so next up we're going to change gears and talk a little bit about electrocardiography an ECG mimic now I've got 10 minutes so I think the title of this was tricks and mimics and I'm only going to talk about one mimic and I'm going to really try to pound this mimic into your heads over the next 10 minutes or so so again back to a real case real case 45-year-old male who was not feeling well complaining of palpitations no surprise blood pressure is 115 so not too bad and what you see up here is this wide complex tacac cardia looks fairly regular and so what is your drug of choice all right now you could say my drug of choice is propal followed by 200 jewels and I would not argue with that all right fantastic it's fast it's reliable kind of fun you build more for it also but let's say that this patient is wide awake and he is like no give me a drug what is your drug of choice well I'll tell you what the the physicians in this case use again this is a real case they chose amone now if you know me I'm not a big fan of amone I like procainamide a lot more for regular wide complex Tac cardias but if you substitute promite or lidocaine for this you get the same outcome this patient Brady down and died and I found out about the case a little while later on we'll go back to what we're actually looking at this is a regular wide complex teoc cardia maybe it's just a tiny bit irregular but when I see something like this instead of calling it an R wct what I actually call this is an RR wct and what does the extra r stand for regular really wide complex teoc cardia it's not just wide it's really wide and what I mean by that is that when you see the curs complexes greater than one big box greater than 200 milliseconds I don't want you to ever think about vtac as your number one diagnosis the first diagnosis I want you to think about whenever you see a regular really wide complex tardia is tox or metabolic and this is so important because if you follow a standard ACS what is ACLS tell you to do when you see a wide complex tardia lidocane Amo or procainamide all of those are sodium channel blockers and if you give this patient a sodium channel blocker it is what I refer to as a c clean kill it's a very reliable way of killing a patient whenever you see the really white complex teoc cardia just give strong consideration to empiric use of calcium and bicarb because if you go with ACLS ACLS will kill this patient all right remember ACLS was never written for tox or metabolic patients ACLS was written for the 65-year old man who smokes two packs per day of cigarettes who eats cheese steaks for breakfast lunch and dinner who one day clutches his chest and falls to the ground that is who ACLS is written for you can go out to the casinos or on Las Vegas Boulevard that is what ACLS was written for honestly it wasn't really intended for a lot of patients that we see in the emergency department and if you employ ACLS this is one of those conditions where ACLS will kill your patient and remember what's the first law of medicine premium no kill them okay and if you follow ACLS you are going to kill this patient really really quickly this was hyperemia the patient's potassium was 9.2 again a real case that was seen at one of our hospitals up on the floor actually this was an inpatient who for whatever reason developed hyper K and the medicine folks that saw this the inpatient Physicians that saw this patient thought this is a wide complex teoc cardia ACLS tells you give them Amo Amo is good for everything procainamide would have done the same thing lidocaine would have done the same thing also we've seen those cases in our own practice and learned from those mistakes so now you learn from the mistakes that we made when it's really wide do not use any of the sodium channel blockers that ACLS tells you to why is it well hyperkalemia is actually a sodium Channel poison condition hyperemia poisons the SEL the sodium channel so it's almost like having a tricyclic overdose and you would never want to use a sodium channel blocker if your sodium channels are already screwed up all right so stay away that's the whole lecture right there all right but I'm going to show you a handful more cases just to really really Hammer home this key point this is a 42y old man short of breath and weakness it's a wide complex Tac cardia but it's a regular really wide complex Tac cardia take a look normal vtac just doesn't get that wide when you're looking at something that's greater than 200 milliseconds think tox and metabolic first just give him some calcium and bicarb if it is tox or metabolic you're going to see the Qs narrow right before your eyes within a couple of minut within a minute or two if it Narrows before your eyes it's not VTEC vtac doesn't do that when you give the bicarb or the calcium on the other hand if you give the calcium a bicarb and nothing happens then fine go ahead call it vtac and use the others but first think about calcium and the bicarb first sometimes people say well what if it really is vac and I give calcium bicarb what's the harm what happens if somebody truly has vtac and you give them a couple amps of B carb what happens to them nothing if I gave everybody in this room two amps of IV sodium bicarb nothing happens it gets metabolized and it's out of your system in about 15 minutes or so what happens if you give calcium to somebody who's not actually hyper K what happens to them right their bones get stronger it's great right there's no harm at all there's no harm just try the calcium if it's hyper K you just saved a life if it's not hyper k no harm all right so few more cases take a look this is another hyper K the patient potassium was in the upper sevens this is a patient that was severely acidotic from sepsis this was misinterpreted as vtac it's too wide for VTEC the other thing as we mentioned earlier in the lecture uh the first lecture is too slow vac has to have a rate of at least 120 or 130 the rate here is only about 110 or so at most this is too slow for vac this is either tox or metabolic when it's slow and really wide tox are metabolic the patient here got some amone and Brady down and died again the reason for this why did this person Brady down and die it wasn't a sodium Channel problem but it's not welln not marketed this way but amiodarone is actually a beta blocker and calcium channel blocker right amone is marketed as a class three anti- rythmic pottassium Channel stabilizer in reality amorin is class 1 2 3 and four class one sodium channel blocker class two beta blocker class four calcium channel blocker would you ever give a beta blocker calcium channel blocker to somebody with a low wide complex T cardia of course not there's no reason to and what happened the amod was given and they Brady down and died all right this patient needed byard here's hyper K you see the answer up there it's eight rates 115 so right off the bat you know it's too slow and let's take a closer look it's way too wide this has to be toxin metabolic look how wide that is and if you follow the EKG machine it's going to have you kill this patient just like we said yesterday in the EKG conference who programs EKG machines plaintiff attorneys they want you to kill the patient right that's how they make their money they want you to kill the patient so don't ever believe that interpretation at the top here's another one nortryptiline overdose sodium channel blocker overdose it's too wide and by the way it's only about 115 it's too slow to call it ventricular tacac cardia give some calcium calcium won't help here but it won't hurt and giv some bicarb you'll see the Cur narrow right in front of your eyes here's a fleen ey toxic patient take a look at V1 that's way too wide to call it vac when it's that when it's that wide just try some calcium and try some bicarb you'll see the car narrow right before your eyes and you'll have your diagnosis this is a great case this is from one of my former attendings from residency he's a program director down in Florida he took care of this patient they didn't know the pottassium was 8.8 it's a regular wide complex tachicardia everybody around him is saying Dale give the patient Amo give him procainamide do something the patient's got vtac he said nope it's too wide and the rate is just a little bit too slow so he said you know what let's just try some calcium bicarb he gave 1 gr of calcium 2 amps of sodium bicarb bam take a look at what happens it Narrows down converts you've got your diagnosis this is just hyperemia if he had treated this patient with Liane AMU or promite he would have killed those sodium channels he would have ended up killing the patient all right so simple take home point this is a common mimic in the emergency department many other Specialties don't see this we see this often times in the Ed we see hyper all the time we see overdoses all the time when you see regular really wide complex tacac cardia don't call it vac until after you've tried some calcium and bicarb if you do that you'll save a life if you go right to ACLS some of your patients will end up dying when in doubt go with the calcium and sodium bicarbonate all right that's it thanks a lot [Music]