance right before syncope is about to happen and it actually uh kicks in and paces a little bit faster in order to prevent the uh the event and this is a small study of about 50 patients somewhere in the control arm somewhere in the cls arm and what they found was that with the cls algorithm uh the patients had significant reduction in the um invasive vehicle syncope they followed them up to about a year so this was published in europe ace in 2004 then there was the spain study that was published in 2017 they also i guess retested the cls algorithm this time everybody got a pacemaker ddi is a non-tracking mode you know you're basically turning off the pacemaker with ddi and uh dd ddd cls was the algorithm if you look on the slide on the left uh this is the proportion of patients with syncope okay with ddd so so this slide shows that this group had the pacemaker on ddd cls for 12 months and then they flipped to ddi and this group in red was ddi for the first 12 months and then ddd cls for the remaining okay and then you can see here that there were no events and then as soon as you turned off the pacemaker from cls to off you had increased incidence of syncope the other group had syncope and then once you turned cls on no more syncope the curve flattened and then here the slide to the right just shows patients who were all along over a period of 12 months on ddd cls and versus you know you can see that there was basically no symptoms no recurrence of syncope the issue three study was published in 2012 again they took patients that had a syncopal episode spontaneous associated with a systole of greater than three seconds or a non-syncopal asystole of more than six seconds and they were randomized to either have pacemaker they all got a pacemaker then were randomized either pacemaker on or off and what they found is that the pacemaker helped there was a 32 absolute risk reduction and a 57 relative risk reduction in syncope at two years but what as you can see here even patients who had the pacemaker on continue to have some episodes of syncope so this was a paradox so they said well why would somebody with a pacemaker still have syncope and then then they took this subset of patience and they gave them a tilt test and what they found is that the patients who had a a you know the patients had a positive tilt were the ones who continue to syncopy so that was probably a blood pressure related issue but you know the patients had a negative tilt table test with the pacemaker did really really well and that made it basically to the national guidelines um and basically you know dual chamber pacing can be effective for patients 40 years of age or older with recurrent and unpredictable syncope who have documented pause of more than three seconds during syncope or an asymptomatic pose of more than six seconds so this recommendation comes from the issue three study uh till table testing can be considered to identify patients with a hypotensive uh response who would be less likely to respond to permanent pacing okay that's also from the subset of the issue three study okay um you you know you're not going to put a pacemaker for unexplained syncope or unexplained false we need some data okay otherwise it's a class 3 recommendation and then this was a study published in 2016 at the new england journal of medicine and it showed that pulmonary embolism pulmonary embolism was identified in nearly one of every six patients who were hospitalized for our first episode of syncope so think of peas also um these are the recommendations education reassurance promoting salt and fluid intake class one reducing backing off on some medications using physical counter pressure maneuvers use of flutter cortisone beta blockers mitodrain the middle drain has a higher this is this is an older data the meteor has moved up um in terms of this is a slide from the most recent 2018 guidelines the european heart journal and i just want to point out some things that have shifted uh from class 1 to 2a or or vice versa if it's a busy slide so you may want to have to review this on your own uh conclusions 12 lead ecg is mandatory in all patients with syncope continuous ecg recording is the gold standard to establish symptom rhythm correlation ilr should be considered early in the workup of unexplained syncope class 1 drug challenge should be performed if you suspect a brugada eps is most useful and sensitive in patients with previous mi and patients with some form of bundle branch block or white qrs based on the composite of available data there seems to be a role for permanent patient in selected patients with neural mediated syncope patients with a negative tilt table test may benefit most from pacing