Resuscitation 2016 – Cardiology Literature Update by Amal Mattu, MD



so most of my talks actually all for my talks have been cardiology literature updates to a large extent and this is labeled cardiology literature update but really this is just a potpourri of a few additional topics that I'd like to address before we we close things out so a little outline we're going to talk about four articles in this talk one that pertains somewhat to education and then we'll talk a little bit about precinct it'd be just a real quick simple article on pre syncope versus syncope mn2 ECG topics just to finish things up before we get into the syncope and ECG topic though I want to introduce the first article based on an email this is in type of email that I oftentimes get and something that I'm sure many of you may relate to as well the email usually goes something like this hey Alma I was at a conference recently and you were talking about this or maybe Haney or someone else was talking about this topic I told my cardiologist or my hospitalist about this new thing that you talked about or a drug or any cagey finding or something and they've never heard of it and they were angry at me for even bringing it up right does anyone air ever experience that right raise your hands up how many people have yet all of us right everybody and so the question is when you hear things at conferences that are based on good literature why is it that sometimes the consultants may not have heard of this this is a fantastic article that was published in the cardiology journals and what I will tell you is that there are similar literature pertaining to intensive care medicine infectious disease and this would probably be true for emergency medicine also so this is not a slam against cardiology it's just kind of a slam against medical education in general so in this American Heart Journal article they asked a very simple question when a defining study a definitive pivotal study gets published leading to a class one recommendation standard of care how long is it before the rest of society medicals society starts practicing that way all right so what these authors did was they found 11 class 1a recommendations things like using aspirin for acute MI right no doubt that's very important based on fantastic literature and they went back and found the pivotal clinical trial the study that definitively says that this is what you have to do it's such a powerful study that it leads to the class 1a recommendation and they asked how long does it take from the time the pivotal study leading to class 1a recommendation is published until the majority of clinicians are actually doing that and they said how long before 70 percent of the people out there are doing it how long before 90 percent of the practitioners out there are following what this pivotal clinical study ended up showing all right so this is a quote from out of the study the time of pivotal clinical trial publication to meaningful uptake of class 1a remember this is not equivalent to a piece and they just looked at ACS therapies and the clinical practice how long do you think it took before this was widely adopted in standard practice amongst these 11 pivotal clinical drug in me a number how many years did it take 3 2.5 8 10 15 16 years it's on average 16 years from the time the pivotal study definitive study standard of care studies published until 90 percent of the clinicians out there are using it let me give you an example aspirin take a look down here aspirin from the time that the definitive study said aspirin saves lives it took two years before it got incorporated into guidelines okay two years and it took an additional 14 years before 90% of clinicians were routinely giving aspirin to their stem ease what about TPA from the time that the definitive studies showed TPA saves lives and stem ease it took eight years before it showed up in the guidelines as class 1-a eight years of people dying before it got incorporated they didn't go out beyond that because then Kath started taking over unfractionated heparin from the time that definitive studies showed that unfractionated heparin is useful for a STEMI patients it took 13 years before it got incorporated as class 1a in the guidelines an additional 17 years that's my math is right 30 years before 90% of clinicians were using beta blockers for years and then 10 years before 70 percent and then there's a little debate now about whether beta blockers are useful early on or not ACE inhibitors and so on and they go through a whole bunch of these but on average it took 16 years before definitive studies got incorporated by the majority of practitioners out there and this is not just cardiologists these are hospitalists probably emergency physicians and everyone else out there it's enormous amount of time so what's the take-home point all right the take-home point here is actually very simple don't get frustrated when you learn something at a conference or you read something that's definitive or you read something in the national guidelines that's already class 1a don't get frustrated that the people upstairs don't know what you're talking about you might take an additional 16 years all right but you've got to share the literature with your colleagues because you can't expect that just because you know about it everybody else is going to know about it your knowledge is based on what you've read and they might be reading something completely different you've got to share the literature with your colleagues in the IDI with your colleagues that are down the hall with your colleagues that are upstairs or downstairs as well share the literature with them I've said this multiple times with regards to the cardiac arrest literature and some of the other literature because they don't know about it yet share the literature with them don't get too frustrated with them alright mental break let's talk briefly about syncope versus pre syncope first of all is this has this patient tim of syncope no of course not because he hasn't woken up yet right so syncope you need to wake up and be normal but pre syncope pre syncope is kind of the swoon sink it bzz you're awaken alert and normal then you're unconscious on the floor no postictal period brief period of unconscious and then you wake up and you're normal again that syncope we all pray have a pretty much standard workup for syncope but what about pre syncope I got real lightheaded and nearly passed up but I didn't completely lose consciousness is that the same thing or not well most people don't consider that to be the same thing but the literature says that it's pretty much the same disease even if the patient didn't completely pass out back in 2012 Shamai Grossman who's up at one of the Harvard hospitals did one of the early studies and he found that 20% of patients with pre syncope had serious outcomes which was almost identical to the syncope patients and in his study he found that the etiology is of pre syncope versus syncope were the same the morbidity and mortality of pre syncope versus syncope were the same so it didn't matter whether the patient completely passed out or almost completely passed out and then moving forward to 2015 a more recent study and we should have a giveaway for anyone who can pronounce this person's name but we're not going to do that so this is from Canada Ian Steele and wells were authors of this study also wells from the wels criteria Fame and in this study they looked at pre syncope versus syncope what they did they looked at two large academic emergency centers pre syncope not that common about 0.5% of patients but what they did was they asked the clinicians what do you think the risk is for this precinct to be patient of having an adverse outcome either death or morbidity in the next month and invariably they almost universally underestimated the risk of these pre syncope patients the actual risk was about 5% of these pre syncope patients had adverse outcomes in the next month what what most clinicians estimate is nearly zero maybe one percent at the most and so in a very very publicized editorial written by James Quinn who's from the San Francisco syncope rules he and some of the other folks that reviewed the study said that this study shows that number one we need to be just as concerned about pre syncope as we are with syncope and number two most clinicians don't tend to appreciate the risk that's associated with pre syncope the bottom line is very simple when you see a patient that nearly passed out you should work them up and worry just as much as if the patient did completely lose consciousness they have the same ideologies and pretty much the same morbidity and mortality in the short-term as in the long-term do the same type of work ups all right so yep very simple point from that article but I think it's a point that emphasized again that we underestimate the concerns associated with pre syncope okay let's move on to a couple of EKG topics this was sent by dr. Chuck Warlow who is a clinical professor of emergency medicine in at Lehigh Valley in Pennsylvania he sent me two really interesting EKG cases which gives me an opportunity to talk about a topic which for whatever reason was a very hot topic in the EKG literature over the past couple of years it's always been an important topic but for some reason there was a plethora of articles that got published just within the past two years on this so let me present the cases he sent me fifty nine-year-old comes in which just beyond exertion for a few weeks no pain it's got a bunch of medical history hypertension obesity anxiety depression and take a look at his vital signs overall he looks comfortable it's a febrile heart rate 69 respiratory rate twenty-six pulse ox 92 percent blood pressure pretty good exams otherwise unremarkable here is the ECG all right hopefully guys can see that and what you probably appreciate is that there's a t-wave inversion in three kind of flattened AV F and T wave inversions v1 v2 v3 even out to v4 and v5 here's the old EKG for comparison right so all of those T wave inversions are new all right so lead three T wave inversions new let's go back to that EKG new flip T wave in lead three new flattening in AVF and all these T wave inversions are new what's the diagnosis alright case number two 66 year old woman comes in with acute shortness of breath for 24 hours history of diabetes lymphedema chronic kidney disease recent pneumonia chronic back pain to the point that she needs to get around in a scooter she had a recent pneumonia and now she's back febrile again to 100.3 heart rates okay rest targets 26 pulse ox 64 percent on room air it's a little bit better on non-rebreather exams otherwise non-diagnostic here's the 12-lead ECG and once again flip T wave lead three flattening in AVF maybe even a little bit inverted Navy off flip T with v1 v2 v3 v4 maybe in v5 also here's the old 12 lead so all of these actually the I'll show you the machines interpretation new ischemic findings in the inferior and the ant receptor Li's be careful about the EKG computer interpretations as I will say EKG computers are programmed by plaintiff attorneys all right so don't ever believe your computer interpretation so anyway here's the old EKG so all of these T wave inversions now are new because the old EKG had normal T waves so once again here's our new EKG flip T waves inferior in anti septal anterior out to v4 and v5 what's your diagnosis here pulmonary embolism alright so the first mini take-home point Pease can definitely produce fevers alright in fact the literature has reported Pease producing fevers up to 102 routinely that's what 39 degrees Celsius routinely all right so don't ever rule it out based on a fever the most important thing is see abruptness of onset as Kevin talked about recently but I want to focus your attention on a lot of literature which has recently been published that has talked about the electrocardiogram findings of massive PE we're not talking about the small PE s that we all have right now okay we're talking about the massive PE s that make patients unstable here's two articles from 2015 mean there's one more that just got published in early 2016 here's three articles from 2014 I'm not going to go through all the details of these articles but I'll just summarize them all in a couple of slides essentially what they say is that massive p/es are notorious for producing t-wave inversions especially in the right precordial leads v1 v2 v3 sometimes out to V for massive PE s can produce St elevation and depression I never learned that before they can mimic STEMI and in particular they tend to produce St elevation in v1 v2 and even an AVR you might remember we talked about asked elevation to AVR and one of the causes I mentioned was massive PE it produces signs of global cardiac ischemia so you get ST elevation in AVR tachycardia that's no surprise new afib that might not be a surprise and signs of right heart strain which can be rightward axis in other words the big s wave in one and tall R wave in v1 let me show you something this are not necessarily specific for PE but the key point here is that if you ever have a PE if you ever diagnose a PE and you see any of these you need to really be worried because the literature says that if your PE patient has any of these findings there's a very high likelihood that if your patients not already unstable they're going to go on to develop hemodynamic instability and have morbidity and mortality these are prognostic findings of a massive PE so you really need to worry about these and you might even lower your threshold for talking your consultants about giving thrombolytics or embolectomy for these patients because these predict a bad in hospital course let me show you some examples that we've seen take a look at this patient look in v1 and v2 there's ST elevation in v1 and v2 and big-time ST depressions out laterally and even out here in some of the inferior leads this was diagnosed as a STEMI the patient went to the cath lab they squirted the dye found clean coronaries fortunately after the negative cath they then did a CTA and found the massive PE but this was a surprise to everybody because it's not well-known that massive PE s can mimic STEMI with St elevation in particular in v1 and v2 and by the way there's ST elevation in AVR as well here's another one I think actually Haney took care of this patient this is a patient that had a massive STEMI and everything went right and I'm not going to throw you under the bus here but everything this patient again ST elevation in v1 a bit in v2 there's ST segment depression a little bit out laterally huge T wave inversions of v1 v2 v3 v4 and some flip T waves in two three and maybe a bit in AVF so flip T waves in the inferior and Interceptor leads some ST segment changes a lot of people would look at that and say my gosh this person has ACS and they need to go for cath no think about PE as well alright when you see what appears to be ischemia on the 12-lead a mistake that people make is that they tunnel vision and only think P only think ACS please don't do that there are a lot of deadly things that can produce ischemic findings on the 12-lead ACS can dissection can also PE can do it pericarditis tamponade can do it you know what if you put your next time you have a slow shift just have a little fun hook yourself up to the 12-lead and just purposely hyperventilate and you'll flip your t waves it's kind of neat you'll pass out after that but nevertheless you'll have a cool EKG alright so hyperventilation can cause T wave inversions pulmonary problems can produce T wave inversions pulmonary problems sometimes PE s can produce ST segment changes as well here's another one once again there's a little bit of St elevation v1 v2 a little elevation in AVR you've got some ST segment depression in the inferior leads ST depression out laterally ischemic findings this was a massive PE and this is a great case this was from a number of years ago at a hospital one of our affiliate hospitals the patient came in with with chest pain now nobody really paid attention to fact that it was chest pain of abrupt onset right em eyes don't usually tend to present abruptly if you really ask them em eyes tend to be crescendo over 10 minutes 15 minutes but this patient said the pain started like that that's not an mi that's PE or dissection think about those up first anyway they got a 12-lead not a great history but they got a 12-lead and the computer and the emergency physician and the interventional cardiologist looked at this and said hey this person is having an acceptance temmie so the patient went immediately to the cath lab and squirted the dye and it was a normal calf right so what do they do they stop the heparin they admitted the patient to the floor to complete the rule-out sandbag on the groin everything is okay patients no longer on heparin now why they just ruled out a finish up getting the troponin what should you do well if you've got concerning chest pain and you've just rule out ACS your jobs not done now you've got to think about all the other deadly causes of chest pain but the mistake here is that they had tunnel vision they saw ST segment changes and suddenly they only thought rule-out mi and then once they did that they wash your hands and said I'm done you know what they should have done is said rule out am I done now I've got to think about other deadly I've got to think about dissection PE pericarditis and tamponade because those can produce ischemic changes also so anyway the patient had a clean cast got a mid to the floor plan was to just finish rolling him out next morning after multiple negative troponin the patient had a cardiac arrest and died and an autopsy was found to have a massive PE and nobody realized that the St elevations could be caused by a PE all right and I've seen medical legal cases just like that as well at least two cases alright one case which was just flipped t-waves patient got admitted ruled out got discharged home and died and after the patient got ruled out they shouldn't have discharged they should have said all right we've ruled out one of the deadly things now we've got to think about the other deadly things before that patient goes home alright the other one was a STEMI just like this case so quick take-home points Pease please remember this it's not commonly taught but Pease are notorious for mimicking ACS not little Pease big Peas are notorious for mimicking ACS t-wave inversions are perhaps the most common abnormality in massive PE s not tachycardia but T wave changes that mimic ACS you can get ST segment changes and what the literature is now showing is that when you have any ischemic looking findings on the 12-lead of a PE that portends an adverse prognosis it portends a significant increase in morbidity and mortality a significant increase in likelihood that the patient if not already they're going to become hemodynamically unstable and be defined a massive PE so when you see a PE who's got any of those findings you've really got to worry no way is that person going home in fact I would argue no way is that person being admitted to the floor those are patients that you should push to get up to the ICU based on no less than five articles six articles actually now in the past two years all right so be very careful about that all right so this was sent to me from Austin Texas I don't know if anyone's from Austin no kind of picnics are down there what I find most interesting also that here's some under picnic supplies there's batteries down here I don't know how that relates to all the rest of this stuff I don't want to go there all right so let's let's finish up with this case alright this was sent by some friends in LA County actually all right Jan chillin burger is the program director down there Ariel is one of the residents and Paul is one of the faculty up there they have a 76 year old woman who presented with twenty minutes of chest pain the pain was very concerning radiating to the neck jaw teeth nausea shortness of breath die freeze this is a slam dunk admission no way this patients going home right so 76 years old we've already established one the laws is the chance of discharge hundred – age so there's only a 24 percent likely that she's going to go home just when she registers right she's staying with the chest pain and everything else what else history of diabetes hypertension hyperlipidemia this is a slam dunking mission if this patient was asymptomatic and came to my IDI as a visitor I'd emitter all right so 12 lead ECG here you go now we talked about left bundle yesterday and I told you I'd talk a little bit about some new criteria here here is the patient this is a just a routine left bundle branch block all right there's no old ECGs for comparison now you recall yesterday I presented it a newer algorithm what we know now is that when patients come in with chest pain and a left bundle you don't need to worry so much if it's newer old left bundle the new algorithm that's been published says the first thing you ask is are they unstable if they're unstable push for calf or if they're in acute cardiogenic pulmonary edema push for calf this patient is neither of the above she's stable and no pulmonary edema okay next step look at the 12-lead now and what you're going to look for is evidence of the scar Bosa concordance criteria scar Bosa A or B if yes either of those then calf if no then just do a routine rule out so what are those scar Bocek criteria again the concordance criteria means scar Bosa a if this ST segment is elevated in the same direction as a QRS complex that's considered positive scar Bosa B if the in v1 v2 or v3 if the ST segment is depressed at least a millimeter in the same direction secured us then call it positive you're done those are the two scar Bocek concordance criteria the third scar Bocek criteria which has been shown to be much less specific so we don't pay much attention to it anymore so I'm going to cross that out I shall tell you what it was now cross it out for now and I'll tell you what it was a little bit later so these are the two concordance criteria and the other article which coming up in a second has also endorse this algorithm now if you look back at this 12 lead initially this patient has neither of those scar bust criteria there's no ST elevation in the same directions to cure s all right Kuras points up there's no ST elevation we're happy with that cure s points up there's no ST elevation we're happy ers points up there's no ST elevation caris points up Kara's points up there's no ST elevation so scar Bosa a know what about cigar boasted B cigar Bosa B says in v1 v2 or v3 is there ST depression of at least a millimeter or looking up here v1 v2 v3 there's no ST depression so this patient does not meet scar Bosa a or a scar Bosa B all right so based on that algorithm the patient doesn't meet criteria now what about scar BOCES C the third criteria that I mentioned scar Bosa C says if the Charis is pointing down and there's ST elevation normally that's good but if the ST elevation is greater than five millimeters that's too much and that should make you concerned well turned out that when they studied scarp this third criteria it didn't tend to work out that well but Along Came an emergency physician named Steve Smith who works up at Hennepin who said well you know maybe this five millimeter rule absolute five millimeters doesn't work because we should be looking at the ratio of the ST elevation to the size of the cure s because you know what if a person's QRS complex is a hundred millimeters I'm exaggerating but a hundred millimeters then a 5 millimeter elevation that's nothing that person's just got gigantic voltage on the other hand if the cares complex is 10 millimeters going down with 5 millimeters of elevation that's pretty significant so maybe we should look at the ratio so what he said is that if the ST elevation if the ST segment heads in the opposite direction of the cure s by more than 25% then you need to worry all right what let's let's look at this visually what saying all right what he said was take a look up here the QRS complex is ten millimeters in height and the ST deviation is four millimeters in the opposite direction for is more than 25% of ten so this would be positive for a STEMI what if the Charis goes down well here's a curious that goes down ten millimeters the ST deviations in the opposite direction 3.2 that's 32% 32% is more than 25 so this would be considered positive for a STEMI also does that make sense hopefully so if the ST segment is in the opposite direction more than 25% of the height of the main qrs call it positive so that's when he proposed and published in 2012 and this got incorporated into the other guideline I showed you yesterday that was published in American Heart Journal once again when somebody's got a left bundle first question are they unstable or in pulmonary edema if yes calf if not look at scar Bosa a and scar Bosa B if yes calf if no then look at this 25 percent ratio business well the validation study has now been published and so now I would argue that this is ready for primetime all right again your cardiologist will probably not know about this because your cardiologists are not reading the EKG literature they're reading other literature this is what you and I have to be experts at so get this article and share it with your cardiologists so anyway let's go back to the case here all right so this was the initial 12 lead EKG what the physicians from LA County did was they repeated the EKG 20 minutes later here's the repeat alright and what we'll do is we'll just take v3 we'll blow it up and take a look at what happened to v3 when they repeated the 12-lead I'm gonna blow this up there's the main QRS complex it's 16 millimeters in depth the ST deviation is 5 millimeters in the opposite direction that's more than 25% so they call this positive based on the revised validated Smith criteria so they called up cardiology activated the cath lab and sure enough a 100% led occlusion that's a life saved and had it not been for them knowing about this criteria they would have just let that left bundle sit and infarct an infarct infarct and left bundles already have lost a lot of tissue they don't do well only in fart so that's a life saved because they knew about this validated criteria and they convinced their cardiologist to take this patient to the cath lab positive all right two days post cast there's new T wave inversions where's your typical after cath but you'll notice all of the scar busted criteria are now gone because the patient has got a stent in there now all right so take-home points about left bundle and MI number one you've got to know the scar Bocek criteria if you're not comfortable with it google search it email me I'll send you videos this is something you as an emergency physician have to know and you also have to be prepared to share this literature with your cardiologist because most of them are not reading the EKG literature you have to be the expert at EKGs alright and even though this is not yet in the guidelines I would argue that best practice dictates that scar Bosa patients go for emergent cath including the validated criteria and if you get argument that's why you've got to have this literature on hand and share it with your colleagues because they won't know about it all right and you're going to see more and more literature about this new validated criteria and when it comes along share it with your cardiologists okay and again here is the algorithm step number one are they unstable or in pulmonary edema if yes the cardiology literature itself is saying push for calf if they're stable as this patient was look for is this scar Bosa concordance criteria scar bow so a or B if yes push for calf if no look for that new validated Smith criteria ST deviation more than 25% in the opposite direction if yes push for calf and this is one of those times where you going to take the article and you're going put it on the stretcher as they roll up to the cath lab all right okay so summarizing these last few articles number one be patient with your consultants and share the literature with them you've got to do that don't ever assume that the other people have read the same stuff or gone in same conferences you have all right you've got to share that literature with your colleagues in the IDI with your colleagues down the hall with your colleagues upstairs don't assume that they know about that all right pre syncope equals syncope in terms of the ideologies and the workup and finally in PE s remember PE s can mimic AC s flip t-waves ST elevation ST depression as television and AV are right and signs have right heart strain taller wave in AV are these all predict impending hemodynamic instability be worried about those PE patients and the corollary to that also is just because you see what looks like ischemia on the 12-lead doesn't mean that ischemia is the only thing you've got to rule out because there's a lot of other dangerous things that mimic ischemia most concerning Li PE dissection and pericarditis all right and then finally know the scar Bosa criteria no this new revised scar buss criteria if you've got questions about this just send me an email I'll be happy to share some of those videos or just go on the internet it's all over the Internet should be all over the internet by now with that we're going to close things out I'll be around for any questions but I sense on behalf of Theresa and me and Sujal and deku and Haney and Mike winners I sincerely want to express my appreciation to all of you for for coming out to Las Vegas and sharing your time with us I hope you go back with at least a few pearls that are going to save lives and I've really enjoyed talking to you all interesting cases you guys are presented and I really hope you all come back next year thank you all have a great evening you

6 thoughts on “Resuscitation 2016 – Cardiology Literature Update by Amal Mattu, MD

  1. 20:00 It is hard to believe that a massive PE that causes cardiac arrest has serielly negativ Troponins. Hs-Assays detect even intermediate-low risk PE's. Maybe that was because you used old (non high sens.) assays?I have never seen a normal hs Trop T in massive PE (multiple years in a tertiary care centre). Second, see also existing literature PMID: 23205283 and Hakemi et al Chest. 2015 Mar;147(3):685-694. doi: 10.1378/chest.14-0700. Normal hs Troponin savely rules out high risk PE.

  2. at 25:55 there is an accidental audible slip of flatus 🙂 Excellent talk, super teacher. Thanks

  3. I'm a student so pardon my ignorance, but shouldn't you wait until multiple studies all show the same thing? It needs to be reproducible before you change a whole practice no? You don't want to bounce back and forth changing practices for every latest conflicting study right? Wait until there's a trend of them?

  4. Thank you for sharing this! You are really helping both Docs and patients!

Leave a Reply

Your email address will not be published. Required fields are marked *