DIP Episode 181 - Comprehensive NBME Emergency Medicine Shelf Review Series 1

Okay, welcome. My name is Divine, I'm a resident. This is episode 181 of the Divine Intervention Podcast. And in this podcast, I'll be going over material that's pertinent to the MBME Emergency Medicine shelf. This will be part one. So because I have a lot to cover, I'm just going to jump right into it. The first analysis that the Emergency Medicine shelf, it's kind of a nebulous show because it's very broad in terms of what's tested. And there's not much in the way of studying material available for it. In fact, there's not much in the way of, you know, adequate MBME material to study or to practice with. So I will say, you know, just study hard for it. And hopefully you'll find these podcasts to be helpful. I'll try to make them as comprehensive as possible. And you should also make sure you can recognize EK Gs. Those things tend to pop up quite frequently on the shelf. And basically, the EK Gs you need to know, you'll see me mention them in those podcasts. So if you see me mention like a particular rhythm, it's probably an EKG you want to know for your test. So let's jump right into it. And I'll talk about these things in big picture, like topics I'll bring up vignettes and things of that nature. Right? So what do they give you a question about a person that has a history of nephotic syndrome? And then so this person, you know, has a history of like FSGS and has chronic reno failure from it.

And then the person presents with like, you know, sudden severe, like this person says that, you know, over the last three hours, he has been having severe chest pain. And he's, he's hard as being racing. And then they give you his vital. That's right. And you see that, you know, he's heart rate is like 125. And he has like this chest pain that's worse when he takes a deep breath. And he's again, he's shot a breath. If you see that, what are you thinking about? Well, I would hope you're thinking about a pulmonary embolus, right? A pulmonary embolus. Remember, people that have nephotic syndrome, those people lose antithromine 3 in the urine. So because they lose antithromine 3, they have less, I mean, antithromine 3 is an anti-quagulant. Right? So they essentially do not have antithromine 3 to inhibit factors 10 and factor 2. So those people are hyperquagulable. So how does a PE classically present? Right? A PE classically presents as a person who have like, you know, they will have like pleuritic chest pain, right? So pain that's worse when they take a deep breath, they'll be tacky cardiac, right? In fact, sinus tacky cardiac is actually the most common finding on EKG in a patient that has a pulmonary embolus. And then these patients also tend to be shot of breath, right? And another thing you may see on an EKG with regards to a pulmonary embolus is a new right-boundal branch block, right?

If you see a new right-boundal branch block, again, in a person that has hyperquagulable risk factors, you really want to think about a PE on those circumstances. But again, remember, the most common EKG presentation is sinus tacky cardiac. They may try to trick you into choosing S133. S133, one is very uncommon, right? And two, it's not very specific for PE. So just something to keep in mind. So the thing is, if a person comes in with a PE, obviously, what kind of diagnostic test would you want to pursue first? Well, you would want to do like a CT angiogram, right? You want to do CT angiography. You know, you would do like CT with contrast angiography. So like a CT of the chest with contrast. But the thing is, if you think with IV contrast, so, but if you think about it, right, there are certain populations of people that should not get a CT angiogram of the chest, right? So people, for example, that have renal failure. If a person has renal failure, like an acute kidney injury, if you gave them a contrast, that would torch their kidneys, right? So for those people, you probably want to consider a nuclear medicine test known as a VQ scan. Also a person that's pregnant, right? Although, to be honest, with you, these days on NBM Is, I mean a CT angiogram with contrast in a pregnant woman is acceptable for PE. It's acceptable in a pregnant woman for PE.

Although VQ scan is probably still the more common answer, you'll see on exams, but I'm here to tell you that a CT angiogram with contrast is acceptable, especially when they do not give you a VQ scan as an answer choice. And the gold standard test, however, to make the diagnosis of a PE is a pulmonary angiogram, but essentially no one does this anymore, right? Because basically you have to do like a right-hat calf, and then you essentially like go all the way to the pulmonary arteries and then inject contrast, right? That's gold standard, it's super sensitive, super specific, but you should never pick that as the right answer. The only time you should ever pick that as the right answer is if they tell you which of the following is the gold standard test for the diagnosis of a PE. That's literally if they ask you like point blank, that's the only time that answer will never be correct, right? So the thing is, what are some, you know, high-yield associations you want to keep at the back of your mind with P Es? Well, one thing you want to keep at the back of your mind is that if a person, you know, has a history of like a DVT, right? And you notice that they get a stroke on the exam. You want to think about that person having some kind of conduit between the right and the left side of the heart, right? Either like an ASD or a PF4 or VSD, right?

Those people can get a paradoxical, paradoxical emblem, because the person has a DVT, they will almost certainly get a PE, especially like again a proximal DVT, right? We have more than a 50% chance of getting a PE. But if you see like like an embolus, like a clot, right, going to the brain, and the person has like a history of a DVT, you know, those circumstances you certainly want to think about the person having, again, like some communication between the right and the left sides of the heart. And then some key things that can close P Es on NVME exams, right? You want to think about things like amniotic fluid embolus, right? So they will give you a question involving like a pregnant female, right? Who is either about to deliver a child or just deliver the child, right? And then she becomes comatose, she becomes unresponsive. And in some cases, she may be bleeding from every vein point of sight. If you see that, think about an amniotic fluid embolus. Remember when the amniotic sacroptures, right? Some finds in some unfortunate situations that amniotic fluid can get into the bloodstream of the female. And amniotic fluid can occlude blood vessels in the lungs, and that can cause a PE, right? Or they can give you a question about a person that you know, like goals, water diving, right? Like underwater diving. And then they arise very quickly, right? Without waiting for pressures to equilibrate. Remember, Henry's law, right?

This is something you learn in general chemistry in college, but Henry's law, the solubility of a gas in a fluid increases with increased pressures. So when you dive to deeper, to very deeper, like, you know, you dive really deep, right? Things like nitrogen, right? I can actually begin to dissolve in your blood, even if ordinarily they are not. But when you come up to the surface, remember, as you go higher, the pressure goes down, pressure dissipates. So if you come up too quickly, you don't give enough time for equilibration to happen, then that nitrogen can undissolve from your circulation. And then those gas bubbles can essentially begin to clog up blood vessels and a person and get a pulmonary embolus under those circumstances. And then if a person also, they can also give you a PE question in a person that recently had like an IV line placed, right? So like an intravenous line placed. Remember, if you're inserting an IV, like an IV, you want to be careful that you're not introducing gas into the person's bloodstream. Because if you do that again, that can include a blood vessel and cause a PE, right? If a person has cancer, especially like these visceral malignancies, like gastric carcinoma or like colon cancer, right? So, some of these malignancies can secret mu sin and mu sin is a powerful activator of the coagulation cascade, especially like secondary hemostasis. And that can cause, that can cause a pulmonary embolus as well, right?

And then remember the case again, a person that has an euphrodix syndrome, right? Remember, an euphrodix syndrome, your glomeruli has been damaged, right? And then those people, because of that, they can lose antithromic freeing their urine. So that makes them hypercloagulable because remember, antithromic freeing is an anticoagulant, it inhibits factor 10 and factor 2. And one tip bit, I'll just go ahead and throw out here is you may see a question, not just about a PE, but about like renoven thrombosis, in a patient that has a histro-nephrodix syndrome. Just if you see a person, you know, histro-nephrodix syndrome, sodium onset, severe flung pain, think about renoven thrombosis. And the nephrodix syndrome that tends to have the strongest association with that is membranose nephropathy. That's actually something to hire to know for your exam. And then another thing that can cause a PE on MDM is, right? If a person has like, you know, like genetic problems, right? So, say for example, a person has like, a factor 5 lighting, radio factor 5 is resistance to degradation by protein C and protein S, right? Or a person has like the Pratronbin G2021 OA mutation, right? Those people make higher than normal amounts of a factor 2 that can make them hypercloagulable. If a person has antiphospholipidantibody syndrome that can certainly make those people hypercloagulable as well.

So those are all high-yield important presentations or risk factors for pulmonary embolus that you want to know for exams, right? And one of the things that predispose, and actually one last thing is a fat embolism syndrome, right? So if they give you a question about a person that, you know, recently had a fracture or recently had like an orthopedic surgery procedure, or if a person has like fat reliever, right? Or the person has like very, like hyperlipemia, right? So they have like very high levels of lipids in their blood. Those things can all predispose to forming a fat embolus. So essentially fat can just go and literally occlude a pulmonary vessel and cause a PE. So you may be wondering divine. White orthopedic procedures and fractures have an association with the development of like fat embolisms in the room. What the thing that happens is if your fracture is bone, remember bone contains marrow, right? And as you get older, right? You probably have like yellow marrow, yellow marrow is literally fat. So if you break off that bone, that fat can break off, traveling the bloodstream and occlude the presence of marivac culture. And remember that in the PE, the classic presentation is the person will have hypoxia and you have the skin finding of PTI. And then they may also have like some brain style symptoms, right? If you see all those things put together, really want to think about fat embolism syndrome, right?

So remember, right, the things that predispose a person to having a PE, right? So Verkos triad, right? The nice harmonic that you can use to remember that is the word she, right? So like Stasis, right? Hyperquagulability and endothelial dysfunction, right? Stasis hyperquagulability and endothelial dysfunction, that's Verkos triad for pulmonary embolism, right? Now the thing is there are many different kinds of P Es, right? And there are some key decision trees that your friends at the MDM expect you to know for the emergency medicine shelf exam. One is if a person has a sub-massive PE, right? So by definition, a sub-massive PE is a person that has some kind of evidence of right heart strain, okay? So you may get like an echocardiogram, and you notice that the right ventricular wall is like, has like aberrant kinetic properties, so it's not contracted as well as issued, or you notice that the person's right ventricle is diluted, right? That tells you that the person has a sub-massive PE, okay? And I will talk about how you treat that shurky, right? But the other big decision tree you want to remember is what constitutes a massive PE, right? A massive PE is a person that is has a PE and they are hemodynamic unstable. So what do I mean by hemodynamic unstable? I mean hemodynamic unstable if the systolic blood pressure is less than 90, right?

Or your requiring pressures to prop up the person's blood pressure, or the patient is like profoundly pretty cardiac, those things all go with the diagnosis of a sub-massive PE. So in general, how do you manage a PE? You know, a person comes in and you know they help just you know your guardian very right TPE. Your first step in management is always to put them on heparin, right? You can put them on on fraction-infet heparin, you can put them on lomo-lecular with heparin. But the thing is keep in mind if the person has a history of renal failure, you actually want to put them on on fraction-infet heparin, not lomo-lecular with heparin. Lomo-lecular with heparin for the most part is contraindicated in people that have a history of renal failure. Now if a person has a sub-massive PE, right? And they have like mild symptoms, right? So you know they have like right heart strain, right ventricular dilation and all that stuff. Yes, you are absolutely fine doing, actually keeping those people on anti-coagulation. So a sub-massive PE will mild symptoms, you know the person's blood pressure is holding up and all that stuff. You can maintain them on anti-coagulation. But there are certain situations where if a person has a PE, you need to subject them to TPA, right? If a person has a massive PE, right? Again, remember massive PE is divided by defined by having like hemodynamic instability requiring preserves to proper blood pressure, bradycardia. Those people deserve TPA, okay?

But if a person also has like a sub-massive PE and they are having severe symptoms, those people also are deserving of TPA on the exam, right? Now you may wonder, define when do I perform an embolectomy, right? So when do I perform an embolectomy? Because sometimes you can actually go on surgically literally extract the clot from the person's acommunary artery. The typical situation where you perform an embolectomy is if you've tried TPA and the TPA is not working and the patient continues to deteriorate, you can consider performing an embolectomy under those circumstances, right? If a patient has like contraindications to getting TPA or anti-coagulation, right? So let's say like they have like a new plastic process going on in the brain or they've had like a history of like a brain bleed, like a sub-racaloid hemorrhage, or they have like a current bleed, right? Like an ongoing bleed, like a GI bleed, right? Or they have aortic dissection. Under those circumstances, it is not prudent to place those patients on anti-coagulation and it's also not prudent to place those patients in, give them TPA because that can kill them relatively quickly. So you don't want to do that. And since I'm kind of talking about TPA now, I think it probably makes sense to just ship this and I'll mention this again during the course of the podcast. Remember if a person has a my hearted infraction, I generally prefer PCI, right? So you prefer percutaneous coronary intervention.

But the thing that can happen is if, for example, they tell you in the question that the person like, oh, that's, you know, the person is not at a site where PCI is possible and the PCI Capable Center is more than two hours away. And under those circumstances, you can also consider giving a TPA. So again, that's a pretty very high yield to know, right? So again, just to, actually one other thing I should mention here is that your friends at the MDMED occasionally want you to pick out the labs that are associated with a person having a pulmonary embolus, right? So remember that if a person has a PE, right, they tend to hyperventilize because they're short of breath. But if you hyperventilize, you're going to get a respiratory alkalosis, right? So you're going to get a respiratory alkalosis. And the thing is when you develop a respiratory alkalosis, right, you create a lot of negative charges in your blood that would want to bind, that would want to bind like calcium, right? So these people can actually have high hypocalcemia on the MDM exam. And then you'll also notice that they are AA gradients will be increased. Remember, whenever you have a problem that is intrinsic to the lung, it tends to be associated with a low A-agridient, right? It tends to be associated, sorry, it tends to be associated with an increased A-agridient whoops. And then remember that people that have a PE, right? Obviously they're going to be hypoxic on the test.

So they will have a decreased partial arterial pressure of oxygen in their bloodstream, right? So again, just to summarize in general, for PE, you perform a CT and drug and with contrast, right? But if the person has like renal failure or the person is pregnant, right? You go to VQ scan. The thing is, again, if a person is pregnant, CTA is actually now acceptable, right? But again, you want to maybe choose that when a VQ scan is not an answer choice that you see on the test. And then remember, if a person comes in with a PE, one thing you can actually do is you can actually go ahead and let's say like they are low, like basically for a person comes in with a PE, it probably makes sense to restructify them using like something like the well score, right? So the well score, the big thing you want to remember is that if your well score is 4 or less, you are low risk for PE. If your well score is 5 or greater, you are at a higher risk for PE. So the thing you typically do in a person that has like a low well score is you order a D-dimer. The thing is the D-dimer has a very good sensitivity. It has very good negative predictive value for the diagnosis or screening in a patient that has a pulmonary embolus. So the thing is, if your person is like the well score is like 4 or less, right? And you know, you measure the D-dimer. If the D-dimer is negative, then you can destroy those patients home safely.

But if the D-dimer is positive, then on the those circumstances you need to proceed to getting an image of the chest, you want to get a CT and geographical of the chest. Okay, you want to get a CT and geographical of the chest. And then if a person is higher, if their well score is like 5 or higher, you don't pass, go, you don't collect 200, you just proceed straight to getting the CT and geographical of the chest, right? Or VQ scan as appropriate. And then I've talked about the goal standard being like the pulmonary angiogram, right? But again, only big that answer, if you tell you that the person, if the question is literally asking like, oh, what's the goal standard diagnostic test for this person's presentation? They then say, okay, I'll go ahead and do the goal standard test, which is a pulmonary angiogram. And then remember, right, for person has a DVT, right? You want to do a compression ultrasound to make the diagnosis. And you usually present as like in a lot of leg pain. And you'll be in one leg, you'll be on both, right? And for the most part, you start the patient on heparin. And you know, after a person has like a DVT or PE, if it's like their first episode, and you know, you've kind of looked and you notice, you don't see any real cause of this person's DVT. You can put them on chronic anticoagulation, or you can put them on war frame, you can put them on the factor 10 inhibitor, so like a pixaband, river oxaband, a doxaband.

Another thing you could also do is to place them on a direct thrombin inhibitor, right? So like the big atran or a guttural band or bivalurity. I'll talk about those in a second. So let's jump to another question, right? So what if you get a question about like a 32 year old male, okay? And he comes in and says that he feels like his heart has been recent for a while, right? He feels like his heart has been recent. And let's say they tell you that, oh, this guy takes, he takes a methemazole, okay? He takes me a thymazole at home, right? And then he shows you an ekegee. And you notice that you actually see like, you know, like a narrow complex tacky redmiya. And you notice that the spaces between the curious complexes are not the same. Well, if you're thinking about, if you if you understand what I just said, I hope you're thinking about a fib, on that those circumstances. Remember, a fib is irregularly irregular, right? And you may say, okay, divine. What does the word irregularly irregularly mean? Well, irregularly irregular means again, the spaces between the curious complexes are not the same, okay? That's the classic buzzword that you used to describe a fib on nbim exempts, right? And again, these patients for the most part will have like palpitations and all that fun stuff. And really for the most part, the way you treat a fib is, you can either treat it, you try to treat it essentially with an even nodal blocking agent, right?

You can treat it with beta blockers, right? Like especially like a selected beta one blockers, or you can also treat them with a non-dihydroperiodine consumption of blockers, right? Like Verapameil or Deltaiaz. Okay? Like Verapameil or Deltaiaz. Now, here's one high yield thing you actually want to keep at the back of your mind, for example. I don't know if whatever is in many resources don't talk about this. So people tend to get this wrong on test, right? So the thing is, if a person has a fib and they're unstable, right? You need to actually, so a person has a fib on stable, they're like hemodynamically unstable. You need to actually like proceed straight to synchronize cardio version, okay? In fact, that's a general rule that I actually, again, I found to be very helpful on exams. If a person has any kind of tachyretmia, so tachyretmia and they're unstable, okay? Your right answer in terms of the next step is to do something called a direct current cardio version, right? And remember, direct current cardio version can have multiple names on NV Me exams, right? So direct current cardio version is also known as a synchronized cardio version, and it's also known as a direct current counter shock, okay? Those are all, those are all terms used to describe synchronized cardio version on NV Me exams. So again, if a person has a tachyretmia and they're hemodynamically unstable, the next step in management is almost always to always to do a synchronized cardio version, right?

And then, so even like for like SVT, for example, and SVT is a white narrow complex regular tachyretmia, if a person is hemodynamically unstable with that, you proceed to doing a synchronized cardio version, right? Now, the thing is, when a person comes in with a favorite, there are certain decisions you kind of need to take, right? So you ask yourself, is it new or is it old, right? If a person has been symptomatic for less than 48 hours, right? Then that's new a fit. For a person who has new a fit, the thing you pretty want to do is you just go ahead and cardiovert them, right? You do a synchronized cardio version like right over the bat, right? But if a person has been symptomatic for more than 48 hours or you don't know how long they've been symptomatic for, then you can pursue one of two strategies on your test, right? So one strategy you can pursue is you can, you can, you know, start antico-avolating them, you get a TEE, not a TTE, you get a TEE, a transess of a gel, a co-cardiogram like right there and there, look for clothing in the heart, if you don't see cloth, you cardiovert them immediately, or you don't need to wait. But another option is that you could put them on a, uh, or a friend for like three weeks, right? And then you do imagine, right? You do again that TEE to make sure that you don't have cloth and then you cardiovert them, okay?

Many people for, for obvious reasons, as sticking with the first option that I talked about, where, you know, you do a TEE right now, put them on HEPRIN for anti-correlation and then you go ahead and cardiovert them, okay? So in general, those are the ways you handle, those are the decision treats for PE, I mean, sorry for A-FEP as you proceed. Now, one thing you want to keep out the back of your mind is that if a person has A-FEP, right? Because the left HEPRIN is almost like quivering, right? Those people are not in a situation where they, they are like protected from cloth, they're actually not, right? So in general, when people have A-FEP, they have a very high risk of forming cloth in the left each term and then that can emboly to the left ventricle and then go from the left ventricle to the cerebro vessels and then it can cause like an ischemic stroke in the brain, right? So the thing is whenever a person has A-FEP, you know, actually you need to use something called the Chad's VASC score, okay? To complete the risk and in general, I'll just go ahead and tell you if a person has A-FEP, you can put them on walk free, right? Or you can put them on a direct thrombin inhibitor again like a datroban, a bigatran or bivalyridine, right? And then you can also put them on a factor 10 inhibitor, right? Like a factor 10 inhibitor, right? So drugs that all have XA, like 10 A, right? If you're going with a Roman numeric, right?

So drugs like a doxaban, river rocksaban, a big saban, those are all acceptable for the treatment of, for the prevention of stroke, right? Like to decrease the stroke risk in a person that has A-FEP, okay? And remember ultimately for A-FEP, right? You know, most people seem to post you like a read-control strategy, but one thing you can also use is, and the read-control strategy already is to give like a beta blocker and a non-diet like either like a, you know, like metoprolophore example, like a beta blocker or like a non-dietroperidine consumption of blocker like verapimil with the TISA. So that's the read-control strategy. In terms of read-control strategy, one thing you would consider doing on your exams is you could give a muterun or you can give the drug propaphenon, okay? Those drugs are good and decent for treating, for you know, essentially going with pharmacological cardioversion of the patient, right? And again, for a read-control strategy, like I say, you can put the patient on those anti-rhythmics, but in general, the electrical cardioversion is what is preferred for the most part. Now, one thing I want to go ahead and talk about, these can be freestanding questions on your exam, but you want to know how to reverse some of these anti-coagulants, right? So if a person obviously like, you know, has like hampering toxicity, you can put them on, you can give them a predominant sulfate to reverse the hampere, right?

But if a person has warframe, your friends at the NBME are kind of counting on you to pick a FFP, right? When you sort of pick an FFP, you may pick like vitamin K. Here's the thing, if a person has like a life-threatening bleed from, let's say you know, from like hamperein toxicity, like I said, you can put them on predominant. If a person has like a life-threatening bleed from warframe toxicity, one thing you can actually consider giving is something called the forfactor pre-thrombin complex concentrates. Some people call it for FPCC, okay? For FPCC is a reversal agent for for warframe toxicity, right? So obviously, the presence I in our would be super high. If you've ever walked in any hospital, you've ever heard of the drug case centra, case centra is the forfactor pre-thrombin complex concentrates. Now the drug of joints for reversing warframe toxicity, that's actually very high to no purposes of the exact. And then if a person has like bleeding and toxicity from a factor, from taking a factor 10 inhibitor, right? So like a pixaband, river roxaband, a doxaband, the way you can reverse those, those drugs is by using a drug known as anddexanet. Notice how, so our spell is, is A-N-D-E and dexanet. So A-N-D-E-X-A-N-E-T and dexanet. Notice and dexanet has the term X-A in its name, right?

So that should help you, hopefully remember that it's used to essentially curb the morbidity associated with like, you know, a person like bleeding, a person that's like, you know, like bleeding from taking a factor 10 A inhibitor. And then the last one I'll mention is the bigatran, right? Remember that bigatran is known as predaxa. So it so happens that a monoclonal antibody was created to rescue patients if they have the bigatran toxicity. So they call it because it's named, the treating is predaxa, it's known as Praxbine, okay? But the name you'll likely see on your exam is a drug known as I-Darrocyziumab. So I-D-A-R-U-C-I-Z-U-M-E-B, I-Darrocyziumab. It's a monoclonal antibody against that bigatran, so it's now- it now helps you reverse the bigatran. That's actually again a very, very high your concept to know from purposes of your exam. So let's go ahead and move to my next avenue. So now, what if you get a question about a patient? Let's see this patient ran in marathon, like yesterday, and then this patient has been having, you know, like, has been feeling funny, having palpitations, not feeling well, and then they show you a picture of an EKG, and you notice that this patient has picked T-Waves on an EKG. What are you thinking about under those circumstances? Well, I hope you're thinking about Robdomionuses, okay?

I hope you're thinking about Robdomionuses, and that Robdomionuses, right, from running the marathon, that has essentially caused like myocyte necrosis, and then you're seeing the picked T-Waves on an EKG because the person has hyperkalemia. Because remember, potassium is an intracellular ion, so whenever you have like large-scale necrosis of cells, that they will release their cell soup into the bloodstream, so that can raise a person's potassium and cause hyperkalemia. Another thing that can cause hyperkalemia on an MBM exam is a person that's getting like chemotherapy for, for like tumor lysis syndrome. Again, as those cells die, right, they release again, they're cell soup into the circulation, and that can cause hyperkalemia. Another one can be a patient that's on dialysis for chronic renal failure, and they miss the dialysis session. Those people can also get a very nasty hyperkalemia, and they can get into trouble with on data on exams, right? So the thing is you want to be able to recognize electrolyte disorders and some drug toxicities, and how they present on an EKG, right? So hyperkalemia, the big thing that happens for the most part is you have topicked T-Waves, right? That's the very first thing you have if you have hyperkalemia. But if the potassium keeps rising and you do nothing, the thing that happens is you can degenerate from having the topicked T-Waves, you then start having white-curus complexes.

If the potassium keeps rising and you do nothing about it, then I mean obviously you do something about it, but if you do nothing about it, you'll then degenerate from having the white-curus complex to having like a sine wave pattern on an EKG, and then after that the patient will probably go into like V-fib, Oasis, Steli, and die, right? So you don't want that. So the thing is how do you treat this hyperkalemia? Once you say like a topic T-Waves, what's the first thing you should always do, right? Obviously you should always give a calcium-based compound, like calcium gluconics, right? That will help you stabilize the myocardium. So that's one thing you can do. Another thing you can do is that you can give the patient insulin plus glucose, you don't just want to give straight insulin, because if you give straight insulin, you make the patient hypoglycemic and then you have a bigger problem on your hands, right? So what you try to do is you give them insulin plus glucose, because remember insulin increases the activity of the sodium potassium ATP is pump. So if you increase the activity of the sodium potassium ATP is pump, that would take sodium out of the cell and put potassium into the cell. So you're essentially redistributing the potassium, right? Another thing you can also do is you can give the beta-2 agonest or butyl role, right? Our butyl role, again, works pretty much like giving insulin plus glucose, it activates the sodium potassium ATP is pump.

So again, that can redistribute potassium from the extracellular environment to the intracellular environment. And then one other thing you can do is you can actually give the person like fluids, but at the same time give them furor some might. Remember furor some might is a loop diuretic, right? And loops, right? They help you, they cause like a potassium diuresis, right? So you're giving that person fluids, you're giving them furor some might at the same time that can help them peel out some of that excess potassium, right? Now one other thing you could also consider doing on your exams, right? Is to give those patients K-excelates, right? Remember K-excelates helps K mix K-excelates out of the body, right? That's kind of a nice thing wanting to remember that, right? So you give K-excelates, they can essentially pull out, it's a sometimes instead of putting K-excelates on your exam, no friends at the MBME, they may try to mess with your head and call it like sodium, polystyrene, sulfonite, you know it accomplishes the same purpose, right? So you can do that to get rid of again to essentially swap out sodium ions, potassium ions, and you can simply pull it out of the body. Now, what if they give you a question about a patient, you know that has some kind of psychiatric disorder, let's say like depression, and they're taking in me preming for depression, right?

And then you notice like a white carousel well, I would hope you're thinking about like a T-C toxicity, remember the tricyclic antidepressants, you know they can cause like anti-hamside effects, so they have anti-histamine allergic effects, so they can cause sedation, they have anti-affelone effects, so they can cause orthostatic hypotension, they have anti-moschronic effects, so they can cause like urinary retention, constipation, delirium in the right patient population, right? Well these drugs, they can also cause like some weird cardiac arrhythmias, right? And the telltale sign of T-C toxicity on an embium exam is a widened QRS on an e-cage, and in general your next step in management for these folks is to give them sodium by carbonate, sodium by carbonate is the drug of choice for treating T-C toxicity. And then if a person has hypochylemia, right? Hopefully remember that, you know, these people have like a prolonged cutine interval, but in addition to that they also have U-waves, okay? They'll have U-waves on an e-cage, it's a wave that comes right after the T-wave if you look at the e-cage or rhythm strip. And then just I guess as a general rule that may help you, most of the notable electrolyte abnormalities that have hypo in their name tend to prolong the cutine interval, right?

So for example, hypochalcemia can prolong the cutine interval, hypochylemia can prolong the cutine interval, hypochalcemia can prolong the cutine interval, but one weird exception, one weird one that I don't know, like people just don't seem to know much is a hypochalcemia, hypochalcemia can actually, um, hypochalcemia can actually shorten the cutine interval, right? So if a person comes in with like a hypochalcemia crisis, let's say that they have like a malignancy, right? Where they have hypochalcemia malignancy, those people generally have like a short cutine interval on an e-cage. And then remember that if a person has hypochalemia, it is not a good idea to give those patients the joxet, right? Because remember, the joxet is that it inhibits the sodium potassium ATP is pump. And we know that the normal job of the sodium potassium ATP is pump is to take three sodiums out of the cell and put two potassiums into the cell. So if you inhibited that sodium potassium ATP is pump. And then that's bad, right? Because potassium will no longer be able to make its wing to the cell and it will still on the outside, right? So if a person already has hypochalemia and then you give them that double dose, the person can get, you can get for sure getting to trouble on the NV Me exams with that. But there's this weird thing, set of things with the joxet that again they love to test on NV Me exams that people tend to get to get to the cell.

The joxet can cause hyperchalemia as a side effect, right? But by virtue of the weight works, if you are hypochalemic, you are more predisposed to getting the joxet toxicity. What do I mean by that? The thing is the sodium potassium ATP is pump that joxet inhibits. It inhibits it by binding to like the potassium spot on the sodium potassium ATP is pump. So if for example you are hypochalemic, then there are most spots available for the joxet to bind on the sodium potassium ATP is pump. And if that happens, then the joxet will accumulate from most sodium potassium ATP is pumps. So you have a higher risk of the joxet toxicity. So separate these two ideas in your mind. In general, if you have a potassium abnormality, you really should not be on the joxet because you can have problems on either end of the spectrum. If you're a hypochalemic, you have a higher risk of the joxet toxicity because hypochalemia predisposes you to having like more the joxet binding. So you have a higher risk of digetoxicity. On the other hand, if you have hyperchalemia, then it's also not good to get the joxet as well because the joxet by virtue of its mechanism of action causes hyperchalemia, right? Causes hyperchalemia. So in general, if you have like a potassium abnormality, do not give that patient the joxet.

Like the classic question, they may give you on the EM show, maybe a person that you know has a history of like heart failure and they take a water pill at home every day and then they come in and they are like in a CHF exacerbation with cardiogenic, complicated by cardiogenic shock. And then you give them the joxet and then they start getting all these PVC's and then maybe they have like a mastiaid me and die. The thing that probably caused it is because they are water pill, they are diuretic causes hyperchalemia and then you're throwing the joxet on top of that and that predispose them to having more trouble. So again, you really want to be careful with that when an NV Me exam. So I think that's what I'm going to say about the electrolytes with recourse to the EKG. I mean, you want to know certain drugs rather than prolong the QT interval, right? So drugs like is it through my scent, right? That's a commonly used drug in the ED, right? So is it through my synch and prolong the QT interval? How do peridol can prolong the QT interval? Most antisoic colleagues can prolong the QT interval, right? So if I press it again, because in the ED you see people that you know, we have like, you know, like they may be belligerent because they have like some kind of intoxication or something. For those people, right? You want to again, obtain an EKG, right?

Or if they give you an EKG and the question, look at it because usually whenever they give you an EKG on an EMET shaft, the EKG usually means something, right? It usually holds the key to the red answer to the question. So make sure you know your EK Gs. And then, so yeah, I think that's all I'm going to say, I think that's all I'm going to see there. So again, those are all just again, how you'll things to keep at the back of your mind because if you have like a prolonged QT interval, right? That can ultimately lead to, that can ultimately lead to like, um, to set the plant and then the vision can die, right? Don't forget that to set the plant is treated with IV magnesium, okay? IV magnesium. Okay. And if a person has like a hypokillemic crisis or a hypocalcemic crisis or hypomagnesemic crisis, you do need to give them back all their missing, right? In fact, one that is especially important is a hypomagnesemia, right? If a person has low magnesium, then they generally would not respond to a replacement of calcium and potassium, right? So if a person's calcium and potassium is not replidian appropriately, even if you're giving them like, you know, you're giving them potassium chloride and all that stuff, then you want to check their magnesium and replete it, okay? Replidian magnesium and everything will kind of fall into place. And then remember that people can, if a person is hypokillemic, right?

You need to correct, you need to correct for, you need to, you know, calculate the corrected calcium, right? So for every one milligram per deciliter drop in your argument, right? That clubbers down your calcium by 0.8, right? So you want to make that adjustment before you say, oh, this person is hypokillemic, just be hypokillemic because the overall, they are hypokillemic, okay? So again, those are all things that can show up on an exam. And then don't forget, right? Like if a person is like, complete, if they give you an MVM exam question and a patient is completely asymptomatic, like clearly they have no symptoms and you know blood was drawn and the potassium was checked and it was like 8, but the patient has no symptoms, has no EKG findings. Then your next step in management from that EM shell question is to perform a blood redraw, right? Because the thing is you may have withdrawn a chemo-like sample, right? And again, remember that potassium is an intracellular ion, so you may have withdrawn a chemo-like sample and then that chemo-like sample falsely deceives you to think that a person is hyper-killemic, okay? So again, these are all high-ealth-insure-remborn exams. I said that hypercalcemia shortens the QT interval, well if a person comes in with a hypercalcemia crisis, the first thing you always want to do is to put them on fluids, give them normal cilin, okay?

Giving normal cilin is always the right first step in the management of a hypercalcemia crisis on the USMLE exams, on the NBM exams, okay? Now, what if you get a question about a patient that you know is complete of like severe chest pain, like it's like severe sodium onset chest pain, they are profoundly hypoxic, they have GVD, and they have blood pressure is like 40 over palpable, and they tell you that recently a central line was placed in the species. What is your next best step in management? Well, I will hope you are saying that your next best step in management for this patient is to perform a needle decompression, right? So like you can do the second intercostal space in the mid-clavicular line or the fifth intercostal space in the mid-axillary line. So what's your diagnosis for this patient? Well, I hope you are saying that this patient has a tension in mothorax, okay? Tension in mothorax. Remember, tension in mothoraces, they tend to arise when you have like this ball valve effect where air is getting into the pleural cavity, but it has no ability to escape, right? If you see that, especially I get in the person that recently had like some kind of an invasive line placed, think about about a pneumothorax, right? And again, if a patient has a tension in mothorax, tension in mothorax by definition is a pneumothorax where there is tension, physiology associated with it. With the buildup of interthoracic pressures, right?

The long one, the apesilateral side collapses, but the thing is, and nothing that happens is that you begin to have mediasis tyno-ships. So whenever you see mediasis tyno-ships and you say that's pneumothorax, that's bad, right? The presence got attention in mothorax, you need to act quickly and immediately, right? And obviously, if a person has a pneumothorax on an immunomy exam, they'll tell you that the person has, you know, like unilaterally decreased breath sounds, the person's lungs will be hyper resonance to percussion, right? So again, those are all things that they love to test on the exam. And that's how you treat attention in mothorax. You do a knee-to-deep compression, right? And then after you do the knee-to-deep compression, you then go ahead and please a chest tube, because the thing is, when you do that knee-to-deep compression, you convert the tension in mothorax to an open-numothorax. And then when you put in the chest tube, that is what actually like led those, led those, that is what will lead those, you know, like the air in the plural cavity sort of like a pass away, but it kind of takes you, you know, it's sweet, sweet time, but it will ultimately happen, right? But not everything mothorax is attention in mothorax, right? Like people can have like a primary spontaneous mothoraces, right? So especially like a young, like tall, thin young male, right?

Those things can all cause, like being a tall, thin young male, that's like a classic presentation of a person, you know, they're a combination of shortness or bread blah blah blah, that can be a person that can have a primary spontaneous mothorax, right? So the thing is, in general, for a primary spontaneous mothorax, if it's a big new mothorax, right? And typically, you know, you try to please a chest tube to fix the problem. But if it's a small new mothorax, right? So let's say like if you look at one hemithorax, right? So like, you know, remember, you have like two hemithoracy, so if you look at one hemithorax and the new mothorax that you see, there's like less than 20% of the size of that hemithorax, and the thing that can actually happen is you can just watch the patient for a few hours in the emergency room, so probably like six hours of their about, and then you get a repeat chest x-ray, right? If the, if the, if the new mothorax has not changed in size, or it's actually started decreasing, then you can go ahead and send the patient home, they'll be fine. But if the new mothorax is like, you know, increasing in size, or the patient is becoming more dynamically unstable, right? Then under those circumstances, you strongly want to consider placing the chest tube, right? Because the chest tube will save that patient's life very quickly, okay? But in general, again, if it's less than 20% of one hemithorax, right?

Observe the patient for a few hours, usually six hours, and then you can send them home. So I hope that's something that makes sense to whoever is listening to this podcast. And then, what if you get a question about a patient? And this patient, you know, recently had some kind of like, operandoscopy for, you know, I don't know, like some esophageal disorder, maybe they had like, girdle, or whatever. And then they tell you that three hours after the procedure, the patient's complaint of chest pain, right? And then they tell you that this person has like a Rice Krispies sensation when you're oscultating the chest, when you're pressing against the chest wall. And then they make sure you like a picture, I mean not a picture, you shouldn't see picture, let me show you an image. And in that image, they make sure like, like a black line, outlining the media's timer. If you see that, what are you thinking about? I would really hope you're thinking about like an esophageal rupture, okay? You're thinking about whether you're an esophageal rupture or like an esophageal perforation. And really, the as you for a diagnostic test on your exam, right? You want to go ahead and administer like gastrography, okay? Remember, another name for gastrography is water solubil contrast in them, okay?

So you, you, you know, you give the person gastrography and you don't want to use barium as your tool, because that barium can cause a very powerful media estimate test and then that will increase the morbidity and mortality in the patient, right? So, you know, you do your gastrography, you find the perforation or rupture, the esophagus. And then your next step in management for those folks is to send them to surgery. It's really only surgery that's used in general to fix these esophageal problems. And remember that esophageal rupture is of a geo-perforation, can also are raising like an alcoholic, right? I mean, the setting of like, perhaps syndrome, like a mile or a white steer, where the, you know, where the, you know, cough, cough, cough, cough, cough, cough, cough, cough, cough, cough, cough, right? So they, they're not, not necessarily cough, I guess they vomit, they're rich, a ton, right? Basically anything that causes like a sudden large increase in intra-theraic pressures, and that can cause, that can cause a surfergeu rupture. And again, you worked out of the exact same way I kind of talked about it, again, for the most part, surgical repairs that means the, means the therapy in a person that has, um, in a person that has an esophageal rupture. Okay. Now, this next head thing, I guess I want to talk about, I, I call them like hypertension-related maladies in the ED, right? So hypertension-related maladies in the ED.

Basically, what do I mean by hypertension-related maladies? These are basically like hypertensive case scenarios that you likely, you may likely see on the NBN emergency medicine or you may even actually see clinically. So let's gonna talk through them, right? So what if they give you a question about a patient, right? And this patient has a history of like really bad chronic kidney disease, or they have a history of like scleroderma. And then you notice that their blood pressure is like super, super high, and the patient is completely of like headache and vision changes. What are you thinking about on the those circumstances? Well, I hope you're saying that this person likely has hypertensive emergency. Okay, remember, you want to be able to differentiate between hypertensive urgency on an NBN exam and hypertensive emergency. And a person that has hypertensive emergency, the blood pressure will be markedly elevated, but they will also begin to have signs and symptoms of end organ damage. For example, they can have a headache telling you which tells you that oh, these people are beginning to have an encephalopathy or they can have vision changes or they can have abdominal pain, right? If you see those things, think about hypertensive emergency. Now, the difference between hypertensive emergency and hypertensive urgency is that in hypertensive urgency, these patients tend to have markedly elevated blood pressures.

To be honest, the exact like blood pressure definition is kind of in flocks in the literature, but a number that is probably safe for you to memorize for the purposes of the NBN exam is the number one, eight, over one, ten. For presence, blood pressure is greater than one , eight, over one, ten. And they don't have signs and symptoms of end organ damage. You can choke that up to hypertensive urgency on an NBN exam. So in general, how do we treat hypertensive urgency and emergency on NBN exams? Well, the thing is, there are group of drugs that you can use. And these are drugs, basically these are your only options because the thing is, your friends at the NBN, one classic thing they tend to do is they will give you the names of many drugs that all lower blood pressure. And then you have to pick out the right one for hypertensive emergency or urgency. Let me tell you the drugs you're supposed to use. So the drugs you're supposed to use, the numonic that I use is observing LENT L-E-N-T in Mothcarolina. Observing LENT L-E-N-T in Mothcarolina. So what does the LENT stand for? So the L stands for Labidolol, the E stands for Esmolol, the N-T stands for Nitro-Proside. And then the Nothcarolina, the N-C, the N stands for Nicardi Pine, and then the C stands for Clavida Pine. These are the only drugs you should use in a person that has a hypertensive emergency or urgency. They usually try to trick people into or try to suck people into picking hydrolyzing.

Yes, hydrolyzing lowers blood pressure, but hydrolyzing is awful for the treatment of hypertensive urgency or emergency. There's some reasoning behind that, but that's beyond the scope of this podcast. And I mean this podcast is ready for the nine minutes, so I think I'm gonna keep going. Now Nitro-Proside, don't forget that Nitro-Proside is associated with cyanide toxicity on MBM exams, right? So remember, cyanide toxicity, there are certain ways you can treat it. You can treat it either by giving M1 nitrate to convert ferric, no ferrous iron, that's Fe2 plus to ferric iron, Fe3 plus in hemoglobin. The thinning Fe3 plus is a powerful binder of cyanide. So when you bind up that cyanide, you then give thiosophite, and then you'll form like a thiosyanide complex, and then you can pee and poop that out safely. Alternatively, for cyanide, Bosnium, you can give hydroxyl cobalamine, right? It's a vitamin B12 derivative, right? So those are always you can treat cyanide poisoning. I'm just mentioning that because I'm talking about a Nitro-Proside. And in general, when a person has a hypertensive emergency or urgency, here's one high-yield thing you want to keep in mind. You don't want to lower their blood pressure by more than 25% within the first hour, okay? You don't want to lower their blood pressures by more than 25% within the first hour.

Now, what if they give you a question about a patient, this patient's blood pressure is like 2, 10 over 150, and this patient is complaining of the worst headache of their lives. Well, I would hope with that, you're thinking about a sub-raconoid hemorrhage, right? Remember, if a person comes in with a sub-raconoid hemorrhage, your first step in diagnosis is to obtain a non-contrast head CT, okay? To obtain a non-contrast head CT, you do not obtain contrast because if you're throwing contrasts with that, the thing that can happen is that you will not be able to see blood because remember blood, especially like hyperacute blood, it kind of serves as its own contrast on a CT scan, right? So that's why you're doing a non-con CT, right? But if the non-con CT is negative, right? Then your next step in mind is to get a longer puncture, right? And the thing you're looking for is an acroemia, right? So if you see like 10,000 red blood cells, that's bad, right? This person likely has a sub-raconoid hemorrhage, right? And one thing your friends at the MBME love to do is, they occasionally give you questions where they almost write it like a meningitis question, but it's a sub-raconoid hemorrhage question. The thing is, if a person, if the worst headache of a person's, you know, kind of study like two hours ago and they have no core rigidity, and you see that their blood pressure is like crazy high, it's very likely to be sub-raconoid hemorrhage, right?

But if a person has been having like headache, brain over like two days, right? And they have no core rigidity, right? Then you're thinking more along the lines of meningitis, right? And the thing is sometimes you also want to be careful, right? Like, seeing a red blood cells in a person's CSF does not always mean sub-raconoid hemorrhage, it could also mean like, herpes and cephalitis, right? Remember like the temporal lobe and cephalitis or like herpes meningitis? But usually for those, right? You see like, you know, like 500 red blood cells, like red blood cells in the hundreds, as against red blood cells in the thousands or tens of thousands on a CSF study. If you see like a ton of red blood cells in a CSF study, you really do want to think about, you know, like, Zanglu Chromia in the setting of a sub-raconoid hemorrhage, right? So what do you do in a patient that has sub-raconoid hemorrhage? I already said again, you do the non-conhead CT. If it's negative, right? You do a lumbar puncture. And remember that sub-raconoid hemorrhage, right? It typically arises from rupture of aberianeurism, most commonly in the anterior comnicidian artery of the circle of willis. Remember the number two artery in the brain? That's a seredal ruptures that can give rise to, a sub-raconoid hemorrhage is the posterior comnicidian artery, okay? So the person comes in with with a sub-raconoid hemorrhage, what's the echo of their lives, yada yada yada, right?

There are certain things you can do, right? If their blood pressure is like markedly elevated, you try to reduce their blood pressures, but the thing is for these people, you only use one of two drugs, right? You can use it a little bit along or you can use my cardipine, okay? Those are the two safe answers that you can pick to lower blood pressure in a person that has a sub-raconoid hemorrhage on an endemic exam, okay? A little bit along when I cardipine to lower blood pressure, right? And then some other things you can also do, right? You can also give like my Modepine, remember? My Modepine is a dihydropyredine calcium channel blocker that you can use to prevent the post-stroke visospasum that is associated with a person that has a brain bleed, aka a sub-raconoid hemorrhage, right? So if you want to prevent the development of an ischemic stroke, superimposed on the hemorrhagic stroke, which is the sub-raconoid hemorrhage they had, one thing you should strongly consider is giving those patients my Modepine. And remember, my Modepine is a dihydropyredine calcium channel blocker. And then other things to keep in mind is, if a person, again, comes in with a sub-raconoid hemorrhage, you also typically want to give them like phenitone or phosphenitone, right? As seizure-prophylaxis, right? And then you may also have to intubate these patients, okay?

You may actually also have to intubate these patients because if they are developing like very rapidly increasing your cranial pressures, I mean, right? You typically call your research to relieve the pressure, but let's say call your research is not an answer choice. Then one thing you could also consider doing is just hype, like you plug, you know, plug them to event, right? And then you hyperventilate these people because remember, the quickest means of acutely lowering a person's intracirbral pressure is actually to hyperventilate those people, okay? To hyperventilate those people, typically hyperventilate till you get to like a PCO2 of like 20 to 25, okay? Those are actually numbers you maybe want to remember for the purposes of the USMLA exams. And then what if they give you a question about a patient that comes in, let's say this patient is like six foot nine inches tall or this patient has like a long history of uncontrolled hypertension and he presents with like sodium onset severe tearing chest pain reditins with a back. What are you thinking about? Well, I would really hope you're thinking about erotic dissection, okay? Erotic dissection. Remember, erotic dissection, again, the classic presentation is a present comes in sodium onset severe tearing chest pain reditins to the back, okay? And classically, right? I mean, there are some risk factors you want to keep in mind, right?

If a person has a history of like chronic hyper, like really bad uncontrolled hypertension, actually, I'll go ahead and see this out loud. Hypertension is the biggest risk factor for erotic dissection. I'll see it again. Hypertension is the biggest risk factor for erotic dissection. And there is a Boswold Pathophysiology behind the erotic dissection that your friends at the NBME expect you to know, right? Your de-disection arises from a person having like cystic medial necrosis or like cystic medial degeneration. So what are some classic risk factors that pop up on the NBM Es? For a person having erotic dissection, right? It can be a person with morphine syndrome. That's why I give you the keys of the person being like six foot nine inches tall, like NB center style height, right? That can trigger erotic dissection. If a person has a history of, let's say they give you a question about an IV drug user or a person like a man that has sex with other men or a person that you know has like promiscuous or sexual behaviors, you may want to think about syphilis, right? Remember syphilis tends to affect the viso-visor that you find in the tunic adventicia, right? Of the urine, it's arch, right? So if you have like a syphilitic or tightis, remember that's like tertiary syphilis. That can also cause erotic dissection. Erotic dissection can also pop up in a person that has a pronounced download syndrome.

Like for the most part, these connective tissue disorders can increase the presence risk of having erotic dissection. And then if a person also has like bicospid erotic valve, right? Remember people that have bicospid erotic valve, they also tend to have like other erotic problems going on as well. Those people can also have erotic dissection. So again, those are all classic risk factors for erotic dissection that you want to keep at the back of your mind on NBM Es' exams. Now, the thing is, one thing I'm also going to say out loud, even if it's not very specific erotic dissection is that for pressing a erotic dissection, if you get a chest x-ray, right? You may see a widened medius thina, okay? You may see a widened medius thina. One thing I also want to go ahead and say is that your friends at the NBME for an image shelf, they may give you a question about a, you know, like a FBI agent or postal worker that comes in with him up to say that, you know, likely has anthrax, a classic finding on imaging, like on a chest x-ray. And a person that also has hemorrhagic medius thinaitis with anthrax is also widened medius thina. That is definitely a question that can show up on the EMEDA NBM Es' shelf. So again, those are all high-y old things to keep at the back of your mind. So the thing is, if a person comes in with an erotic dissection, right? And, you know, they are stable. Well, if they are stable, you can actually do like CT&Gogram with IV contrast, okay?

That will help you a lot with decision making. But if, for example, the patient is hemorrhagic on stable on your NBME exam. And the thing you want to do for those people is you want to get a TEE, or get a TEE, a transverse of a gelico cardiogram. The reason you get a TEE is because you can do that at the bedside, okay? And that can help you clearly make the diagnosis, right? So that you can proceed with management. So the thing is, the million dollar question is, what is your first step in the management of erotic dissection? You always want to give a beta blocker first, okay? Given a beta blocker first is always the first step in management of an erotic dissection, okay? It's always the first step in management of an erotic dissection. And then, after you've given the beta blocker, and again, let me try to trick you to give hydrozene, don't give hydrozene, one of the drug you can give, I guess, if they don't put a beta blocker as an answer choice, is you can actually give a nitropercyte, nitropercyte can also be used in patients that have erotic dissection, okay? But beta blockers are the first-line agent. So the thing is, why do you get all those images? Why do you get the TEE or why do you get the CT and geogram with IV contrast? Well, the reason is that there are two kinds of erotic dissections, right? There's the Stanford type A dissection, and there's the Stanford type B dissection.

The thing is, if a person has an erotic dissection and it only involves the descending order, that's a type B dissection, okay? If a person has an erotic dissection and it only involves the descending order, that is a type B dissection. Every other kind of erotic dissection is a type A dissection. So the quick question is, right, how do you treat these things? So a type B dissection, if you give the beta blocker, right? But you also need to send those patients to surgery. But if a person has a type B dissection that only involves the descending order, then those people can be treated with medical management only, right? So you can go ahead and give those people a beta blocker and you kind of watch them. I mean, you likely send those people to an ICU. Now, some other key things you want to keep at the back of your mind with these erotic dissections, right? If an erotic dissection, you know, if it dissects proximally, that can actually cause a schemia of a person's coronary vessels. Classically, that's the RCA, what it means, the right coronary artery. Now, what is another hypertensive melody that can occur on the MBM Is, right? What if they give you a question about a patient? Let's see, the theory that this person has like a histone, like some thyroid problem and this person comes in and, you know, they get like a CT scan with IV contrast for some kind of a procedure, or some kind of imaging test that he needs to get done.

And then they tell you that, oh, like, you know, on the second day after the person got like the scan, they tell you that, oh, this person is like markedly tachycardic, right? Has like a mild hypertension. The person has like a fever, right? So like, the temperature is like 103. And the person has like altered mental status. If you see that, I would really hope you're thinking about thyroid storm under those circumstances, thyroid storm. Okay? Thyroid storm, right? Like, what are the classic populations that tend to get thyroid storm on the MBM Is exams, right? Well, these are people that are, they're like hyper thyroid, right? For the person has a history of hyper thyroidism that can increase the risk of a thyroid storm. If a person, you know, that has hyper thyroid disease misses their medications, right? So they miss taking the amethymasol or the Ptu, right? That can again also trigger like a, thyroid toxic crisis, right? Like a thyroid storm kind of presentation. If a person has, um, if a person has, you know, like gets contrast for image and remember, most images, right? That like most cut scans or CT scans, right? Most of the contrast agents contain iodine, right? So because those things contain iodine, right? They can trigger, um, in again, a person with a susceptible thyroid and they can trigger a thyroid toxic crisis on that those are circumstances. And then other things that can cause that, um, that can cause thyroid storm, right?

If a person is on a muterome, right? So let me give you a question about a person that you know, has some kind of credit this problem. And then they were recently studied like on a muterome, right? To help control the aritha, whatever, um, a muterome can also trigger a thyroid storm, right? I mean, look at the name of the drug, a meyodero, right? So a meyodero, it literally has iodine in the name, right? So again, through the wolf chikof effect, it can trigger a thyroid toxic crisis, right? It can trigger thyroid, thyroid storm, okay? It can trigger thyroid storm, right? And the thing is, if a person has thyroid storm, it obviously that'll be suggested by if you, you know, if you check the thyroid labs, the TSA should obviously be low, the T3, T4 are typically high, okay? So those are all high of things to keep in mind, for exams. So now, how do we treat thyroid storm? Well, the thing you do for thyroid storm is in general, you go ahead and give a bit of blocker first like proprenolol, okay? Proprenolol, remember, proprenolol is a non-selective bit of blocker. It blocks what bit of one and bit of two receptors. But the thing is, um, proprenolol also helps in a person that has thyroid storm, because it inhibits an enzyme known as a 5-prime diodinase. And the job of the 5-prime diodinase is to convert T4 to T3, right? So proprenolol can certainly help with your hyperthyroidcent symptoms.

Another thing you'll give next after proprenolol is you give, um, you give, um, actually you can give us more low, instead of proprenolol, let's more low, let's not know that, but as more as more as more like a selective bit of one blocker, right? So one of the the thing you give next after proprenolol is P2 U, right? So purple, fire, or a cell? Remember, P2 U, P2 U is an, um, P2 U is an, um, um, you know, it's an anti-thyroid medication, but it also has that ability to inhibit that peripheral, right? So P in P2 U, P in peripheral, it also has the ability to inhibit that peripheral of 5-prime diodinase that converts T4 to T3. And then after you've given P2 U, you actually have to wait an hour, right? And then after you wait that hour, you can give something known as Lugol's solution, occasionally on MBME exams, instead of calling it Lugol's solution, from the Mekollib SSKI. So SSKI stands for super saturated, um, solution of potassium iodide, right? So you can do that. And when you do that, that can help you with, um, that can help you with again, you know, like sort of treating the present symptoms, uh, because you're essentially like trying to inhibit the production of new thyroid hormone. Okay, but you do it one hour after you give in P2 U, right? And then, um, um, so actually let's hold it for a second there. So I mentioned the Wolf Chycoff Effect, whoops, I mixed it up.

So the thing is the Wolf Chycoff Effect is an effect that you take advantage of when you're giving a person in thyroid storm, um, Lugol's solution, or like the super saturated solution of potassium iodide. So the Wolf Chycoff Effect is when you supply an iodine load, you inhibit organification in the thyroid gland, right? And that will prevent the formation of thyroid hormone, right? So you are taking advantage of the Wolf Chycoff Effect when you give Lugol's solution or when you give the SSKI solution to a present that's undergoing a thyroid storm, right? Uh, the thing I was thinking about when I was talking about a mutler, right? Um, or if a person gets like contrast, like iodine contrast and then it triggers a thyroid storm, I guess I was thinking more along the lines of the Yod Bistal phenomenon, okay? We're giving an iodine load causes the person to have a thyroid toxicosis, okay? So please don't confuse that like I did on the example, right? So Wolf Chycoff goes with, um, becoming a, um, like, shutting down thyroid hormone production, Yod Bistal deals with, uh, ramping up thyroid hormone production, right?

And then the thing is after you're giving like, so remember I said first step you give per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per per So you can prevent the development of that in general in efficiency by giving the Xamethasone or Hydro Corysone by giving the Xamethasone or Hydro Corysone. And one thing I guess I'll just go ahead and throw out there if they give you a question right and like a non-spezive question and they're asking about the kind of that a person that has a history of hyperthyroidism will have they will likely have a fib. Okay. A fib is the most common arrhythmia in a person that has a history of a hyperthyroidism.

That's actually like a weird nucleoid, high hyalurphactoid, you need to know for the purposes of your exam. And then another hyper-tensive melody that you mention an Mbim exam, right? It can give your person that you know, they tell you that this person has like a neck mass and then they tell you like two or three like uncles or whatever. Have died of like some thyroid problem, right? And then they tell you that this person presents and this person says that he has had these episodes where he has like severe headache and his blood pressure occasionally like during those episodes of severe headache, the person's blood pressure shoots as has like 250 systolic, right? If you see that, you want to think about a thiochromositoma, right? So these thyroid thyroid, like crap I've been talking about essentially refers to medallary thyroid cancer, right? Remember Mm2 A and Mm2 B associated with people having a few chromositomas, right? And remember that Mm2, the Mm2's inherited in an orosomodominant fashion and they are associated with a mutation in the ret, so R-E-T in the ret, okay? So remember Mm2 A people have a few chromositoma, they have primary hyperthyroidism and then they have medallary thyroid cancer, right? But on the other hand, people that have Mm2 B, right? They have like, they have a few chromositomas, right? They have medallary thyroid cancers, they have like the mucosin aromas, right? And they also have the martyloid body habitus, right?

So those are all high yield things you want to keep at the back of your mind in a person that has a, um, um, um, in a person that has a few chromositoma, right? And obviously the person comes with a few chromositoma, how do you want to treat these people, right? The first thing you want to do is you want to, you know, block alpha receptors first, right? So you can give an irreversible, alpha-1 blocker like phenoxybensamine or you can give a reversible alpha-1 blocker like phentolomy. Alternatively, you can give an alpha-beda blocker like, um, like, um, labidol, okay, you can give labidol, okay? You can give labidolol, it can really help in these kinds of circumstances. And then, um, so you block alpha, you block beta, the other things would like the MIBG scan and all that. So that's my fine internal medicine shop. I discussed those very adequately in my internal medicine videos. And then, um, another one you may see, another hypertensive malady. I think probably this is the last one I'll talk about. Um, another hypertensive malady emission on an MIBG exam is, you know, they give you a question about a patient, you know, has a history of depression, they're taking like phenolzine or tris- trineolceperumine or isocraboxazine as their medications on MIBG exams. And, um, you know, they go to a restaurant, they are eating and then they start feeling altered and they become almost like comatose and they come into the emergency room, their bloopers are like 252, 260, systemic.

If you see that, you really do want to think about, um, um, like a tyronin crisis. Remember phenolzine. Uh, so pH, N, E, L, Z, I, N, E, um, trineolzine, perumine, I believe it's spelled T, R, A, N, Y, L, C, Y, P, R, O, M, I, N, E. And then isocraboxazine. Um, um, isocraboxazine, right? Those are all M, E, Y, they are monotonyneoxidies and hematocytes. So remember those drugs are not safe in people that get a tyramine, in people that get tyramine rich foods on the MBM exam. So again, that's something very high, you have to give out the back of your mind for purposes of the MBM, for purposes of the MBM exam. Now, um, so how do you treat these people right? Again, you can treat them with an alpha-beta blocker, like labeta law, or you can treat them with phantolamine. Okay. So again, tyramine crisis with M, E, Y's, you can give phantolamine. Remember, it's a reversible law for one antagonist or you give, um, um, you give phantolamine, sorry, you give phantolamine, that's the reversible alpha one antagonist, or you can give labeta law, which is an alpha-beta blocker. And I said that I talked about some genetic syndrome associated with a medallary thyroid cancer, right? So like M, E, N, 2, E, N, 2, E. But don't forget that when people, um, don't forget that when people lend out VHL, chromosome 3 defect, also the modem of the inheritance, also tends to be associated with, um, with a few chromosidomans, right?

So there are many, um, those are just all things, again, you want to keep in the back of you. Like all these things I've mentioned, you just want to know them well, because this probably covers most of the hypertensive scenarios you see on M, on M, M, M, E, M, E, M, shelf, right? In a person that comes in with like very high blood pressures, although maybe one I didn't mention what I'll talk about this likely later, when I talk about drugs of abuse, although I've actually made the podcast on drugs of abuse, what I mean, discussed it in an emergency medicine context. Well, basically, if a person over doses on cocaine, cocaine is a sympathetic agent, right? And he is the reoptic of caracolomins. So that can cause a hypertensive crisis. For instance, a hypertensive crisis from cocaine, you can treat them with a little bit of law, you can treat them with, um, um, um, treat them with a little law, and you can also treat them with, um, um, what do I want to say? Oh, come on, do I think you can also treat them with like a fentanylamine, right? Or you can also treat them with like, uh, actually, unless some situations, you can actually treat them with nitro-perside as well for the hypertensive, tyramine crisis that arises with taking an immune. Okay, so I think these are all the hypertension related maladies I want to discuss. So let's move on to the next thing I want to talk about. Okay, so what if you get a question about a patient, right?

You know, this patient is an IV drug user and they come in, they say for the last four days, they've been having like feverers and then they tell you that, oh, that's your school day, the chest I hear a memory you've never heard before, right? Let's say the like the memory is her best, uh, like you hear this whole systemic murmur at the left, turn on border, right? Um, in the tricospit area, but what are you thinking about? Well, this is endocraditis, right? This is endocraditis. Endocraditis, there's really not much you need to know for the eating shelf because again, uh, the chronic management is likely going to be under the overview of internal medicine, but you know, in general, the person comes in, they haven't no credit is, um, the classic presentation is like fever, new murmur. Sometimes the patients may have, you know, like these symptoms that have been going over a long time, um, the person may have, um, um, like, you know, you may get in the gym and see like the septic pulmonary embolite or the person may have like these embolic phenomena, right? So like the genuinenotes, right, that have been less or the osler nose that have been full, right? Um, so you know, you may see all those things, right? And again, it's classically an IV drug user. And usually why?

Because most times if you think about endocraditis, endocraditis tends to affect the left side of the heart, well, not so in an IV drug user because I mean, think about if you have an IV drug user, where you injecting the drugs into IV into a V, and all the veins drink to the right side of the heart, right? So people that IV drug users tend to get like, um, um, they tend to get, um, with the IV drug users, they tend to get like vegetations on their tricospit valve, right? And usually when they get like a ovular anomaly from having these vegetations, they tend to get a tricospit regurgitation, okay? They almost always tend to get regurgitant lesions on embankment exams, right? Um, and really for the most part, right, if you want to diagnose endocraditis, right, you need to get blood cultures, that's always what you do first, right? You always get blood cultures first. And then, um, you can also obtain like a TEE, okay, to see if there's any vegetation on the valve, right? And then, uh, you know, you send off these four sets of blood cultures, you, you, you, you know, you get the TE to see if there's any vegetation, right? And then after that you stack treatment, right? And the thing is until you get back like, you know, your positive blood cultures to know what blood you're treating, um, in general, you want to treat these people empirically, right? With like something that will cover at least MRSA, right?

So you typically give some kind of, um, like then commising for example, that can help with the endocraditis until you can be more targeted with therapy, once you figure out, um, exactly what blood is, uh, growing from the person's bloodstream, okay? Um, so, uh, yeah, so I think those are, you know, kind of like the big things to keep in mind with, uh, with endocraditis. So let's go ahead and, uh, jump to the next topic, which will be about, uh, infact, in fact, I'm presenting as a vignette. Okay, now what if a patient comes into the emergency room, you know, you're coming to see they have chest pain, um, that they've been having this chest pain for the last like two weeks, and they have this chest pain whenever they walk like two blocks, but once the rest for, was the rest for like 10, 15 minutes, the pink goes away. Well, what's your diagnosis for that patient? Well, this person clearly has stable engine, right? So stable engine, chest pain, bad with rest, I mean, for bad with rest, uh, bad with physical exertion, right? Come on physical exertion goes away when the patient rests. And if you see that, think about stable engine, remember, stable engine is not an acute coronary syndrome. Here's one making that point. The thing is when a person has an acute coronary syndrome, almost always the right next step in management for those people is to take them to the cath lab.

Not so for a person that has stable engine, for a person has stable engine, uh, you kind of need to like, restructify them, right? But if you know they're like high risk, um, and they have stable engine, uh, typically what you do is you refer them for stress test, okay? But in general, when a person has an acute coronary syndrome, you need to send them for cardiac catheterization. So what do I mean by a acute coronary syndrome, right? A acute coronary syndrome, uh, basically start from unstable engine, right? So unstable engine and stemmies, stemmies, those are all examples of a acute coronary syndrome. So, uh, so let's sort of go in progression. So I've talked about stable engine, uh, well unstable engine, the thing that happens is, um, um, these people, you know, the way we present is, it will be a person that has a history of like stable engine, but the presence symptoms seem to be getting worse, right? So they may tell you that, oh, you know, before I could walk to block before my chest being comes, but now I walk one block and my chest being comes, right? So that's on stable engine, what's the stable engine is on stable engine or the person is beginning to have like chest pain at rest or the person is beginning to take shorter, like it's, it's taking longer time periods for them to recover from the chest pain of an engine, right?

So let's see before they say, oh, doc, um, if I walk 10 minutes, I get chest pain when I rest before like after 15 minutes, the pain goes away, but now they say that you know, doc, 10 minutes, I get chest pain, and it's even more severe, and it takes me like an hour, like an hour of rest before the chest pain goes away, that is unstable, right? But the thing is a non stable engine, you know, you may see like STD pressions, you may see TV inversions, but they don't have any troponin innovations. Now, in a person that has an end stemming, right? And not a non ST elevation, my credit infraction, these people have elevated troponins, what else? You see, am I in the name of something? Those people have elevated troponins, right? So in an end stemming, you have elevated troponins, where you do not have ST elevations. Instead, the thing you have is, you have things like, again, TV inversions, STD pressions, right? And then a full blown stemming, you have ST elevations, you have troponing elevations as well, right? So that, I mean, again, for all these acucuronious symptoms, you send the patient to cardiac catheterization. But unfortunately, it's not that simple on the MBM exam, for there are many kind of like decision trees, they want you to understand. So let's sort of talk through those. The thing is, this is more for like a clinical peril, you may not necessarily use it much on your test.

You probably use it more like the email rotation, but if a person comes in with chest pain, right? You can risk stratified them with a corner as the heart score. Okay? Or if a person has, if a person has like unstable and an end stemming, and you want to predict the like, you know, like relatively immediate mobility mortality, you can use something called the Timi score. Okay? TiMI, the Timi score, it's classically used in patients that have unstable and an end stemming, right? So the thing is, obviously, the person has a stemming, right? You want to know how to, like, I mean, you obviously order an EKG and I'll kind of talk about like reasonable steps in management when a person comes in with chest pain, I use suspect and MI, right? You want to for sure know the EKG leads, right? That go with certain infarcts, right? So you know that obviously if a person has like ST elevations in the inferior leads, like two, three and AVF, then you know that they have like a right cornering or infarct, right? Or if a person has ST elevations in like V1 to like V5, right? I mean V1 to V4, and you know, you want to think about some kind of anterior infarct, like an anterior septal infarct. So that's LED territory, that's like the left anterior descending artery. And then don't forget that a person that has a problem with like V5, V6, 1 and AVL, right? Those people likely have like a lateral wall infarct, right? So like from a lateral circumflex, that kind of problem.

And if they give you a question about a person that has an MI and the person seems to have like this new onset like heart block, you want to think about an RC infarct, right? And RC infarct classically can cause a heart block because the R's, the right culinary area in most people, supplies the signal, the SC nodal artery, right? Or the AV nodal artery, right? So you can get heart blocks if those, if you have an RC infarct down to those circumstances. And then let me, I guess again talk about some associations here that you want to know for your NBM image shelf. The thing is, if a person has an RC infarct, is there a particular kind of drug that's contraindicated? It's actually nitrates, right? Don't want to give those people nitrates because if you give them nitrates, remember people that have an RC infarct, they're identical, they're not working as well, right? So those people are really depending on preload a lot, right? Because they essentially just take advantage of the Frank Stalin principle to provide any sort of cardiac output that ultimately would mix its way to the left to the left heart, right? So the thing that happens under those circumstances is those people you don't want to give them nitrates because nitrates are Vinodilators, right? Remember nitrates increase Vinos capacitance, so they have Vinodilators, so they make blood pool in the lower extremities, right?

So you don't want to give a nitrate because that would decrease preload and that can throw a person that has an RC infarct, right, into like really bad a cardiogenic shock. So you don't want to do that, right? And other case you may see already, maybe a person that you know they have a history of like erectile dysfunction and they are taking like a phosphodiester, it's 5 inhibitor like cell dena film, those people should also not get nitrates, right? Because they can get like a profound hypertension and die, right? Or you know like just hypertension that's really hard to treat. So you generally don't want to do those kinds of things on NV Me exams, right? So in generally for prisoners an RC infarct, you can actually consider giving them like fluids, like gentle amounts of fluids, right? To support their preload so that you can at least spursop cardiac output to the left side of the heart, right? So the thing is if a person comes in with an MI, right? The first thing you do is you obtain an EKG, right? And if you see you know again ST elevations that are territorial, right? Or you see like a new left bundle branch block that the person has no heart before, you want to think about an MI, right? Although remember that typically before you see the ST elevations, one thing you may see is you may see these things known as hyperacute T-waves, okay? You may see hyperacute T-waves. These things you shop like within minutes to like the early hours after an MI, right?

And then after that the hyperacute T-waves can progress to ST elevations, right? And then those ST elevations over time they can become Q-waves, okay? They can become Q-waves within a few hours to digs, right? So you get the EKG, right? After getting the EKG, don't forget to give the patient a spray, right? In fact, in general, the patient comes in with chest pain, you have this suspicion of MI, you don't go ahead and give them like 320, 4 milligrams of aspirin, right? I remember aspirin actually does reduce mortality in the setting of an MI. On that like certain circumstances, the mortality benefit of giving aspirin is almost like taking, it's almost like getting thrombolytics for like TPA, it's almost like getting TPA. So you're absolutely right. If a person comes in with chest pain, usually within like 10 minutes of arrival, you want to have those patients on aspirin, okay? You want to have those patients having got in their first dose of aspirin. And then, so after you give the aspirin, you know, you obtain troponins, right? Like you'll be elevated, if the person has an MI, if the initial troponins are negative, what you can do is you can repeat them like 6 hours later, right? For pressing like has like true MI, they'll begin to declare themselves at some point. And then, other things you want to do, right? Remember if a person, you know, has an infarct and you're trying to diagnose a like a reinfaction, right?

You want to use CKM beyond those circumstances, because it takes like 7 to 10 days for troponing I to return back to its normal levels, right? So typically, on that, those circumstances to detect your infarction, you go ahead and proceed with with a CKMB. Now, so what are some drugs you gave us already talked about you giving aspirin, right? If the patient is hypoxic, you can actually give them oxygen, right? You also give the patients a P2 Y12 blocker, right? So like clopinogrel or prestogrel or tycagrel or remember those P2 Y12 blockers, those essentially ADP receptor blockers, that you can use as an antiplet lead agents, right? So, you know, you give your P2 Y12 blockers like a probidogrel, prestogrel, tycagrel, you also give unfraxionated heprin, right? And then if the patient is completely of like chest pain, right? You can go ahead and give them a nitrate, okay? You can give them a nitrate, you can also give them morphine, morphine also helps for the chest pain. So you can give either morphine or you can give a nitrate. So again, these are all important things you need to know for the purposes of your test. Now, the thing is one of the drugs that you know you can give, it's very loyal though, right? So it's on a regular shop on your exam. But basically, if you know a person who's going for a precutinous coronary intervention, one thing you can actually do is to give them a GP2 B3 receptor antagonist, right? So what are the GP2 B3 receptor antagonist?

They are drugs like, like, um, up six-symab, right? Up six-symab is a monoclonal antibody against GP2 B3 A. Another drug is aeptifibatite. Soeptifibatite is spelfas, ep, ti,eptifibatite. Soep, ep, ti,eptifibatite. Soep, ti,eptifibatite, right? So up six-symab is ab,ci,x,im,ab. That's easy to spell. So up six-symab,eptifibatite, tyrophibans, ti,r,o,eptifibatite. Okay? Those are all GP2 B3 receptor antagonists. You usually give them an IV formulation and those can be given prior to a person going for pre-cutaneous or coronary intervention. Right? And one thing you should actually keep in mind is that if a person has renal failure, that can actually slow the clearance of, um, troponins, right? So the presence of troponins may remain elevated for longer than you would expect on an NBM exam. So, um, so what are some other things, right? You want to keep in mind with MI, right? So the thing is if a person has an MI, the preferred method is PCR, right? In fact, you want to know something on the door to balloon time on an NBM, right? So between the time when the patient hits the door, complain of chest pain, and when a balloon is inflated in the occluded coronary vessel, that time period should be more than 90 minutes. That's actually a very high-yield thing to know for the image shelf. And then remember that, um, don't confuse this door to balloon time with time to a PCI-capable center, right? So let's say a person is having like, um, an MI, right?

You know, you see the STL visions, everything. And the hospital, wherever they are at, is not capable of, um, precutinous coronary intervention. Then one thing you can actually do is to consider, uh, thrombolytics, okay? But the thing is thrombolytics are really the correct answer, because typically the, you know, the, there's a PCI-capable center nearby, right? So, but the timeline you want to remember is two hours. If a, if a person is at a spot, where they cannot get precutinous coronary intervention, and the next spot they can get that PCI is less than two hours away, transport them to that center, let them get PCI there. On the other hand, if the person, um, um, if the person is, if the PCI-capable hospital is more than two hours away, then you need to consider thrombolytics, thrombolytics, under those circumstances. So you give, uh, you give a TPA, right? Now, the thing is TPA can actually be given for up to 12 hours after a presence that's complaining of like, uh, MI-style symptoms. Okay? So again, these are all important things you want to keep at the back of your mind, for example. So please don't conflict the two hours like, oh, like, time to a PCI-capable center with the 90 minutes door to balloon time. There are timelines, but they mean two totally different things for purposes of the USM Ls. Um, now one thing that I should I guess mention, right?

So you may see on your exam is they can give you a question and they may say, oh, you know, the person has like a geogenic shock from an MI, and then they ask for the next step in management. Um, and then you know, they usually put a bunch of like bogus answers, and then one answer may be to do something called, uh, an intra-eotic balloon pump. For purposes of the image, I think it's actually highly important that you know how to, like, you understand how an IABP works. Basically, the thing that happens is, you know, you make like a nick through the femoral artery, and then you put this pump into the other, right? So you travel like retrovider from the femoral artery all the way, uh, close to the, uh, to the other, right? Now, the thing that happens is that the probably like the biggest buzzword you want to remember with the intra-eotic balloon pump is that it inflates in diastole. Okay? So the thing is when it inflates in diastole, right? It prevents blood from sort of like going past it into the rest of the, like, the descending order or whatever. So the thing that happens is that because there's little blood going past it, then you actually encourage profusion of the coronary vessels and the cerebral vessels. Okay? Because again, it's inflating in diastole, right? And if it inflates in diastole, remember, when do blood vessels in the, when do, when do your coronary vessels have blood flowing through them? Well, they have blood flowing through them in diastole, right?

So if you inflate the balloon during the process of diastole, right? Whatever, uh, you will essentially like almost before simple, almost like retrograde back into the coronary vessels. So it helps in that regard. Again, there's most of it in diastole, diastole, but maybe make like a separate podcast on like all these devices that I used in the ICU, sometimes, sometime down the line, right? But intra-eotic balloon pumps, the inflating diastole, so the increased coronary profusion that way. Second thing they do is that, uh, they deflate in systole, and the thing is there isn't a deflate in systole is that, or the good thing about them deflate in systole is that by deflate in, right? They call, they help the heart with afterload reduction, right? So because they help the heart with afterload reduction, they can cause like a mild increase in cardiac output. Okay? These are, again, this is something you do need to understand for purposes of your exams, right? Now, um, remember again, like I said, in general, you perform pre-gathering, coronary intervention for, for a person that has an MI, but please don't forget, if a person has, um, you know, like left main coronary artery disease, so they have like triple vessel disease, um, then yes, those people do deserve, um, um, a cabbage, right? So coronary artery bypass graft, I remember that, um, the arterial, the arterial vessels that I use for cabbage, they tend to perform longer and do better than the venous side.

So, so like using the softness, venous not as great as using like, like an artery in the body, basically is what I'm saying, like the internal memory artery, for example. And then, um, you also want to know about like MI complications for this exam, right? So remember, right? Like if they describe a person that, you know, they had a recent MI like two, three days ago, and then they have like this, you know, like flash coronary edema, and you hear like a holosis stomach, no matter the left-lower sternal border. Um, you want to think about, um, an interventricular septor rupture, right? So that will present us like a VSD kind of murmur, right? You'll present us a VSD kind of murmur on the exam. And then if they describe a person that, you know, again has like flash pulmonary edema, um, and you know, they tell you that all the person is like regurgititinal ton, right? Well, you notice that the person's ventricular size is more or more for the most part. Think about acute mitral regurg, happening from like papillary muscle rupture, right? So these people have like pulmonary edema, but you have a normal heart size because it's a cute problem. Conscious of the person that has chronic mitral regurgit, people that have chronic mitral regurgit, um, because they've been having like regurgit for a prolonged period of time, right? They've now had time to exert like overload on the left side of the heart, a volume overload on the left side of the heart.

And the thing is that volume overload in the setting of chronic mitral regurgitation, right? We'll cause like an esteric heart sound, they'll cause like eccentric hypertrophy. So those people get like systolic dysfunction, basically like heiferif, right? So like, I feel you'll reduce ejection fraction because they have systolic dysfunction. Again, these are all high of things to know for, for exams. And then, uh, they can also give you a question about a patient, you know, recent MI and they say, oh, this person has been doing well, but all of a sudden the patient becomes unresponsive. And the person has like JVD, this person has like, um, like a blood pressure of like 60 over a poppable and the tell you that it's hard to ask what like here anything from the chest, right? Well, if you see that, um, I really hope under those circumstances you're thinking about like a ventricular feral rupture, okay? Uh, ventricular feral rupture can actually almost present like cardiac tamponact, right? That's why I give you essentially becs try out. Again, if you see that in the context of recent MI, that's what you really should be thinking about on the exam. And then, if they give you a question about a patient, you know, they tell you they come back to the emergency room, they say that, oh, you know, I had a PCI like a week ago, right? And then I've been feeling funny, like I've noticed that my, my toes have started turning blue and I have to take care of my low extremities.

And then, uh, they tell you that, oh, you know, you obtained some loves, I know these presents creatinines and they did. If you see that, what should you be thinking about? Well, I'll really hope you're thinking about something called bluto syndrome, okay? Bluto syndrome. Sometimes people call it cholesterol embolization syndrome. That is something that classically happens after a person gets like cardiac catheterization for like an MI, right? So as you're trying to, you know, like stand up vessel, you may square off some or shoot off some cholesterol embolite that can then embolize like vessels in the kidneys. So the person can get an AKI from that. It can embolize an obstruct like the digital arteries in the lower extremities, right? So that person can have, um, that person can have, um, again, like ischemia of their lower extremities so they can have like a, that's why it's called bluto syndrome. These people also tend to have like BTKI on the skin. They may have this finding known as a lividoretical virus, right? Those are all things that are associated with a bluto syndrome. Now, another thing you may also notice is they may give you a question about a patient, you know, they'll tell you that a few hours ago, this person had like percutaneous coronary intervention and access was established through like the femoral artery. And then the person, right, becomes like profoundly hypotensive. And this person is completely not like severe back pain.

If you see that on your exam, you really don't want to think about something called a retroperitoneal bleed, okay? You want to think about a retroperitoneal bleed, many physicians call it an RP bleed, right? Because again, remember, whenever you're doing those vascular procedures involving the vascular procedures involving like the femoral artery, you run out, there's certainly a risk that exists of a retroperitoneal bleed, okay? So that's actually something you want to keep at the back of your mind for purposes of the NV Me exam. And then also do not forget that if they, what if they give you a question about a person, you know, again, they got like percutaneous coronary intervention for an MI, or maybe they get got like some kind of ablation for like some weird pathway that's causing a redmiya. And then they tell you that, oh, this person's check, this person, this person's hemoglobin for surgery was 12. Now it's like seven and he's dropping and the person's chest is big, right? Under those circumstances, I really hope you think about potential cardiac tamponat, right? Because remember, if you are bleeding like pathways or you're doing TCI, you're booking needles in a person's heart, right? So you can book the right kind of hole and that can cause a lot of problems, a lot of problems for a lot of problems for for the patient, right? So obviously for those people, you need to take them right back to surgery for like exploration of the thoracic cavity, right?

And then if they give you a question about a patient that you know recently had an MI like three, four days ago, or this patient has an issue of A-Fib, right? And the patient presents with like sodium onset, severe abdominal pain. If you see that, you want to think about acute mesenteric ischemia, really the way you make the diagnosis is with mesenteric angiography, it almost always involves the superior mesenteric artery, right? So again, those are all things you want to keep in mind, or similar presentation, right? Like a person, oh, recent MI, they got a PCI like three days ago, and then right now, you're having like severe low extremity pain and tenderness. If you see that you're thinking about acute limb ischemia, right? The first step in monument is always to give those people a apron, right? For acute limb ischemia, you give apron, and then you typically do like an arteriography of the lower extremities, but you almost always have to call a vascular surgery to kind of help you out there. Okay? So again, high yield, high yield, high yield to know for exams. And then, remember, people can get like paracaditis after an MI, right? They can get like the fibrenospheric aditis like a few days after an MI, or... Oh... If a person has like paracaditis, right? Like paracarial symptoms like... So like chest pain works with lying back, better relate us, springing forward, and you tell me that this person had like an MI like six weeks ago.

They want to think about a dressless syndrome. Remember, that's an autoimmune paracaditis. And please don't forget that in general, right? If a person has paracaditis, they'll have the fused ST segment innovations on the immediate, and then they'll also have the fused ST segment... Sorry, they'll have the fused ST segment innovations, and then they'll have the fused PR segment depressions on an EKG. And in general, when a person has paracaditis, right, you give them an inset plus coacheset. Okay? You give an inset plus coacheset. Now, if for example the person has like renal insufficiency or like... Yeah, if the person has renal insufficiency, they may want to consider giving like steroids under those circumstances. But in general... In general... Giving insets plus coacheset is preferred, because the thing is coacheset decreases the risk of recurrence. What steroids actually increase the risk of recurrence of paracaditis. Okay? Now, remember that the most common cause of death within the first 24 hours of a patient having an MI is a... Is V-Fib, right? Is V-Fib. That is actually one high-year thing to keep in mind, for example. And you want to do... We have lost my trend of thought. Okay, you want to in general do insets plus coacheset instead of giving steroids. Let me sort of retrace my footsteps. I don't know why I can't lose my trend of thought there. And again, like I said, the fused ST segment innovations, the fused PR segment depressions for paracaditis.

And then, I guess, last thing I think I would mention here, actually two more things. So much that one can learn from us. This EM show is very broad. This would probably end up being one of my more comprehensive podcasts. But, Prince Metal, right? The new name these days is V-Ran Tanjena. So the classic presentation will be a person, you know, comes in. They'll tell you that they have chest pain. They've had like multiple episodes of this. Tens to be in a smoker. Tens to happen at night. Right? And then they'll come in. We take them to the cath lab. Yeah, coronaries are clean. They have like, you know, ST elevations on EKG. So ST elevations for putting elevations. We take them to the cath lab. And they're like, good to go. Right? Yeah. Coronary versions are clean. If you see that, think about V-Ran Tanjena. Right? And really, for the most part, you treat those people with calcium channel blocker like... like the entire set on MDM exams. I remember people that have these Prince Metal, and Jena, or have a other visospastic diseases, right? Like... Like Reynolds phenomenon, right? Those people should not be given... Those people should not be given... Sumatraptan, right? Because Sumatraptan causes viso-construction. And that can trigger an MI in those kinds of populations, right? So, with the most part, very much, V-Ran Tanjena, you treated with... non-dihydroperiodine calcium channel blockers like Delta-AZP, for example, for purposes of the NV Mes.

And then, if a person has an MI and sending them home, right? Obviously, you want to send them home with like a bit of blocker, right? Remember, you want to use one of either Metoprolol, or Carvedi-Lol, or Bisoprolol, right? And then you also want to send them home with an A-senator, right? So like, you're a lysinopril, you're anala-pril, and then you also want to send them home with a statin, right? A high intensity statin, right? So like, at over statin, like 80 milligrams, or over-sava statin, 40 milligrams, okay? Those are two examples of like high intensity statins, right? And then... For the most part, that's what you want to do. Although, remember that these beta blockers, or you don't want to give them... If a person has like acute, discompensated heart failure from like their MI, right? Like if a person is decompensated initially, you don't need to... You don't need to give them a beta blocker first, or non-dihydropreeding consumption of blocker weight, for... Wait for them to kind of stabilize from a cardiac standpoint before you're throwing a beta blocker, okay? Before you're throwing a beta blocker on the exams. So, let's go ahead and talk about arrhythmias, right? Let's go ahead and have this free-for-all discussion relating to arrhythmias. So the thing is with arrhythmias, right? There are just many facets you need to know, right? If you don't know about arrhythmias, you probably should not take the EM shelf, right?

You're gonna be doing this on a huge, huge, huge disservice, right? So what is the deal with arrhythmias, right? So I'm just gonna talk about things from many different perspectives, right? So, first thing you want to understand, you wanna know things that can prolong the cutie interval, right? You wanna know things that prolong the cutie interval, right? So, electrolyte abnormalities can prolong the cutie interval, right? So things like hypochylemia, hypochalcemia, hypomide-mysemia, those things can all prolong the cutie interval, and then drugs like is it traumatizing your microlates, your fluoroquinolones, right? Your anti-rhythmias themselves, right? Those things can all prolong the cutie interval on NV Me exams, right? And remember that there are certain people that can also have some congenital long cutie syndromes, right? Like the two big ones that they tend to test for whatever reason on the NV Me are like Romano word syndrome, right? Remember Romano word, it's like Rosomo dominant in Heritans, these people tend to have like, you know, like a prolonged cutie interval, but they also tend to get like all these like weird ventricular tachyritmias, right? And that's pretty much all that's going on with them, right? So, again, Rosomo dominant ventricular tachyritmias, and then they tend to have again like a prolonged cutie interval. That's why it's called a congenital long cutie syndrome.

So you want to be able to compare Romano word syndrome with a gerval and lunged male syndrome. That's actually inherited in an Rosomo recessive fashion, right? So, a gerval and lunged male syndrome is inherited in an Rosomo recessive fashion. And the thing that typically happens is that these people, in addition to having like the ventricular tachyritmias on the congenital long cutie interval, they also tend to have like a deafness, okay? They also tend to have a deafness on NBM exams. So again, that's hopefully something that you keep at the back of your mind for tests. And the thing is for these people, right, that have these congenital long cutie syndromes, you need to essentially put them on a bit of blocker for life, right? So they don't, again, they don't get like, because that suppresses the hyperageneric state so that they don't get, um, nasty arrhythmias. But one other thing you can also do is to place an ICD, right, so that you can shock the... You place an ICD so that you can essentially shock the person back into like a good rhythm when it detects, having like a... when it detects that the person has like, you know, like a bad rhythm going on. Although they may actually give you a case on the H-shelf, and they may talk about a person that you know has an ICD in place, maybe they have like heart failure and their EF is like very low, or this person has like hypertrophic cardiomyop... like a H-C-M, right, like the...

the long athlete that collapses and dies, or the person has like... like one of these congenital long cutie syndromes, and you know you've placed an ICD, but the person has been noticing the ICD firing and the asymptomatic, and you check an EKG, you notice that, yeah, these people actually don't have an arrhythmia, right? Typically the thing that triggers that situation where like the IC Ds are firing inappropriately, is when those people have been exposed to some kind of magnet, right? So let's see, they've got in like an MRI scan, for example, right? Now mess up the settings, right? So typically the thing you do is you take a magnet that you may find in the emergency room. You please that magnet over those people's... over the device, and that will inactivate the device, and then you likely have to consult... cardiology to come and like reset, reset the device, so that it functions appropriately. So again, very high-yield things to know for your exams. Now, the thing is... so what are some key things with again with arrhythmia, right? So remember the QT interval, right? I said, oh, you know, QT interval, if it's more than like 440 milliseconds, it's prolonged. The thing is if a person has a very fast heart rate, then you need to be a little careful with calculating the QT interval. The way you calculate the...

a person's QT interval, if they have a fast heart rate is, you get the QT interval that you're getting from like the EKG strip or whatever, and then you divide it by the square root of the arr interval. Okay, that will give you a more accurate measure of the person's... of the person's QT interval, right? And then don't forget to your wolf Parkinson's and white syndrome. So, you have to do the association like the bundle of Kent, right? Classically, this will present on an EKG as a person having like a shot, like you'll be a young person, completing of like, competitions. And then the person will have like a short PR interval, they'll have like a delta wave on EKG, and then they'll have a white care complex. So if you see this, think about WPW, right? And remember, WPW is actually an example of an anti-dromic, EVRT, so it's an anti-dromic, EV nodal, reentrant attack cardia, right? So it's good anti-dromic because the signal from the atria goes straight to the ventricles through the bundle of Kent, and then they go up the EV nod back to the atrium, right? So you essentially create like a reentry circuit, which can actually be obliterated. But again, that's like the thing that... That's the thing that tells you that it's anti-dromic, EVRT versus orthodromic, where the signal comes from the atria and takes the normal route, right? So it goes from the atria through the EV nodes, and then you have depolarization of the ventricles, okay?

You have depolarization of the ventricles, right? And the thing is that orthodromic EVRT tends to be associated with narrow QRS because it's taking the normal route. And the dromic EVRT tends to be associated with a white QRS because it does not take the normal route. So that's actually again a very subtle, but important difference between those two things that you want to keep at the back of your mind, for exams. And then if a person has WPW, right? So typically, what do you do? So you typically give Prokina Mide, right? Remember Prokina Mide is a Class 1 B, and they make that has an association on drug induced lupus, so don't forget your fancy, schmancy, anti-histone antibodies. But yeah, you can use Prokina Mide, right? The thing is, more than knowing what to use, you also want to need to know what you should not use, right? So the thing is if a person has WPW, you actually do not want to give them an EV node block in agent, right? So you don't want to give them a beta blocker, you absolutely don't want to give them a dihydroper... Sorry, a non-dihydroperadiene calcium channel blocker, like Verapame, Lodil, Taihasem. You also don't want to give them the joxin, because the joxin, yes, it's a positive nitrope, but the joxin is also a most chrysanic receptor, agonist, right?

So the joxin can actually slow conduction on the EV node, and again, that'll be bad for a person that has WPW, because if their hearts are going at very high rates, and then you transfer that rhythm, let's say they have like AFI band WPW, and transfer that rhythm from the right atrium to the... Like from the atrium to the ventricles, the present ventricles may be going up to like 300 bits per minute. That's V5 territory on the visual likely diagram, so you want to try to avoid that if you can, right? So that's all I think I'm going to say about WPW, and then some other, I guess, classic murmurs, for the purposes of the USMLE exams, but also the NBME emergency medicine show, which is my primary point of discussion here, are the hard blocks, right? So you want to know your hard blocks, remember? Like you have like the Type 1 EV block, right? The Type 1 EV block, the present just has a prolonged PR interval, right, but they don't have any drop bits, and then you go to the second degree EV blocks, right? Those, there's two types, right? There's movies, one and more bits, too. Remember, Mobits 1 is also known as Winky Buck, all right? Okay, so the thing that happens in Mobits 1 is that the person has successive PR intervals that are prolonged gain, right? So it's like, oh, the first one was 5 little boxes, second one was 6 little boxes, third one was 7 little boxes. They have like a prolonged gain PR interval before the drop of bits.

If you see that, think about Mobits 1, but if a person has a fixed size, so like these people, they are dropping bits, but you notice that the PR intervals, they are prolonged, but they are all the same size. If you see that presentation, think about Mobits 2, okay? And then Mobits 3, I mean not Mobits 3, it's Mobits 3. A third degree hard block is all over the place, right? All over the place. Third degree hard block and cause multiple problems, but typically the way I spot that on an exam is that there's no relationship between the P waves and the QR's complex. Well, what does that mean? What I mean there is that if you measure the person's PP intervals, they match out well, they are roughly similar. If measure the person's RR intervals, they also match out well. They also roughly similar on the exams, right? So that's the way I've always learned to recognize a third degree of block. And obviously, the person seems to medic from an EV block, right? But they have like a Mobits 2 or a third degree of EV block. And those people need to be paced, okay? Typically you start with transcutaneous pacing, because that's much easier to arrange. But after you do the transcutaneous pacing, the next thing you need to do is, and even if in fact let me tell you this, even if they are not symptomatic yet, but they are high risk, go ahead and put those paths on your chest, just in case you need to initiate treatment emergency. Right? So you do transcutaneous pacing.

If the patient is still a crush on you, you can do a transvenous pacing, okay? You can do transvenous pacing. Or if they don't give you like pacing, as an answer choice for anything, you can actually give, um... What am I thinking about? You can actually give atropin. Remember atropin is a most chronic receptor antagonist, so you can actually speed up a person's heart rate. Okay, so that's all I'm going to say with, that's all I'm going to say with that. Um, and I mean, I guess let me see some more things about these EV blocks. Remember, mobids are too or higher, right? Those people need pacemakers, but mobids one in general, and mobids... Sorry, why do I keep seeing this? Mobids two, which is the second type of the second degree V block, and third degree V block, those people get pacemakers, right? But mobids one, and a type one degree EV block. Those people generally do not need treatment. Usually, you don't need any kind of treatment. And actually, it's very high, you know, that a person that has... uh, mobids two EV block, has a very high risk of progressing to a third degree EV block. Has a very high risk of progressing to a third degree EV block. Now, what if they give you a question about a patient? And this patient has like a regular neuro complex tackier with me. What are you thinking about? Well, I hope you're thinking about SVT, right? Superventricular taggy cardio, right? The third neuro complex, because it's a resin from above the ventricles.

So, it's a resin from above the ventricles, right? If you have an arrhythmia that arrides from above the ventricles, it's almost always... narrow complex, right? So, the curious complex will be narrow. The curious complex will be narrow. The only exception that I really see for a patient has like a SVT with a barrency. It may look a lot like VTAC, because it'll be like a white complex regular tackier in me. But let's... Right, so, if you see a patient have a narrow complex regular tackier with me on your exam, think about the superventricular tacky cardio, SVT, right? The first thing in my life for these people is, you know, I mean, obviously you can obtain vitals and all that stuff. But the things you're classical to do for these people is... You can start with like vagal maneuvers, right? So, you put the patient's head in cold water, you can do the carotid massage, you can have them blow into a syringe, right? But one thing you can also do simultaneously is that you can actually give... You can actually give a denocene, remember a denocene? Because it's like hyperpolarization of cells, right? So, it can essentially stop conduction down the evening, and almost like reset, you literally stop the person's heart, right? So, you can almost reset the person's heart on that those circumstances.

But if, for example, you know, like that is not really working, because typically for a denocene, you give three doses, you give six milligrams, and then give 12 milligrams, if that's not working, or you know you are able to, you've been able to like stabilize the patient's cell, you can then put them on something to control the heart rate. So, you can put them on a bit of blocker, right? Or you can put them, which is a class two anti-retinic, or you can put them on a non-dihydroperidine-consumption blocker, which is a class four anti-retinic, like verapamele or delta-azen. Again, all the important things to know for purposes of the exam. But if they give you a question about a person that has, again, I've mentioned this rule already. If a patient has an SVT and the hymnodynamiclyon stable, how do you treat? You persist right to direct current cardiversion. Remember, that thing has three different names. It could be direct current cardiversion. It could be direct current counter shock, or it could be a synchronized cardiversion. And what do I mean by the word synchronized? Well, by the word synchronized, I mean the presence of, you don't want to avoid the R and T phenomenon. So, what does the R and T phenomenon mean? Remember, the T wave on an EKG represents ventricular repolarization. Okay, represents ventricular repolarization.

So, the thing that can happen is that, if you shock the person when the ventricular repolarizing, you can actually make, throw those people into like V-fib or sad, the point, and they can die. So, you generally want to try to avoid that. So, that's why you press the sync button. And you can actually do a synchronized cardiversion. The only times in emergency medicine that you do an on synchronized cardiversion, is if a person has V-fib or a person has post-lesvy tech. Those are the only rhythms that go through on synchronized cardiversion. Remember, on synchronized cardiversion is also known as defibrillation on tests. So, I guess that's maybe all I want to say about a SVT. A flotter is treated essentially the same way as an SVT. But don't forget, your classic, your classically described a sawtooth pattern. And the sawtooth pattern is actually seen a lot easier in leads to three and AVF on the exam. So, that's something you should maybe keep at the back of your mind when you are looking at an EKG, where they're trying to get you to make the diagnosis of etroflotter. And then, don't forget like your multi-focal etro-tachi cardia. You have like three or more different p-wave morphologies. For the most part, you tell those people to stop smoking. And usually, three of those people would like calcium channel blockers, like a non-dihydroperidine calcium channel blocker, like verapermil, or tyazine. It's very common in patients that have COPD.

And then, if you see like a regular white complex stack here with me, you want to think about V-tack. The thing is, if a person has V-tack, and they have no pulse, well, your decision is easy. You need to shock that patient. And also, this is the same management principle for V-fibs. I'll talk about both together. So, V-tack with no pulse or V-fib. You need to do an on-synchronized cardioversion, and then you need to essentially initiate like E-cellus algorithm where you give them like, you alternate, you give epinephrine two minutes, and then you give a muter, and then you alternate to epinephrine, and then I'm muter, and then to epinephrine, and then I'm muter. Contrast that with a person that has an MI where, for the most part, you give epinephrine, and that's it. Okay, give epinephrine, and that's it. So, I've talked about the pulse-less V-tack decision. If a person has V-tack, and they have a pulse, right, but they are hemodynamically unstable, you want to post you a synchronized cardioversion on that of circumstances. Now, the third decision with V-tack is if a person has V-tack, and they are hemodynamically stable, the first line of medication can actually give those people is a muter, okay? A muter is the drug of choice for treating a patient that has V-tack that is hemodynamically stable.

But if you don't see a muter as an answer choice, so the person has like an allergy to a muter or has like a history of a muter or toxicity, you can consider giving those patients a light-okin, okay? A light-okin is the second line agent for the management of a patient that has V-tack. Again, regular, white complex tachyridmia that is hemodynamically stable. And again, I've talked about V-tack. I mean, if a patient has PEA, sisterly, really all you're going to be doing for those people is high-quality CPR in epinephrine. High-quality CPR in epinephrine, that's pretty much it. You don't shock, sisterly, you don't shock PEA, right? Although I'll talk about those Hitches and T's probably in a future podcast. And then one thing I want to talk about is what if you get a question about like an athlete, you know, he's brought into the emergency room because he collapsed during a basketball game. And if you see that, right, hopefully you're thinking about like hyper-traffic cardiomyopathy. Remember, it's autosomodominant in heritins. These people tend to have like mutations in sacchomia proteins or proteins like amyazine binding protein C or like the beta-myocene heavy chain, right? Those are all things that are associated with like mutations giving rise to hypertrophic cardiomyopathy. The thing is your friends at the MBM, they want you to be able to differentiate the murmur of hypertrophic cardiomyopathy from erotic stenosis. I mean, one thing that can help you is just age, right?

HCM will be in a young person on the exam. Erotic stenosis will be in an old, like, person on your test, right? And then remember that erotic stenosis, the murmur is heard best at the right of personal border. Contrata would HCM with the murmur is heard best at the left lower sternal border. Okay? And then the thing is people that have erotic stenosis, the murmur radiates to the carotids. People that have HCM, the murmur actually does not radiate to the carotids, right? And then you've probably come to associate the term pausos pervus etardus with erotic stenosis, right? So like a slow, delayed upstroke of the carotid pulse. It's kind of different with HCM, HCM. They have something known as pausos bicepheriens. Okay? B-I-S-F-E-R-I-E-N-S pausos bicepheriens. The thing that happens in pausos bicepheriens is that those people have, like, a small upstroke of the carotid pulse. And then it's followed by a big upstroke. If you see that, think about pausos bicepheriens. That's a classic ambient exam finding in a person that has hypertrophic cardiomyopathy. And then don't forget that if you increase preload, that will actually make the murmur of erotic stenosis sound louder. Because when you have increased preload, you have an increased endastole volume for the left ventricle. So you have more flow of blood across the stenotic valve. Okay? You have more flow of blood across the stenotic valve. So the murmur will get louder.

On the other hand, if you increase preload for a present that has HCM, that will actually make the murmur sound softer. Because when you increase preload, that will actually take away that anterior leaflet of the mitral valve from the left ventricle valve flow tract. So that will relieve the obstruction. So that really makes the murmur sound softer. Okay? That actually makes the murmur sound softer. And also if you increase afterload, that also makes the murmur of HCM sound softer as well. Because again, essentially anything that puts more blood in the left ventricle will make the murmur of HCM sound softer. Now again, people that have HCM bit of blockers, right? Because you want them to spend, you want their hearts to spend more time in the asteli so that you can, you know, you can essentially augment the astolic feeling and hopefully relieve some of their symptoms. And those people again, if you're having like nasty, nasty, nasty arid meas, they also need placement of an, of an ICD. Okay? They need placement of an ICD. Now, I guess I'll talk about the quick boss phrases with the other vavular disorders, right? So like, mantra vav prolapse, right? It's like, it will be a person that maybe has like some psychiatric disorder or a person that is pregnant or a person that has morphine syndrome, right? And then the utility that the person has like a murmur that meets its astolic click, right? That's my mantra vav prolapse for you.

Remember, the boss of pathophysiology is a mix of some other degeneration of the vav, right? And then if the utility that the person has like a holo systolic murmur heard best at the apex, we're eating to the axilla, that's my true regurgers, right? Remember, mantra regurgers causes a volume overload. And don't forget that mantra regurgers, right, can happen as a result of a papillary muscle rupture as a complication of an acute myocardial infarction. And then, oh, erotic stenosis, right? Like systolic ejection murmur, heard best at the right of personal border, radiates to the carotids, old guy, you may see early AS in a patient that has a bicospeediotic valve or so like a ton of syndrome style patient, right? And then don't forget the odicrygurgitation, right? Odicrygurgitation, you'll be a systolic murmur, heard best at the left sternal border or the left sternal border, right? And you'll be a systolic bluing murmur, right? That'll be a serial white pulse pressure. In fact, let me teach you a trick. If you ever see white pulse pressure on an embankment mix and you want to think about two pathologies, eroticrygurgitation or patent doctor satiriosus, PDU obviously being a kid on the mbm exam, right? And eroticrygurg, again, you'll have a white pulse pressure, so you'll be seeing a blood pressure of like 160 over 40, that's very bizarre, right? That's a white pulse pressure, right?

Remember, pulse pressure is the spread between your systolic and your dastolic blood pressures that is classic and pathonomonic for eroticrygurgitation, right? And then a VSD is also heard best at the left sternal border, right? You'll be a holosis stomach murmur. And then again, remember that that can arise as an acute complication, like an interventricular septor rupture in the setting of a recent acute M-I. So I think those are the viola disorders I want to talk about. And let's see. Okay, let me talk about a few quick topics here and then I'll be done. I'll try to be done within the next 10 minutes. I know I apologize to whoever is listening to this podcast. This is probably the longest like audio podcast that I've ever met. My apologies, but they're just certain things I want to get through because there's a lot to get through in EM. I don't want to have like 50 different podcasts just for the e-match show. So let's go ahead and talk about a CHF exacerbation, right? So CHF exacerbation, you're presenting a person that has a history of CHF, right? And you know, it may be something that, there's usually something that triggers the exacerbation, right? But classically, they'll have like pulmonary dima, crackles when you're scotate the lungs, they'll have like, they may have GVD, they may have like congestive hepatopathy, right?

Where they have like hepato-megaly because fluid is backing up in their livers, they'll have like pitting a dim of their lower extremities, they may have like an anasacr state, they may have like hyper volimic hyponitremia, right? So they can have all those things, right? If you see that, they may have like an S3 heart sound, think about a CHF exacerbation, right? And remember, right, there are many things that can trigger CHF exacerbation, probably one of the most common causes, at least that I've seen clinically, and you may see on your exam, is a person not being compliant with your medication, right? That's a very common cause of a CHF exacerbation. If a person misses dialysis, that can make them volume overloaded, right? If a person has like a myocardial infraction, right? Or a person has like huge metabolic stress, like an infection or something, or the aceptic that can again trigger CHF exacerbation, right? And I think maybe one sidebar thing I should maybe kind of discuss here, is being able to identify right heart failure versus left heart failure. I don't know if whatever is in a lot of people seem to get this wrong on exams. So let's talk about it, right? So the thing is, in a right heart failure, usually those people will not have crackles in the lungs, right? And they'll probably have like a Hischof smoking, so they have like COPD causing like corpone alley, or they have like a cystic fibrosis, right? They've had like really bad pulmonary hypertension, right?

So people that have heart heart failure, they'll have GVD, they'll have like hepato-mechaline, they'll have like peripheral edema, because remember, everything ultimately drains to the right side of your heart. But they'll typically not have like, and they'll have like elevated central venous pressures. Remember, your CVP is a proxy, you can see a surrogate for your right-itro pressure, why is it called central venous pressure? Well, guess what? All your veins drain to the right-itre, right? So it should make sense that the right-itro pressure should also be known as the CVP, or the central venous pressure. And people that have right heart failure again, they'll have a normal pulmonary capillary wedge pressure. Remember, a pulmonary capillary wedge pressure is a proxy for left-itro pressure on NV Me exams. Now, um, um, versus left heart failure, if a person has left heart failure, they'll have like pulmonary edema, they'll have essentially all the signs of right heart failure, or they'll have pulmonary edema, they'll have an elevated pulmonary capillary wedge pressure, so their left-itro pressure will be elevated with more than 18. Remember, that magic number of 18 will help you differentiate between a cardiogenic cause of pulmonary edema on an NV Me exam, right? versus a non-cardiogenic cause of pulmonary edema on an NV Me exam. Remember, cardiogenic pulmonary edema, PCWP will be more than 18, because fluid is backing up in the left-itre.

A non-cardiogenic pulmonary edema will be something along the lines of, um, of ARDS, okay? ARDS causes an, is the post-archal cause of a non-cardiogenic pulmonary edema. And, um, that again will be a pseudo-dip pulmonary capillary wedge, but should there be less than 18 on an NV Me exam, right? And, I remember that, um, again, if a person, you know, comes in with a CHF examination, how do you want to treat them, right? So, um, you know, typically you want to go ahead and, uh, I mean, if you get imaging like a chest x-ray, you may see that they have like, you know, like fluid everywhere, you have like, civilization of the, of the pulmonary vessels. Um, typically, uh, one of the quickest ways you can actually relieve the assurance of breath-believe it or not is to give them nitroglycerin, right? Remember, nitroglycerin is a venodilider, right? And, because it's a venodilider, it decreases preload, right? So, it's like increasing like the capacitance of the veins in your lower extremities. So, the blood, the, if you, when you see something has increased capacitance, you hang on to the blood, right? Like, you are able to hang on to things for longer periods, right? So, the, the venodiliders, right? So, they keep blood in the lower extremities, right? So, that keeps it away from the heart. And when you do that, right? That kind of like, reduces my ocadioloxygen demand, right? And it sort of like, reduces the stress on the heart.

That is actually one of the quickest means of relieving the dyspnea that is associated with the CHF exacerbation, right? So, you can give nitroglycerin, as you actually your first drug, and then after that, you can give like fewer summits, fewer summits of lipdiarrhetic, that will over time help, help the fluid get away. And the less than you are giving a person fewer summits, and you know, they are not having like vigorous diuresis with that, you can actually go ahead and add a thiazide diuretic to that regimen. You can add like metola zone, for example, right? And that can help with achieving like a very vigorous diuresis. So, now, let's assume you've tried these medications, you know, you've tried fewer summits, you've tried nitroglycerin, and the person is still, you know, you've given medical therapy, the patient is still struggling, and they ask for your next best step in management on the shelf. The thing you want to do is you want to switch to putting those patients on like BIPAP or like CPAP. The thing is BIPAP and CPAP, they are colloquially referred to as NIPPV. What does NIPPV stand for? NIPPV stands for non-invasive, positive pressure ventilation. And remember, NIPPV is also something you can use for a person that has like a COPD exacerbation, right? But the thing is, those things actually decrease the work of breathing of the heart, right?

And one of the ways they decrease the work of breathing is that they essentially give you like peep because you're blowing air down the earring to the lungs, right? So that keeps the, of your life open because the fluid, the pulmonary dimmer, the fluid in the lungs actually tries to like compress those pulmonary ovulite, right? So you can actually try to decrease those patients' work of breathing by, you know, putting them on CPAP or BIPAP, or again, you may see, the term NIPPV on your exam, that will keep the ovulite open, that will like give them peep, right? So that will decrease the work of breathing. But the thing is, those CPAP and BIPAP, right? They also decrease, actually increase the interest or arctic pressure so that decreases preload. And by decreasing that preload, right? Again, you're decreasing the work that the heart has to, essentially decreasing like all the trouble that the heart has to go through. So you're decreasing your cardio oxygen demand. And again, you're keeping the blood away from the heart. And then CPAP BIPAP also actually increases, I mean, actually decreases after low. And the decrease preload and the decrease after load and the decrease the work of breathing. And those are all high yield things you want to know on your exam. And then again, if you're trying NIPPV and the patient is not doing well, the patient is still struggling, then you need to proceed towards into beating the patient. You need to proceed towards into beating the patient.

And I mean, if a person, you know, has a C-chef exacerbation, or a person has like a reoginic shock, right? You want to consider using pressers, right? You want to use like a drug like Dubu de Min, right? Dubu de Min is a beta-1 agonist. You can use it to trick a reoginic shock. But one other drug you can actually use is something known as merino, okay? You can use merino, right? Merino. Merino is a force for diasterease inhibitor. So think about it. If you inhibit force for diasterease, that would make cyclic NP persist for longer periods of time. Well, the thing is, you may hear attending physicians or you may read in texts that merino is an I know dileter. Let me see, like, how? How is it an I know dileter? Well, the reason that I know dileter is elevated level of cyclic NP do different things in cardiac muscle versus smootmossal. In cardiac muscle, elevated levels of cyclic NP actually cause, actually cause, like, contraction of the muscle, right? So that is why merino is a positive I know trope. But if you're going at the level of the blood vessel and you have high levels of cyclic NP, that actually causes smootmossal relaxation. So the person actually has visual dilation. So merino is almost like the perfect drug because it's increasing your cardiac output because it's a positive I know trope. But it's also making it easier for your heart to work because by causing visual dilation, right, your heart has the faces decreased after load.

So it's much easier for the left ventricle to empty. That's why merino is a phenomenal drug, right? In fact, there are some patients that have treated where, you know, they're in like a CHF exacerbation and they are not making urine. You put them on the vitamin or merino and boom. They start making phenomenal amounts of urine, okay? So that's one thing you can use to those drugs like the vitamin merino, you can use those to treat cardiogenic shock in the in the setting of a CHF exacerbation. And then remember one thing that can actually cause like a CHF exacerbation like picture and a young person on your MBM exam can actually be a person that has myocarditis, right? So they can give you a question about a patient, you know, it will be a young person and maybe they have like upper respiratory symptoms, like, you know, like a few days ago. And then now you're having like new S3 heart sound, they tell you that you get an echocardiogram and you see like global enlargement of the ventricles. And the person has like new S3 heart sound, they have JVD, they have pulmonary Dima, right? That's myocarditis. And classically, it's caused by viruses on MBM exams, especially like the Cox-Aki B virus, right? The thing is these people may actually have like elevated troponins, but one classic unique finding on MBM exams, whatever bizarre reason in myocarditis is that these people will have tacky cardiac, that is out of proportion to the fever, okay?

So they may be like minimally febrile, but you're like, man, this person's heart is like sleeping away at like 140, 150 bits per minute. If you see that, you really want to think about myocarditis, right? That can cause a CHF style presentation. And really the way you treat a CHF exacerbation is the way you treat these people as well, okay? So again, these are all higher things to keep at the back of your mind, for example. And then I guess my last topic, I promise, my last topic is syncopy, right? And again, I'll talk about this real quick. You just want to be able to recognize these different kinds of syncopy, right? So like viso-vigal syncopy, classically, that will arise in a present that, you know, they'll tell you that, oh, before the present passed out, you know, they heard bad news or they were sweating and they had like, power of the face and then they passed out. That's viso-vigal syncopy, typically make the diagnosis with a tilt table test. Cardiogenic syncopy will be the one where the person like just like without warning, they just pass out. And then it lasts for like a very short time interval and then they come right back without any sequelae. If you see that, think about cardiogenic syncopy, they likely have like a dangerous arrhythmia that's causing their problems. And then your genocyncopy, right? AKA seizures or stroke, right? Those people tend to have either have like neurologic deficits or they may have like a post-itopsyroid, right?

And after they have the arrhythmia, they may be like confused for, I mean, after they have the syncopylepsote, they may be confused for a while. So that's like again, something I want to keep in mind with that. So I think I'm going to go ahead and stop here for the day. Thank you for listening. Apologies for this podcast going really long, but I want to make, I mean, there's going to be more in the series for emergency medicine. So as I do at the end of every podcast, I do offer one or one tutoring for many exams. Step one, step two C case, step two CS, step three pre clinical medical exams, 30 year shelf exams, including the image shelf. Also offer tutoring if you're a medicine resident for like the medicine training exam or the ABI and board exam. And if you're a college student that needs to be doing for like general chemistry, organic chemistry, physics, biochemistry, histology, physiology, I tutor for all those things. And then also do this thing I call longitudinal tutoring where if you're a first second or 30 medical student, I tutor you for either your block exam, so your shelf exams. And then at the same time, I tutor you for your upcoming USMLE exam. Again, I've done this with people and they found it to be very helpful and they've been actually very successful with it. And then also offer this thing that I call a USMLE booster course. It's 10 hours for step two C case, step three, and it's 20 hours for step one.

And basically it's something that's good for a person at the end of the day, they get it period or feel like their knowledge base is good. And you just want to use like a Q&A format to put everything together, like the most notes, the high yields for the test, for those respective exams. Reach out to me and I'll give you some more details about the course. But again, people have done this with the foundation to be very helpful for the exams. So I do issue, and oh, one last thing, if you're a medicine applying to residency, right, so like an ERS application or like a college student applying to a med school, so an Amcass application, I'd offer like one or one advice in slash, I guess coaching, right, so like rec letters, personal statements, mocking reviews, editing applications, all for all those services. Again, I've worked with tons of people and vast majority of people have worked with have much of their first choices. So have a wonderful rest of your day. I hope you enjoyed this podcast. I will see you in the next episode. God bless you. Thank you.

Stasis, hypercoagulability, and endothelial dysfunction.

Antithrombin III.

Sinus tachycardia (or sinus tach). A new right bundle branch block can also occur.

Non-contrast head CT. Contrast agents can obscure the visualization of hyperacute blood on CT.

< 48 hours: Synchronized cardioversion is appropriate. > 48 hours or unknown duration: Anticoagulation plus TEE/TTE to rule out clot, followed by cardioversion (or waiting 3 weeks).

Age (AS is older; HCM is younger), murmur location/radiation (AS heard best right sternal border, radiates to carotids; HCM heard best left lower sternal border, does not radiate).

Alpha-beta blockers (e.g., labetalol) or Phentolamine (a reversible alpha-1 antagonist).

Hypokalemia, hypocalcemia, or hypomagnesemia can prolong the QT interval. Magnesium sulfate is often required if hypomagnesemia is present.

Unilaterally decreased breath sounds and hyperresonance to percussion on the affected side. Treatment requires needle decompression followed by chest tube placement.

Administering a beta-blocker (e.g., labetalol) to reduce shear stress and blood pressure.

Orthodromic EVRT (narrow QRS) vs Anti-dromic EVRT (wide QRS). The wide complex suggests an anti-dromic pathway.

It helps stabilize the myocardium and can improve cardiac function by correcting associated hypocalcemia/hypokalemia.

Prothrombin Complex Concentrate (PCC or 4-factor PCC) for Warfarin; Andexanet alfa for Factor Xa inhibitors.

Alpha-beta blockers (e.g., labetalol) or Phentolamine (a reversible alpha-1 antagonist).

Hypokalemia, hypocalcemia, or hypomagnesemia can prolong the QT interval. Magnesium sulfate is often required if hypomagnesemia is present.

Unilaterally decreased breath sounds and hyperresonance to percussion on the affected side. Treatment requires needle decompression followed by chest tube placement.

Administering a beta-blocker (e.g., labetalol) to reduce shear stress and blood pressure.

Orthodromic EVRT (narrow QRS) vs Anti-dromic EVRT (wide QRS). The wide complex suggests an anti-dromic pathway.

It helps stabilize the myocardium and can improve cardiac function by correcting associated hypocalcemia/hypokalemia.

Prothrombin Complex Concentrate (PCC or 4-factor PCC) for Warfarin; Andexanet alfa for Factor Xa inhibitors.