High Yield Cardiology for Shelf Exam & Step 1 + Step 2 CK

Getting 80% on cardio is the gateway to a 260 on step two. It's also where most students plateau. Not because cardio is impossible, but because they're memorizing instead of thinking in blood flow. Every cardio question asks the same thing. Is blood getting where it needs to go?

Today, I'm revealing exclusive footage from our paid course. [music] Real teaching showing how to think through cardio like a 260 plus score. These patterns don't just boost cardio, they improve every vignette where hemodynamics revitals matter.

Last time we talked about making key concepts automatic. This is all in the service of on your test. The more that you can automatically know what every sentence means, the better you will do. I can virtually guarantee that. You read a sentence and you just know what it means, your test is going to go much more smoothly. I don't think that's I don't think that's a controversial thing to say. The hard thing is to figure out how do we do that?

Last time we talked about making key concepts automatic. This idea that you want to be able to see someone that's hypotensive and tacocartic and immediately be thinking about the bar receptor reflex. That's the first step. The second step though is to actually be able to put it together in an actual vignette and to drill these vignettes. What I've done here is I've created vignettes where we're going to a drill those automatic key concepts that you they just become something that you reflexively see when you're doing questions, but b I'm going to give you cards and that you can then turn into vignettes that you can drill these concepts and continue to reinforce the connections.

We're going to start with Hadra. The way that this is going to work, actually all of you guys are going to read this vignette and I'm going to call in Hadra because I want her to tell me what the path of physiological chronology is. But for all of these, I want you all to do it and I will choose one of you to go over the path of physiological.

So, a lot of people have been asking about additional practice for these concepts and other some of the more common concepts on the OSM less. We actually have a free 14-day video series that breaks down even more some of these topics. And we include some test taking strategies that we use to help some students who have gone literally from failing to, you know, 250s or even 260 plus on step one or even step two. So be sure to click in the link in the description below if you want to check it out.

Everyone read this. You don't have to read it out loud, but I want you to tell me what's the pathophysiologic chronology. walk through the pathophysiological pinology and I want you to specifically tell me what's the mechanism for developing type two diabetes and why is he orthostatic.

>> The mechanism for type 2 diabetes is uh malitis is that there is insulin resistance and that insulin resistance results in increased in insulin production and increased amin production and that amin production whenever there is increased production of proteins in our body there's always going to be increased phase production of misfolded proteins in our body and some of those misfolded proteins can be ubiquitin ubiquinated and others are not degraded by ubiquitination and those proteins aggregate and one of those proteins aggregating and through hydrophobic interactions is amoid. When we have type 2 diabetes malitis, we have a lot of insulin production because the cells are essentially resistant to proteins and we have a lot of production of listed proteins and we have a lot of production of myoid and that amoid aggregates because of hydrophobic interaction into beta pleated sheets and then that actually deposits in the pancreas and that results in dysfunction of the pancreas. Over time, the pancreatic beta cells become dysfunctional and there is decreased even more decreased production of insulin which really results in a relative insulin deficiency.

>> That was really good. I am really impressed. I don't even think I need to teach that what I was planning on teaching. That was really good. Great. So why is your orthostatic walk me through the path of physiology? What how do you connect all this?

>> It's this that obviously diabetes malitis equals hypoglycemia. The blood has a lot of blood glucose inside it and because of that blood glucose there is non-enzyatic glycoilation of the arteries and because of that I think there is basically less blood flow when the normal response of when a person gets up is that initially when a person gets up there is pooling of blood in their veins and because of that there is decreased preload in the heart because of which there is decreed decrease stroke volume. When the stroke volume decreases, there's degrees cardic output. And when the cardic output decreases, there's degrees MAP. When the map decreases, there's a decreased stretch on the barrel receptor reflex. And there's a decreased stretch on the bar receptor on the barrel receptor.

>> Okay. So, that's good. You're walking through the normal healthy mechanism. What I'm asking is why normal. But in diabetes malitis, the there's basically the nerves are basically weak because the blood can go to the nerves and it's not providing the nutrients. the nerves are not functioning at their best. The when we get laded lightadedness and we have enough activation and we have ways of constriction that is basically being prevented and the blood is not able to go to the person's brain and that's why they're laded.

>> Okay. How did that feel?

>> Yeah, that feel felt okay.

>> Yeah, it was not bad. It was a little it was a little it felt a little meandering at the end. In a test, it would be a little hard because I I feel like the risk that you run with going into so much detail on the normal mechanism is that it's going to take too much time. Granted, this is a artificial scenario, but in an actual test, that would probably be a little like going over the normal barrel receptor reflex is probably too much, but otherwise, that was actually quite good.

What I'm going to show you is this is the level at which in an actual timed test, this is probably the level at which I would think about it. You don't have to go into details about how do you get diabetes. I I asked you to go through the details of why you get diabetes. People Someone was asking what do you do in an actual test? What should you actually do in a test scenario? You can't go through oh thinking about amlanin every time diabetes. You can't be thinking of amlin production because of insulin resistance that's just too much. You just say diabetes in a test setting. This is about the level at which I would think about it. There's some sort of diabetic neuropathy of the autonomic nervous system. You get verosceptor reflex dysfunction and that's why you're getting hypotensive and orthostatic. That's it.

However, when you're not doing this in a test, in a non-EST scenario, I would want you to go through as much detail as possible. And the reason is because the more detail you can give, the more that this will become natural in your test and the more that you'll be able to review it.

Let's talk about some of this. This is the mechanism of type 2 diabetes, which Hadra just explained. There's insulin resistance that leads to overprouction of insulin. at insulin overprouction also amaline is released along with insulin which leads ultimately to amaloid production. The amaloid leads to beta eyelet cell dysfunction and now you have a decrease in insulin supply to go along with increase in demand that diabetes technically it just means diabetes technically just means you have high blood sugar.

This we took I took directly from the lecture endocrinology the diabetes valadis and thyroid lecture briefly to walk through the mechanism of getting amaloid. You have a protein some proteins there's a non-greable part and if there's misfolding you'll get ubiquitination of it and if you're stuff one they love ubiquitin love the proteosome it's it seems to always be the answer when that's one of the answer choices you can degrade the degradable part but the the non-degradable part the hydrophobic part you can't degrade when you're making more and more proteins in the case of having insulin resistance and having increase in insulin you will then accumulate these non-degradable parts where the non-degradable parts will accumulate and eventually Eventually what happens is that they polymerize. They now join together to form the superructure of the beta sheet which we call amaloid.

Great. What what's the significance of the fact that he had 20 years of diabetes and that is poorly controlled? Why did I say that in the vignette? Why do they say that in other vignettes? Bjo, what do you think?

>> You wanted to draw attention to the fact that poorly controlled diabetes can lead to the renal Did the guy have renal failure? I forget.

>> He had renal failure. Yeah. Why did I say an adrenal failure? Why was that important? Why would you have to include that or why would I include that in the vignette?

>> Play directly into the orthostasis, right? It didn't necessarily play directly into the vignette, but it was still important. It's because the point is that a lot of these late manifestations happen similar in combinantly, right? Kidney disease often times happens with like retinopathy, but if you're going to get peripheral neuropathy, it's also reasonable to think that you could you are at risk of having autonomic neuropathy. I was building towards this idea that he had autonomic neuropathy. Tingling in hands and feet may seem like a distractor, but really what it's telling you is just the overall state of his disease. If someone says, "Oh, this is someone who's got insulin dependent diabetes, insulin dependent type two diabetes, it just means it's really bad diabetes." Someone comes in with diabetes and they've got kidney failure, it just means that they have really bad diabetes and they are at risk of having these other complications.

Great. We talked about this last time. I don't want to I don't want to spend too much time talking about this, but the normal barrel receptor reflex was what Hajger was going through. If I was going to make a tattoo, it would say map is cardiac output time TPR equals heart rate time stroke volume* CPR and then treated load after load and contractility. Sometimes you can think about rhythm. And this is the mechanism. But hopefully you guys have every single time that you've been standing up, you have been thinking about the bar receptor reflex that you can make this an automatic key concept because I guarantee if you're not drilling this into your head now on the day of your task, it's not going to come to mind naturally. You're going to be time pressured. You're going to be stressed. This is the last thing you're going to be thinking of. The time to practice this is when you're not in a timed setting. when you're exercising, when you get up, when you stand up from a seated position, when you get up from bed, whatever it is, but you want to make this, you want to learn how to make this automatic because the more that you can make knowing the right answer or knowing what every sentence means automatic on your test, the happier you will be with your score. I can guarantee that.

We talked about heart rate last time. I don't want to spend too much time talking about this, but the reason that M1 causes an increase in heart rate is is because of the phase 4 deolarization. Danielle, what's the equations for cerebral profusion?

>> Cerebral profusion pressure equals mean arterial pressure minus intraraanial pressure.

>> Great. And how generally can you think about when I say profusion pressure? What's a good way of thinking about that?

>> Resistance is that like in the

>> Oh, no. Like in general, if I think of blank profusion pressure, what's the generic equation for profusion pressure? That's a bad question. Basically, what's the pressure of the system you're coming from? Right? In this case, it's the arterial system.

>> Minus the pressure of the system you're going to, right? In this case, it's the brain inside. In general, cuz a lot of people will just memorize this. I'm saying you don't have to memorize this. You can actually make sense of it. The profusion pressure on your brain is what's the pressure of the blood going to your brain minus the pressure inside your brain. Pretty much it. The other famous profusion pressure equation, which we'll talk about eventually, is coronary profusion pressure, which is usually written as a aortic diastolic blood pressure minus left ventricular diastolic pressure. Your coronary is fill during diastillate usually at least the leftsided ones and they're going to the heart where ultimately right the the blood is going to end up in the left left ventricle. You're looking at the diastolic blood pressure but it's coming from the aorta it's ending up in the heart. The profusion pressure is just pressure is coming from minus pressure is going to tell me why is he lightheaded using the cerebral profusion pressure abrasion. Why does he get light? Why does he get lightheaded when he stands up? He gets headed because the MAP decreases and the intracraanial pressure is high. Basically the cerebral profusion pressure decreases.

>> Yeah. I don't even know that I would say the ICP is high. The ICP is probably normal.

>> But the point is that the ICP isn't pain. If this decreases relative to this then yeah your cerebral profusion pressure is going to go down.

>> Yeah. Cool. Great. When someone might day when someone presents with lightheadedness or syncopy when they're standing, what's the general mechanism behind lightheadedness and could this be a stroke? Puja, can you tell us what's the general mechanism behind lightheadedness and or syncopy?

>> Oh boy.

>> Remember you were saying before you were like, yeah, you know, someone comes in unconscious. Yeah, I don't know what that means. What you're supposed to know what that means? Yeah. Yeah, it's pretty much Yeah, the general unconsciousness is a little different from Singap, which I'll explain. But yeah, you should you it should be automatic. I've bolded all the questions that I want you guys to make into cards. We'll give you the cards.

>> The whole chronology.

>> Well, so yeah, there's going to be two kinds of cards. There's going to be the ones that I bolded. This is this is an automatic key concept. This is a concept that I want you to make automatic. When you see someone that's lightheaded, you want to think hypotension. In a general in a very general sense, if someone's intermittently lightheaded or if they're syncable, maybe not 100% of the time, but I'd say 90 to 95% of the time, particularly in questions, particularly for syncopy, if it's truly presinopy or syncopy, virtually 100% of the time it's going to be I know there's going to be haters out there who are going to say actually technically you can be syncable from

>> Yes, technically it's true. But that's really uncommon. That's hot air balloonists. Yeah. But in general, in general, you should think hypotension when someone's lightheaded. I bolded this because I want you to make this an automatic key concept. In other words, I want you to be thinking about this when you see. Oh, I know they're hypotensive. It should just come to your mind. That's what I want. Fuja, does that make sense?

>> Yes.

>> Perfect. I'm just spelling it out for you. This is this is what I wish that people told me. Could Fuji, can you tell me? Could this be a stroke?

>> Could uh

>> possess with lightheadedness? What's the likelihood that this is a stroke if they're lightheaded? I think it could be.

>> H no, almost never a stroke. That I would argue is probably a cognitive error. And I think if I had to reconstruct it, I think that the way that it happens is that people think of lightheadedness as a brain thing. Then your system one just goes, you know, oh, brain pathology. What's a brain pathology? Oh yeah, stroke. Strokes a brain pathology. Here's a case where sometimes you do get a a patient that comes in and said the scenario will say, you know, the patient comes in with the lightheadedness and the syncopy blah blah blah, but then the vignettes talking about the symptoms of a stroke.

>> I've yet to see a vignette like that. Please bring that next time.

>> I'm not saying that I've seen it. What again I struggle with is when I see something like this and I associate it with the hypertension, am I going to lock myself in? That's what I kind of get scared of.

>> Oh, great. Yeah, exactly. This is why you have a system too, right? I'm not saying that if you say hypotension for syncopy, you're going to be right 100% of the time. There's maybe a couple percent or 5% of the time where it's not going to be that. In other words, what was the trick of using your system too? What did we call that last time? Trust but verify. In other words, say, "Oh, yeah, totally. I think that they are most likely hypertensive." But then verify, do they have other symptoms of hypertension? When you look at the blood pressure, is it low? You still have to check it. I'm not saying I'm not saying that your test is just going to be like you're not thinking at all and everything is going to be automatic. No. Absolutely not.

>> Yeah. Roaching questions with system one and I'm doubting my questions with system one as well. Like system two is like non-existent for me.

>> Exactly. What I'm trying to do with this is I want to strengthen your system one. I want to strengthen your system one. Your system one is giving you the right answer more frequently. However, we also need to strengthen your system too that it can take that answer and actually evaluate it and say, "Oh, does this make sense or not?" But I think the problem is that a lot of you guys you your thinking is more this oh lightheaded. Oh yeah, lightheaded. Oh, it's brain. Oh, brain problem. What's a brain problem? Oh yeah, I think of stroke. No, that will lead you down the wrong path virtually 100% of the time. I've bolded this because I want to make this an automatic concept. When you see syncopy or preyncopy, you should be thinking hypertension because in virtually 100% of I'd say 95% of the time, just read just fair. You should be thinking this will guide you in the right way. M said in her text to me, she said, I think it's good to think of stroke as focal neurological deficit, which is totally true. Trust but verify. What's the classic presentation of stroke? Well, the classic presentation of stroke is a focal sudden neurologic deficit. You suddenly have trouble speaking. You can't move your leg or something. That's the classic presentation.

Great. Next, let us Danielle, I want you to walk us through maybe just the the overall big picture in terms of the pathophysiological chronology. Basically this elderly man was born healthy. Some probably some poor life choice choices poor diet maybe decreased exercise led him to develop diabetes type two well to have insulin resistance increased insulin resistance which caused an increased production of insulin to compensate for the resistance and then this caused an increase in analine. Do you want me to go through everything?

>> But that's I think that's big picture. That's actually yeah this is a delicate thing. I guess I would say when you're doing it on your own, I would want you to go through everything. For the interest of time to make sure that we can cover enough vignette to reread a little bit.

>> Since we already discussed the whole process type occurs, I'll just go over that. Skip that. Basically, his long-standing type diabetes led him to have these kind of endstage factors such as renal failure and the autonomic dysfunction. And the autonomic dysfunction caused him to have a receptor reflex dysfunction. So he's not able to the job, but he stands up.

>> He pent out. I think what you're saying is that he can't augment his cardiac output, which means his MAP doesn't increase. And because his map doesn't increase, his cerebral profusion pressure falls. I think that's what you're getting at.

What I've included here, the bolded questions are the key concepts you want to make automatic. You see someone that's pre-syncable, you should think hypertension. You should not think stroke. Presinopy or syncopy. virtually I don't know 100% of the cases at least for vignettes and even in the real world is almost always because of hypertension basic syncopy hypertension cardiac synopy any of the causes a stenosis hypertention non-custain vag hypertension all of them they're all hypertension in the test this is about the level of detail in a question that would be one card or the bolded things we will include that the other kinds of cards that I'm going to include is this one the front of the card would be this vignette and the back of the card would be this and when you're reviewing it should Should you do the summary or should you use the detailed one? Which do you think is better? Dales, what do you think? If I'm reviewing this and I'm not in a time setting, which do you think I should go through?

>> Detailed.

>> Absolutely. Yeah. And a fair question is, Alec, isn't this just a god- aful waste of time? Why would I do that? Why would I? Seriously?

>> Muscle memory for your brain.

>> Yeah. Exactly. Cuz all of this stuff, I guarantee certainly for step one, but even for most of this, for step two, are things that are going to be on your test. Yeah. It's going to take you a little bit longer for sure, but then you're look at all the things that you're reviewing. It's crazy. There's all this stuff. And the other benefit is that yeah, you're essentially creating muscle memory that the next time you see someone who has some form of autonomic dysfunction and they've like got diabetes and kidney failure, you're like, "Oh, I like totally makes sense cuz maybe next time it's not going to be that they have maybe it's not that they're going to have autonomic problems of sympathetic system in terms of blood pressure, but maybe it's that they're going to have diarrhea. there just there's just no clear reason why and oh they've got tingling hands and feet and kidney failure. It stands to reason that they might have autonomic dysfunction as well. Maybe they've just got a problem with their sympathetic system into their GI tract. Their parasympathetic system is overactive and they're getting diarrhea because of that. You want to train yourself to be able to make these connections on the spot. And if you wait until your test until you try to make them, you'll never make them. It's not going to happen cuz it just becomes that much harder on the day of your test to do this in a timed setting when you're stressed. Just not going to happen.

That was great. I'm going to ask all of you guys to read this quietly to yourself and then I'm going to have Derelis walk us through what the pathophysiological chronology of this one is. This one's pretty tough.

>> Born healthy male. I guess you the whole he's probably had some unhealthy lifestyle changes or habits, sorry, that like with the smoking and um now at elderly age is actually I don't know where to go to here. I know what

>> It's hard. This one's hard.

>> But I don't know how to get to the from this.

>> Yeah, I know. Okay. Can someone else Does someone else want to give it a shot? This is one of the harder ones. But again, this is totally fair game for your test. You want to give it a shot?

>> I just man working neck pain. There can be a lot of things but he has lightheadedness. One month history of upper mid throatic back pain. I think of something aortic maybe already.

>> Okay. So stop. Let me point something out to you guys. Your system one is unaware of time. Let me repeat this. In other words, your system one doesn't really know what happened first, what happened second, happened third. It just it doesn't. It's just completely oblivious to time. You have to if you're going to think about the actual chronology, you actually have to arrange the vignette in chronological order. I want you to actually arrange this in chronological order. What happened first and then what happened second just in terms of the the elements of the vignette. You don't have to tell me why it happened but just which

>> He was a healthy man and then he started smoking which is a risk factor for to develop um 20 years ago. That's a long time and that increases your risk of a lot of but he has a CT that demonstrate that he has a mass [clears throat] lately. He started smoking this increas who developed pancreatic cancer and pancreatic cancer develop how do I say this hyperongability also he doesn't know it's a sexist young man who start smoking develop pancreatic cancer to develop triangle he has a DBT and then he developed PE and the D pain is the DDT embed the DDT progressed to a PE pulmonary embolism that gave him lightheadedness.

Perfect. That was fantastic. That was great. Do you see how different it is though for those of you that maybe weren't able to make all those connections? My guess is as you were going, it was hard to tell cuz you were going down the wrong path of I don't think I was being very clear in what I was what I wanted. But the key is that you often times what you'll see this is exactly how this is exactly how they're going to give it to you in the vignette because this is the chief complaint. He comes in. They might not even give it to you like this. They might even say a six, seveny old guy comes in with a two-day history of lightheadedness and that's it because that's a chief complaint. And then they might tell you for a week he's had worsening left leg pain and then they'll say he's had a month of worsening upper thoracic pain cuz this is HPI business now. And then they're going to tell you about their smoking history, this 20 pack of your history way down at the bottom because that's where the social history goes. What I see a lot of you guys do with your pathophysiological chronologies is they're not actual chronologies. You're just going sentence by sentence, which is essentially what you were doing, I think, right? That's not what I want.

>> I want to ask you a question while I practicate. What? Why do I

>> When you do your test, do this. You should also arrange them chronologically in your mind because Yes, it's hard. It's harder. Yeah. Cuz if you don't if you don't arrange it in your mind, your system one's not going to do it right. You're not naturally going to do this. No matter how many times you do questions, you're not naturally going to make those connections. I would argue that if I when I present it like this, I guess a lot of you guys were like, "Oh my god, I have zero idea what's going on." But if I were to present it like this in the actual chronology in which it happened, I didn't even tell you that he had pancreatic cancer. I didn't tell you any of the background of any of these things, right? I just now have just arranged them in order of the actual timing of them. It became much more clear what was going on when you arranged it in that order. Yeah, I think I as I finish because when I read the head start taking I finish before they download but I do it really quick. That's maybe why I think I might not do it but yeah cuz it's a secondary like I don't know how to explain it. Puja, what are your thoughts? If you puja, if you saw it this way versus if you saw it this way, which is easier for you, puja, what do you think?

>> I think the bottom it's it's a little bit more clear why one 20 20 pack year smoking history is is the reason that he's got the pancreatic mass, is the reason he's got the weight loss, is the reason he's got the upper back pain. I I would think that this would be the easier one.

>> Totally. Yeah. Are you naturally going to do this though?

>> I'm trying.

>> Yeah. Yeah, I guess my point is that your system one will not do this. Just reading a vignette, this is not going to this will not become immediately obvious to you. Instead, when I read a vignette, whenever I see like days, weeks, I'm actually I actually take an extra second and actually think this happened first. I would read this and I would say, okay, he's got leg pain and then lightheadedness. Oh, actually before that he's got back pain, then leg pain, then lightheadedness. They like, oh, actually, no, it's smoking then pain or sorry, smoking, back pain and mass, leg pain and lightheadedness. I I actually think and and as I'm going I'm trying to put the put those pieces together.

>> Well, if you think about that then they should put the social history as the first thing in the min.

>> Not necessarily because the social history isn't always one of the one of the key things. The reason why that the reason why the H&MP is laid out the way that it is because then you know what to expect, what to listen to in every step. You could argue maybe that you could put it in the HPI, but they will not always do that for you. They will not both clinically and on your test. But I want you guys to see that it's much easier to see the connections if you actually arrange it in chronological order. Which is why I keep telling you guys you have to make actual chronologies. It's not sentence by sentence in terms of that's not what a pathophysi chronology is. You have to read it sentence by sentence. But what you're trying to build in your head is this happened first, this happened second, this happened third, this happened fourth. Now I would argue that this is the exact same process that you should be doing guay because if you just think about it in the order that the patient tells it to you it is much much harder for you to make sense of it than if you're saying take me back from the beginning when it's the first time that you were well actually think okay try and make it in chronological order. So this would be the summary as you're going through the test. This is about the detail that I would want you to go through it in a time setting. Smoking leads to cancer. Pancreatic cancer a lot of things but in this case it was the major risk factor for getting pancreatic cancer and then smoking and pancreatic cancer are two right so what you guys didn't talk about was the fact that it's not just pancreatic cancer he was smoking too. That's two out of three of your cause triad that leads to DBT leadup hyperusion. Very triads. What are the three elements in var triad? hyperraulability, venous stasis and endothelial damage. Danielle, what does Veros try predispose you to and how many are necessary in order to be predisposed?

>> Yes, it'll predispose you to getting two of the factors.

>> Yeah, it's basically Venus clots, Venus clots, DBT. Yeah, I typically need two out of the three. Great. As Danielle, which of the which elements of your cause does this patient have? So our patient has the pancreatic cancer causing the hypercoagility and then the long history of smoking which is going to cause endothelial damage.

>> Perfect. Smoking is endthelial damage. Pancreatic cancer is hyperquagility. Great. Durales, what is it generally? What does it mean when they say that there's a provoked or an unprovoked DBT? What is that refer?

>> I'm not sure, but I'm assuming it has to do with if you're causing it due to something that you're doing, lifestyle changes, problems, or versus no.

>> Yeah, provoked basically means that there's a very clear precipitant very obvious. Unprovoked is where it's not immediately clear what is like causing it and hajra which would be more concerning the provoked or the unprovoked and why.

>> I think the unprovoked is more concerning because in provoked you have a clear precipitant that you can take care of for example in our case smoking we could tell the patient to stop quit smoking for unprovoked I think we're more concerned as to now we have to dig in by.

>> Like would you be concerned about.

>> Yeah, usually unprovoked are much more concern Often times the thing that you worry about is genetics or some sort of undiscovered factor. For this guy, they didn't necessarily know that he had cancer. Presumably he didn't know he had cancer when he presented to the emergency department. It's a double whammy. Oh, by the way, you have DVTP. Oh, and by the way, you have pancreatic cancer. But the pancreatic cancer was that unclear precipitant. It was the one that you didn't know about, but that's what you that's what you really worry about. Actually happened to one of the one of the one of the professors at Stanford. He just just developed a DBT. And it turns out, right, it was an unprovoked DBT. used playing tennis and it turns out that he has factory 5 lighten. Wow, this stuff is real. That's crazy. But yeah, that was great.

Now I want to talk about resistors. Let's talk about resistors in series versus in parallel. Louise, you can think about blood vessels resistors in series of parallel. This is series. It's where one resistor is after the other after another. I have no choice. I've got to go if I want to go from this point to this point, I've got to go through all the resistors. It's parallel. I've got a choice. Basically, technically, I'm not choosing, but there are multiple paths through the different resistors that I can take. These are resistors in parallel. Louise, can you tell us what is what's the total resistance equal to if there are resistors that are in series?

>> Would it be the sum of the four resistors?

>> Yeah, it is. Yeah. Total resistance is just you just add them up. It's the easiest one. If I remove a resistor in series, what's the effect, Louise, on the total resistance? Increase it or decrease it?

>> It will decrease it.

>> Yeah. Great. Right. Because it's just a story. Take this out. It's going to decrease it. Great. Puja. For resistors in parallel, what's the total resistance?

>> 1 over R1 1 + R2

>> Equals what?

>> Equals I don't know.

>> Does it equal the total resistance? Yeah. What was it equal to? Yeah, everyone remembers this side of the equation. No one remembers this side of the equation. It's actually 1 / R total. And I've made this mistake multiple times. I used to think that it was R total equals 1 / R1. Right? That's why I asked you cuz I've definitely made that mistake before. But no, it's actually 1 / R total equals 1 / R1 + 1 / R2 + 1 / R3 because that's important because PUA what is the effect of removing a resistor in parallel? What effect does it increase the total resistance or does it decrease the total resistance.

>> In parallel? I think it increases.

>> Yeah, it increases it. Great. Let's prove it. Let's prove it to ourselves. Let's assume let's just make the math easy. We've got three resistors. They all have the same resistance and that resistance is two. I mean use the units just to make it really easy. One over R total. This is for parallel. This is in parallel. It's gonna be 1 and 12 plus 1/2 one. If we rearrange the terms we'll find that R total, right, is 2/3. Agree?

>> Now let's say that we remove one of the resistors. Now we've taken out R3. Let's say now it's just two resistors. 1 over R total equals 1/2 + 1/2. But what do you know? the total resistance is now it's one of those weird because you haven't really thought about reciprocals for a really long time but do the math prove to yourself that removing a resistor in parallel will increase the total resistance great in other words if I have a PE what's it going to do to my pulmonary resistance Danielle would I consider my left and right pulmonary arteries to be resistors in series or in parallel.

>> Resistors in parallel.

>> Great. And if I had a pulmonary embolism to my right pulmonary artery Danielle, what would be the effect on my total pulmonary arterial resistance If I were to think of them as resistors, this is a key concept. I've bolded it.

>> Yeah. If we're thinking about our pulinary arteries in parallel, then if you were to remove or block our right artery, then you removing one of those resistors parallel. Then your total of resistance would increase.

>> Perfect. Yeah. Exactly. Excellent. Excellent. It's durales. How could a PE lead to hypertension? That's a key concept. it in since the PE that it's in parallel and you're taking away one of the resistance on one side. It's causing an increase in total resistance though. Then that increase in total resistance is going to lead to a decrease in for forward flow. That's going to cause you to have less blood pumping forward including to your left side of your heart. Meaning less stroke volume, less cardiac output.

>> Skipping a step. What why is there less volume? Think of your tattoo. You're going to make a tattoo.

>> Okay. So, you anything going anything that's in front or I guess after the pulmonary embolism is going to have an decrease in preload. You have an increase in preload. It's going to cause a increase in volume to your left sorry decrease in volume to your left atrium which causes a decrease in volume to your left ventricle and that's how you get the decrease in stroke volume. Sorry, this might be a technicality, but really I I guess the way that I I would think about it and I think the way they to test this would be I I would say there's decrease in volume to the left atrium, decrease in volume to the left ventricle. That's great. I would say that that means that there's a decrease in preload because I think what you were saying maybe I'm suggested was that a decrease in preload leads to a decrease in volume. It's not usually how it's described physiologically. Usually you think of it from the context of the left ventricle itself. There's a left there's a decrease in left ventricular volume which means that there's a decrease.

>> Okay, that's true. Left. Yeah. Left ventricular and diastolic volume.

>> Yeah. Exactly. Yeah. That's what you think of as preload. Not that preload leads to a decrease in your left ventricular. Yeah. Decrease in stroke volume.

>> Decrease in stroke volume leads to decrease in cardiac output which leads to a decrease in your MAP.

>> Great.

>> Decrease in your mean arterial pressure means less blood in your arterial system which means less blood to your brain. Remember, you want the key is that you want to use these concepts that we just talked about. If you don't use them now, you're not going to use them on your test. It's not going to be automatic on your test.

>> I don't know what's the term for that. Maybe I wasn't here.

>> Profusion pressure. Oh, you might not have been here. Yeah. Cereal profusion pressure.

>> Oh, so is that the cerebral the cerebral perusion pressure equals.

>> Matt minus ICP?

>> Because your map is decreased.

>> Yeah, your profusion pressure is decreased. Yeah, exactly. In other words, yeah, larger pees are more likely to give you dynamag effects to drop your map. And it's that decrease in map, which is ultimately decreasing your cerebral perusion pressure and that's where you're headed.

Great. Now, I want you to read this exact same vignette. Now that you've learned those key concepts, now that we've drilled those key concepts, right now I want you to read the vignette and I want you to tell me because my hope is that now you're able to make the connections automatically much more. In order to further that, I want you to make this into a card and actually think why does he get a DVT? Why is he lightheaded? Why is it tech cardic? Hadra, can you tell us what was the can you give us the high level? Don't go into really excruciating detail, but just the highle summary and then we can save the excruciating detail for when you guys go over this on your own.

>> Yeah, the pathophysiology chronology will be such that this 67 year old has been smoking for the last 20 years and that's a risk factor for pancreatic cancer and both of those are risk factors. They kind of make their vowels tri. There is endothelial damage and there is hypercarobility which causes which results in DVT and the DVT from there and ambulance which causes PE and that PE actually increases resistance to blood flow and there's decreased cardiac output which decreases the MAP and which decreases the cerebral profusion pressure and when the cereal profusion pressure decreases there's there's and the decrease in MAP also results in activation of the sympathetic outflow because of the barrier receptor reflex.

>> Perfect. Honestly, that's okay. Like that level of detail cuz again, I want to train you in two ways. I want to show you when you're going through this in a time setting, you have to know which details to cut and which to not, right? What are the big picture elements that you need to still have a complete story, reasonably complete story versus what are you going to do when it's on your own and you want to go over these details because these are details that could certainly be tested in other for in a test. This is it. I'd say smoking pancreatic cancer at least a DVT to PE low MAP street done in a test this is about as much detail as I would give but outside of a test this is the level of detail that I would try to do I would even get down to the point of saying yeah you get a PE the PE leads to you're removing the resistor in parallel because that's a really important concept thinking of resistors in parallel versus in series and then yeah go through all of it cool I think we might even have time for one more Louise I'm going to have all of you guys read this but And I'm going to have Luis go over the pathophysiologology. Luis, would you like to give us the path of physiolog?

>> A 36 year old woman who was born healthy. She they they don't specify for how long she has been smoking or using the oral contraceptives, but but let's say that she was born healthy. When she gets to a reproductive age and starts having sexual activity, she starts taking the oral contraceptives and she probably starts smoking as well. She probably develops a DV or.

>> She smokes some then she takes a flight.

>> Yeah. Yeah, that that sentence in the chronologic sequence. She was a 36 year old woman. She was born healthy. She Yeah. She's most uses OCP and then she takes a long flight from South Korea to LA. From sitting down for quite a long time, she develops DBTs. During the flight, she gets to LA and all of a sudden she starts complaining. She probably develops DVTs and then those clots.

>> I'm just happy there. That was that was not bad. What I want to point out is that this is probably how a lot of vignettes feel to a lot of you guys. you're reading it and honestly you probably don't even give it as much effort as Luis just gave. You probably just oh I don't know you just like you choose an answer that's usually about the level that I think most people understand most vignettes and there are two choices that you have when you see a vignette this first is to just say look at the answer read the educational objective and say oh yeah I get it oh yeah I'll get it next time. The second thing, which is what I want you guys to do, is to actually go through and make sense of the path of physiologic anology. I actually walk you through step by step when you have the the answer in front of you, cuz what you'll find, and the reason why I'm showing you, there's a very I'm very intentionally showing you the vignette at the beginning and at the end of each of these is because I want to show you in the beginning you're often not sure what's going on, but then afterwards, you're like, how could I not how could someone not see this? And Louise, this is what I want to prove to you. I want to prove to you that you're going to you're going to be like, "Oh, this is I totally got this. Makes total sense." And if you make a card on this and if you repeat this card using detailed pathophysiological knowledge every single time, when you see a question like this, and I guarantee you're going to see a question like this in your test, may not be this exact same scenario, but it'll be very similar. You'll know it. You'll know it because our goal is to make sure that you know automatically what every sentence is trying to tell you automatically on your test. This is the summary. Basically, she's, you know, our previous guy smoking and pancreatic cancer was two out of three if you're constrained. This lady's got three out of three smoking damage and she's got.

Hyperability and right, because of the OCPS and she's got venthesis. She's got a wamping DBT which becomes a large PE that leads to right-sided heart failure. And the fact that it's right-sided heart failure is critical because that's why she doesn't have crackles in her lungs, and that's leading to hypertension and ultimately against cerebral hyper.

Let's talk about heart failure. Puja, what does heart failure mean? This vague term.

Well, the heart's not able to pump blood adequately.

Adequately for what? Adequate for what?

For the body's needs. I know it's the one time that the medical student answers correct something really vague, but yeah, it's true for basically, it's if you can't meet the body's blood demand, right? Or and/or, right, you need excessive volume or pressure to do it adequately. The classic heart failure patient is they've got JVD up to their earlobe and they've got inspiratory crackles and all this stuff. They they have adequate flow to their, they may have adequate flow to their body, but they need so much volume to do it adequately that's still considered heart failure.

Let's talk about, oh yes, I did about the previous vignette when we were talking about the virtual house triad. When we're doing this on our own, should I think about what specifically in the blood is causing the hypercoagulability and it's allowing, I don't know if it was, if it was a timed setting, what do you think?

Oh, no.

No. I probably wouldn't do it. Yeah. But if it was not outside of a test, maybe not every time, but I would say, yeah, you should think about what's, what exactly is the mechanism in which OCPS cause hyperability? Sometimes I don't know. I don't really understand why cancer. I guess they say that there's mucin or something and it causes tissue factor. I don't know, substitute or blah, blah, blah, but yeah. Yeah. But in, in theory, yeah, you should try to walk through exactly one at least once. Yeah. Cuz the more that you walk through it, the easier, the more automatic you're going to make it on your test. That's the goal. As long as you remember that, I think it will guide it will make it a lot easier for you to think, oh, should I do this or not?

Luis, do you have a question?

Yes. I was going to ask something related to the the clinical vignette that I was reading. Usually the DVTs will be the cause for pulmonary, the DVTs they will go into the pulmonary artery causing a PE, but then I got a little confused because when I saw the the distension of the jugular veins, I didn't think of,

Let's talk about this. Let me ask a question. So what are the signs of right heart failure? It's like I planned there to ask that question. What are the signs of right heart failure?

Increased. Yeah. Jugular distension because of the overload in the superior vena cava and there from there up. Yeah. Basically, jugular vein distension.

What else?

This is good. I'm glad that, yeah, basically every, almost everything that you think of as signs of heart failure are basically signs of right heart failure. Hepato-splenomegaly, ascites, jugular distension, lower extremity edema. All of those things are essentially right heart failure. I would actually, we should even, let's make this, we should make that into that. That should be something that you should know. You should absolutely know that is a key concept that I want you to make automatic.

Puja, or I think, Luis, what's the mechanism of getting lower extremity edema and right heart failure?

Because you're, for whatever reason, your heart is not able to either push that fluid forward, it's causing a backflow of the fluid. There's an increase in pressure due to the backflow.

Yeah, it depends on the cause. In this case, there was an increase in afterload for the right heart, but not that's not always true.

But you can, when you say increase in a fluid, it could be be calling it the right heart and you would just have to say as opposed to just,

Yeah. Yes. Exactly. Yeah. You have to specify afterward for the right heart.

Anyways, there's a back or an accumulation of fluid that is causing your heart to fail in the sense of not letting it push forward. That's going to cause that to move from the ventricle, all that fluid from the ventricle up to the atrium and then go into your venous system. That tends to cause the JVD, the jugular venous distension, peripheral edema. We're focusing on one symptom or one sign.

In the end of the day, all that backflow is just going to cause an increase in your venous system to the point that your capillaries have a high hydrostatic pressure and cause that filtration.

Yeah, exactly. Yeah. You get venous congestion, particularly the dependent areas. Yeah. You have capillary, it's in the capillaries, not really the venous system. Your capillaries are the thinnest part. That's where the, if there's going to be fluid, fluid leak, it's going to be across the capillaries. There's more fluid leakage in the venous system. That's what gives you peripheral edema.

Great. Hadra, on a test or just in general, how do you differentiate between left and right heart failure? Because they always say, "Oh, the most common cause of right heart failure is such heart failure." How do you differentiate between that combined left and right heart failure versus just having isolated right heart failure?

In isolated, isolated right heart failure, a patient will present with edema, hepatomegaly, ascites, JVP raised, but clear lungs. The lungs will be clear. But in left heart failure, because of the backup of blood, the lungs will not be clear. Yes, we'll have pulmonary edema and pulmonary capillary wedge pressure will be raised.

Not.

Yeah, exactly. Usually what they'll say is they'll have inspiratory crackles. If they have a pulmonary artery catheter, which is pretty rare, but if they did, right. But both, both actual in real life, very few people get pulmonary artery catheters. But also, in in vignettes, they don't really have pressure or pulmonary artery catheters that often. Almost always, it's going to be the lungs. I can't tell you how many times I, I'll see your question, it's about heart failure, and you'll say, "Oh, yeah. Oh, yeah. There's, you'll see pulmonary edema or something." And they have no idea why they like, "Oh, clear lungs. Oh, that's because there's no pneumonia." Something that's completely unrelated. Oh, no. Anytime that they give you signs of heart failure, you want to listen to the lungs, both in real life and in your vignette, especially in the vignettes, because they can't just, they're not going to come out and just tell you, "Oh, it's just right heart failure." They have to give you a sign that it's just right heart failure to give you a sign. And really, they're really restricted in the signs they can give you because almost every sign of heart failure is really right-sided heart failure. If there's signs of right-sided heart failure without pulmonary edema, you should think isolated heart failure. Sometimes, literally, that is the only clue that they're going to give you, and that's how you're supposed to answer the question.

Now, I want to go back to Luis. Luis, I, it's always hard. It's always hard to be put on the spot. It's always hard to do these questions. But I want you to tell me now that you've, we've reviewed these key concepts. Right now, I want you to tell me, what's the pathophysiology here? 36-year-old woman is born healthy. She starts smoking and using oral contraceptives. She takes a very long flight from South Korea to LA where she where she develops DVTs in her lower extremities. Those those those DVTs will, those DVTs will go to the pulmonary artery as a pulmonary embolism that will decrease the preload.

Preload to,

That will decrease the preload, causing a decrease in the stroke volume, causing a decrease in the cardiac output, causing a decrease in MAP and causing decreased cerebral hypoperfusion.

That's awesome. It's really interesting. I heard you say, PE causing, there's a lot of hesitation, decrease in preload, but then did you guys hear it was like, decrease in stroke volume, decrease in cardiac output, decrease in MAP, super hyper. It was just like, that part was automatic. Did you feel that, Luis?

Yeah, basically what I was being practicing from the session from Tuesday about just making sense of something and then just try to be automatic. Once you get to the point where you understand the clinical vignette and then just from there on, just try to connect what variable affects the other variables from the, that's why I, yeah, just like you said, I hesitated a little bit, but from that PE for all the way to the decrease in the preload, the rest was basically automatic, decreasing the stroke volume, decreasing the cardiac output, and then decrease in MAP and then decrease cerebral brain.

But I think one of the things you said that struck me was you said you've been drilling it since Tuesday and now it's, it's just become automatic. My thought when I hear that is that the same thing is going to be true for this vignette. Yeah. The first time that you saw this, it was pretty slow. The second time you saw this, part of it was slow, but other parts of it were faster. I guarantee that if you were to continue to just repeat this vignette, right, in your cards, and just, just the repetition, the practice, and make the connections every single time, that the next time you see this or a similar vignette, because there'll be similar vignettes, it will just be much faster. Just the end of, end of this vignette was. What are your thoughts, please?

Yes, I couldn't agree more. I think that if you, yeah, if you just, the rest of the vignette cards, if you see the same card over and over, it doesn't matter if you don't, if you don't study the card for a month or a month and a half, whenever it's, whenever the card appears, then the, the basic or the idea of the card just comes up automatically because you've been seeing it for quite a few months now. It doesn't matter if you go a couple of weeks without seeing that same concept. Once you, one of the either the back or the front part of the card, you automatically can recall the clinical vignette related to the card you were seeing. Yeah, I think that repetition is the most effective way of just remembering stuff because if you read it one time, if they change that, the clinical vignette, and you haven't, if you haven't practiced the same, the key concepts of that card over and over, you might hesitate a little bit. And I just did. I knew that it had to do something with the DVTs and the PE. But then I, I hesitated which was the parameter that was affected in this case, the preload, but I hesitated because I wasn't sure at the beginning. But then the rest of it just came out automatically, and I think it's thanks to the, the session we had three days ago. Yeah, it's, it's because the other thing is, yeah, like you can see as you're doing the pathophysiological question, you can see where the rough spots are. It's just telling you, yeah, maybe that's the area that we want to focus on. That's the area. Cuz you guys were asking, what do you, where are you supposed to focus on? Focus on the parts that are slowest. It's, I know it's more pleasurable to do the ones that are faster, but it's, I think Puja was mentioning before, it's really pleasurable. It's hard, but you get this sense of satisfaction when you can see a vignette and you know exactly what every single sentence means. It's just, it just feels good. It just feels awesome. And I can tell you, it feels doubly awesome when that question is on your test, your actual exam. You're like, "Oh, yeah. I know what every single, literally, I know what every single sentence means. I know what, why they're trying to tell, why they're including it. You know, why there's a pertinent negative. I just, I, you just get it. You feel such a boss." Yeah. But it comes from, you want to continue to make these automatic.

I have a question. She obviously she had a PE and because of that it's causing the lightheadedness. But I'm assuming I guess PE is going to have different severities because I guess this wasn't that severe. She's having no hyperventilation or like,

Oh, just, just because they didn't, they don't say something doesn't mean it's not there. That's a,

But is that something like it might not,

Hyperventilate? Oh, yeah. If they told you her, her respiratory rate, it would be high.

Okay. So it's like a for sure thing like she actually is having a trouble breathing and all that. It's just not like, oh, I feel kind of, I might have a DVT. It's not anything like that.

In other words, the lack of a symptom doesn't necessarily mean that it's not there. This is one of my pet peeves about rule in, rule out is that often times you guys will say, "Oh, this is ruled out, ruled out because if it was this, and I would expect all of these symptoms." That's not necessarily true. First of all, clinically, that's not necessarily true. The diseases don't present in the classic way every time. There is such a thing as sensitivity and specificity of clinical signs and symptoms, and that doesn't even work in real life, but it certainly doesn't work in tests either. In this case, oh, the fact that she does, she's not hyperventilating means that it can't be a large PE. They didn't tell you that her respiratory was normal. You don't have a pertinent negative. Does that make sense?

Yeah, that makes complete sense. Yeah, that's good to know that it can't just rule it out because it's not there. But I guess for future knowledge, PEs generally like, it's not because like, oh, she has small,

Large PEs are the ones that are human to significant.

Okay. Little ones probably would even cause lightheadedness. Small PEs would not cause lightheadedness unless you were very fragile,

Or you had some lung prior lung disease or something.

Yeah, if you're, if you had heart problems to begin with, yeah, a small PE might be the one. But yeah, just think about it. A small PE is likely only to remove a very small resistor in your pulmonary arterial system. Removing a small resistor is not going to change your pulmonary resistance that much. A large PE is going to remove a large resistor from your pulmonary circulation. If you knocked out the right pulmonary artery, that's a huge resistor. That's going to cause a dramatic change in your pulmonary arterial resistance. That would be enough of a drop in preload to cause hypertension. But notice I have made that concept automatic. This is my view. But you see how how quickly that came to mind. It's because every single time I see these these changes either of increase in resistors or decrease in resistors. If I see a patent ductus or I see an AV fistula or something like that, I'm thinking about it in terms of resistors in parallel. You can see it as a side note. But yes, to your point, large PEs are the ones that are that will cause hemodynamic changes. Small PEs generally are just going to give you chest pain and hypoxemia.

Thank you guys. This was great. I want you to come up with your own automatic key concepts, or you can even just, you can take the ones that we have here or in the, the previous presentation, but I want you to, I want you to post them as a comment on this video. Knowing the right answer automatically. I want you to post them here so that we can all see how each other's doing and also to give feedback. Awesome. I want to, one of the, one of the ways to reinforce information is to go back and talk about previous concepts. That way you can again reinforce it and learn how to use it. I want to go back to our discussion of resistors in series and parallel because I think that this is actually a really useful concept that can be applied to both Step One and Step Two questions to help you predict what the answers will be. If you model blood vessels like resistors in series versus in parallel, series would be this, parallel would be this, right? Series means I have no choice. I have to go from basically one resistor to the next versus parallel. If I'm an electron, I have essentially a choice or there's a number of different options of which resistor I would go through.

Danielle, can you tell us what's the total resistance equal to for resistors in series?

Resistors in series would be like R1 plus R2 plus R3 plus R4 equals, um, our total.

Perfect. Deb, can you tell us if I removed a resistor in series, what would the total resistance be?

It's to subtract the resistance in, in the resistor.

Yeah, perfect. One of the resistors in series, total resistance should go down. That's pretty straightforward.

Padra, can you tell us for resistors in parallel, what's the total resistance equal to?

Oh, yeah. For parallel, it's one over total resistance equals one over R1 plus one over R2 plus one over R3.

Boom. Great. Hadra, can you tell us then based on that equation, if I removed a resistor in parallel, what would the total resistance be?

That would increase the total resistance.

Okay, this is critical. This is, and this is what makes it so useful from the standpoint of modeling it physiologically. In other words, if I remove, unlike a series where if I remove a resistor in series where I reduce the total resistance, in parallel, if I remove a resistor in parallel, I am now going to increase the total resistance. That's just a brief reminder of this concept. Now I want to actually go through some applications of this.

Joyce, can you walk us through and can you tell us what would be the afterload and the left ventricular cardiac output be relative to normal if someone had a PDA and why?

Patent ductus arteriosus is an abnormal pathway in between that of the left and right atrium. Is that correct?

PDA is actually between the aorta and the pulmonary artery.

It's between pulmonary artery and aortic. The cardiac output would be greater.

Okay. Why? How about the afterload?

The afterload would be less.

Great. Why? How would you model it? I don't care that you get the right answer. I care that you understand how to apply the concept.

Yeah, that was a system one answer. Let's see. The cardiac output is,

Let's take a step back. Think about this in terms of resistors in series versus in parallel. If I am, I've essentially added a conduit from my aorta. Now there's an extra path. Would you model that as removing or adding a resistor, and would that resistor be in parallel or in series?

That would be in parallel.

Well, which means it reduced the total resistance.

Perfect. And if I reduce my resistance, so think back to again, if I was going to make a tattoo, this would be my, the, the crux of my tattoo. MAP equals cardiac output times DBR, which really is just pressure is flow times resistance. Another way of thinking about that, what would then my cardiac output be relative to normal if I had a PDA?

Cardiac output would be,

Cardiac output would be increased. Yeah. In other words, if my resistance goes down, my cardiac output would go up. Perfect. Again, the concept is very applicable. If I add a resistor in parallel, my afterload goes down, which means in response, my cardiac output should go up. Cool. Does that make sense?

Yes.

Perfect. Well done. If I closed a VSD, what would be the afterload effect and what would be the left ventricular cardiac output effect relative to before I closed it? And what do you think, Ariel? If I closed a VSD, what would happen?

If you close, wouldn't that go back to what it normally should be?

Sure. Again, I, I don't care that you get the answer. I care that you use the concept. So, the hardest thing to do early on is to train yourself to use the concept, cuz the natural tendency is to try to just like what Joyce said at the beginning, like just say what you think is probably going to be the right answer. Again, like that, you can get some questions right just through like sheer logic, but I'd rather that you learn how to apply this concept because this concept is actually very broadly applicable. The concept of resistors in series versus parallel.

Okay.

Ultimately, what I want to train you to do is to see the concept behind the questions because I think what a lot of people get struggle with is they see a question like this and they're like, "Oh my god, I never knew I didn't, I never saw in First Aid what would happen to the afterload if I closed a VSD," and they panic. Yeah. Exactly. But really, it's just a concept. There's one concept and there's, I don't know, maybe 10 different ways that they could ask it. But this is the same thing again. Like you'll see every single one of these things has literally the exact same concept. And instead of trying to think of that specific VSD, the VSD part, honestly, is it's essentially irrelevant. It's the concept that matters.

Assuming by what you're saying with the closure of the VSD being something in comparison to this resistance, I would say that we're taking away a resistance and this is in parallel. If that were the case, then that you would increase, you would increase your resistance would then increase. So that means that your afterload would increase, your cardiac output would decrease.

See?

Awesome. That's actually really awesome.

Pretty cool. In other words, completely different from the typical approach, right? The typical approach is to look at a question like this and be like, ah, I don't know. This wasn't in First Aid. You will never ask me that. But instead, the key thing that you have to to learn once you start getting the pathophysiological analogies down, the next step is to figure out what's the standalone question. In other words, what, what really are they asking me? This question isn't really asking you about the closure of your VSD. This question is asking, do you understand how to model the blood vessels as resistors in parallel versus in series? That was very good. Nice. Well done.

Bartina, you are up next. Martina, can you tell us if I removed the left kidney, what would be the afterload and the left ventricular cardiac output relative to normal?

Left kidney.

Again, is it, does it matter? Does it matter that I'm asking you the left kidney? No. How should we think about this? First, whether it is in series or if it is in parallel.

Exactly. Yeah. What do you think?

This is in parallel.

Yeah. And why is it in parallel? Explain to me why would that, why would it make sense to model the kidneys or a kidney as being in parallel with the rest of the system?

Because it goes in loops. It's not set on the same plane like,

Yeah. So in other words, if I'm like, you know, if I, if my choice is, if I'm trying to get to my abdominal aorta, I have to go through my thoracic aorta. Those are in series. But if I have to begin with, I want to continue down it or do I want to go down my, my left renal artery?

Yes.

Great. If it's in parallel, if I remove my left kidney, what again, what would be the effects?

Total resistance would increase. That decreases your cardiac output and your afterload will increase.

Yeah, that's awesome. Yeah. Well done. Remember, just remember, guys, like, I, my one of my favorite quotes of all time was the Marcel Proust quote. The true process of discovery isn't in seeing new lands, but instead of having new eyes. When you learn a new concept, this is why before when we talked about how to improve your system one, a lot of it just comes down to training yourself to see these problems as the concepts underneath them. I, I think it takes a little bit of practice, but it's very good to see it this way.

Totally. Yeah. But again, but you hit the nail on the head. It's just, it's really just practice because I think people think, "Oh, I'm not smart enough." No, it's not. It's just, you just have to do it and you do it enough. Like what we're saying before, I hope you guys have been, I hope you guys have been every time you stand up thinking about venous pooling in your legs, decrease in left ventricular preload, which ultimately leads to a decrease in cardiac output, decrease in MAP, and then walking through the baroreceptor reflex to compensate. My guess is that when you've done that, the more that you do that, the more that now when you see a patient who is hypotensive and tachycardic, you just know intuitively what that means. In other words, you can see the concept without even really thinking about it. That's my goal with this. Again, your tendency, the tendency when you do a question like this is to try to just like answer it based off of logic and not use the concept, and you will get some questions right. The problem is that you're robbing yourself of the larger opportunity to actually see these things with new eyes, to use the resistors in series versus in parallel to actually understand and predict the answers to all of these problems.

Yeah, I have never done this before. This using a basic concept which you learned in school and then try to put it in here and,

Yeah, but you use it. I remember I was, when I was a resident at MGH, there was this visiting student, I don't know from where, but he was, I wanted to go to Harvard for surgery, and he was like, you could tell he was trying really hard to impress them. And we were doing like a nephrectomy, and so you have to clamp the pulmonary artery. They were asking him all these questions about EQ, and he was just totally following it. He just had no idea. They're very simple concepts. They're very simple questions. Again, like, it's not, they're not hard. You just have to do it. That was good. That was awesome.

Nicole, if I made an AV fistula, what would the afterload and the left ventricular cardiac output be relative to prior to making it? Prior to creation is really what that should say.

I'm an AV fistula. Would this be like adding something in series?

First of all, let's start with what is an AV fistula?

It's just a connection between an artery and a vein that shouldn't be there.

Yeah, great. In other words, it's like a PDA, essentially, except I made it instead of it was there to help my fetal circulation.

Then it would be more like it in parallel.

You tell me. You reason through it and tell me which would make more sense.

If I have a connection where more blood is going from my artery to my vein, I feel like that would decrease.

Again, I want you to think about, you can use logic, but that should be your secondary check. I want you to apply this concept first. Again, is this more like a series where I have literally no choice? I have to go through these resistors in sequence, or is it more like parallel where there's going to be a branch point and I essentially have a choice of which direction I go as blood?

I think it's going to be in parallel because you can go either through the artery, continue through the artery, or go through the fistula, correct?

Yeah, exactly. Great. If I make, in other words, am I adding or am I subtracting resistance, series or in parallel?

You're adding in parallel.

Great. Now it should be relatively straightforward. What effect will I have on my MAP and my left ventricular cardiac output?

If you're adding in parallel, then your resistance will decrease, and your cardiac output is going to increase, and your afterload is going to decrease.

Perfect. Yeah. Yeah. Exactly. Resistance, afterload, essentially they're technically different, but they're essentially the same thing. Like for our purposes, they're essentially the same thing. Yeah, that was awesome. That was great. Thanks. Remember this concept again. Now, every time you like blood vessels, I want you to think about them as just resistors and think of them are they in series, are they in parallel? Because there's a lot of questions for which this has a lot of relevance. Like PEs, probably the most obvious one. What's the systemic resistance if you take out a kidney? These are very real questions. What if I clamp the pulmonary artery? In an ectomy? These are, yeah, these are real. They help a lot. Yeah, this concept, again, these are your new eyes with which I want you to see problems dealing with blood vessels.

Now we're going to switch back to vignettes. Nitia, what I'm going to do, I'm going to, I'm going to mix this up a little bit. What I'm going to do is I'm going to have all of you guys read the vignette and I want you to come up with the pathophysiological chronology. I will choose one of you at random to go through the pathophysiological chronology. All of you guys are eligible. Read through the vignette and tell me what the pathophysiological chronology is.

Can you walk us through the pathophysiological chronology?

Yes. We have a 63-year-old man who got to the position because of climbing episodes.

That's not a pathophysiological chronology. I can tell you that from the start. Anytime you're just going in the order that they're telling you, because remember, like these vignettes are in the, the typical order of an H&P. The first sentence is the chief complaint. That's usually the end of your pathophysiological chronology. What happened first?

We have a healthy man who started to develop fainting episodes since two months.

No, that's, I don't think. Let's give someone else a shot. I think that that is again, that's not a sentence by sentence analysis is not a pathophysiological chronology. Let's go with Hadra. Do you want to give it a shot?

Yeah, I can try. Yeah. First, we have to arrange the vignette according to what happened first. A 63-year-old man was born healthy and then he had a poor lifestyle and he acquired hypertension and diabetes, which was poorly controlled, and then he develops from the past two months, he has episodes of fainting and easy fatigability, and that fainting has been,

Yeah, but what's the pathophysiology, right? You have to tell me why. You can't just tell me the symptom.

Because of his, uh, poorly controlled hypertension and diabetes mellitus, I think he started developing autonomic neuropathy, and because of that, I think he does not have the baroreceptor reflex to give him the, he gets hypotensive when he gets up, and that's, I think the hypotension is causing him the fainting episodes for the past two months.

That's not a bad thought. It's not, yeah.

There's evidence that that's a second thought as well. Yeah. And the second thing which I was thinking about that because of his poorly controlled hypertension and diabetes mellitus, he's getting some kind of ischemic cardiac myopathy, and that has is causing him the cardiac output to decrease and the MAP decrease.

No, that's not it either. Someone else want to give it a shot? This is a hard one. This is actually one of the hardest ones I think I wrote because there's, it's pretty complicated. All right, I will share it with you. What's interesting about this is that no one talked about his EKG. I'm going to guess it's because you guys probably didn't make sense of it. And this is pretty common. They call this confirmation bias or anchoring. In other words, we anchor on a particular diagnosis. We think like, or system one says, "Oh yeah, long, long-standing diabetes certainly diabetes could give you syncopal episodes because of autonomic dysfunction." That makes total sense. And yeah, that that makes total sense. The problem is that the EKG doesn't fit with that. Nor does the EKG fit with the idea of ischemic cardiomyopathy. Both of which could explain fainting episodes. Both of which are very reasonable hypotheses. The problem is this EKG doesn't fit with that. And so what ends up happening is that you know, we kind of like just completely gloss over the EKG. Again, you call that confirmation bias because you ignore the evidence that goes against what we're thinking and we only look for the evidence that that shows it. Yeah. The other thing is to think about what causes could be the, and again, because the key is why is ventricular rate is much lower than it's the, the summary of the pathophysiological, because again, there is the question of how, like how in detail would you do this during an actual timed question like on your test versus how would you do this if you had more time to think it through. If I was doing this on a test, this is what I would have thought. RCA, am I the right coronary artery supplies the AV node. In other words, if I have ischemia to my AV node, then guess what? I may not get conduction from the atria to the ventricles. That would cause ventricular bradycardia. And really, the ventricle is the one that sets your heart rate, your pulse. If that's really low, then my heart rate's going to fall. My cardiac output's going to fall. I'm going to be hypotensive, and that's going to lead to syncope. We'll go through in detail what this would be later. But again, in a, if I was doing this quickly, once I've reviewed this pathophysiology again and again, this is all I would need to do on a test to check to see if that made sense.

Let's start by talking about syncope. Priya, can you tell us what's the general or the usual general mechanism of syncope?

Vasovagal syncope.

That's a little bit too specific. What's the mechanism? What's the underlying cause?

I think the blood pressure falls.

Yeah, that's it. That's pretty much it.

Yeah.

Global hypoperfusion of the brain because of hypertension.

Technically, you can have hypoxemia. There are like less common causes, but I'd say 95% of the time syncope can be because of hypotension. Some form of heart, like vasovagal syncope is a hypotension because you have your vagal stimulus is too strong, get really bradycardic, your cardiac output drops, your cardiac output drops, your MAP drops, your cerebral perfusion pressure drops. And Priya, what equation can you use to explain this? Why hypotension would cause syncope?

I think it's, is it MAP minus ICP?

Equals what?

The cerebral perfusion pressure.

Very good. MAP minus ICP equals cerebral perfusion pressure. If my MAP goes down, my cerebral perfusion pressure goes down. My brain hypoperfusion goes down. Five seconds. Again, you want to make that your eyes, though. You don't want it to be this thing where it's like digging into the deep recesses of your memory, trying to hopefully find it, right? You want to make this your eyes. When you see someone that's lightheaded, or if I stand up, right? Sometimes I get lightheaded, or my wife recently was like, "Oh, you know, I stand up quickly. I get lightheaded." I was like, "Oh, wow." I literally thought of the cerebral perfusion pressure and then thought about what are the reasons why her MAP, I know she's dehydrated, all this stuff, but this is, this becomes natural the more that you use it. Just like using the resistors in series versus parallel can help you to explain the blood pressure and the afterload in tons of different situations where you have either abnormal connections between vessels or decrease in abnormal connections.

Let's talk about heart blocks. Trade, starting again. This is bolded. This is going to be a question that you're going to want to make cards on. We'll make the cards for you afterwards, but again, this is one of those, one of those key concepts that you want to make automatic. Can you walk us through, starting with the SA node, what's the order of depolarization of the heart?

From the sinoatrial node, goes to the atria, and from there it goes to the AV node, to the bundle of His, and then Purkinje fibers, then left bundle branch, and then right bundle branch, and then ventricles.

Yeah, perfect. In other words, SA node to atria to AV node to His-Purkinje fibers to both ventricles simultaneously. Perfect.

Allison, what exactly does it mean? It's embarrassing. I didn't really understand. I didn't really make sense of this until I was like an intern, but what exactly does it mean when when we say that there's a sinus rhythm?

I think it means that there's a P wave before every QRS.

That's how you determine that it, that's like a way to tell you that there is sinus rhythm. But what exactly does it mean? Cuz that was kind of what I memorized as a medical student. Oh,

That's what we're told, man. That's what I mean. Sinus.

What does rhythm mean? I didn't even, I never thought about that as a medical student.

Yeah.

Let me tell you. Basically, it just means that the, the electrical depolarization of the heart originates in the SA node. It makes sense why the thing that we all memorize, there's a P before every QRS and QRS after every P. It makes sense why, because again, you're saying that like the atria depolarizing before the ventricles. That makes sense. Technically, although technically you could have, you could not be in sinus and still have that be true. But if you had like an ectopic focus in your atria that was going off, it'd be kind of hard to tell, but yeah, generally we still assume that it's sinus in that case.

Danielle, what does it mean to have third-degree heart block?

That means that the AV and SA node are beating independently of each other or conducting independently of each other.

Kind of. Now tell me, the SA and the AV nodes. Think about what are, what exactly are independent?

Oh, sorry. The, yeah, the not the nodes, the, like atria, like the atria and the ventricles.

Perfect. Yeah. Exactly. Yeah. In other words, like your AV node is not functioning. Your AV node is like the one electrical connection between the atria and the ventricles. Kind of cool like that, right? You have this one sort of like bundle of electrical tissue that is the sole connection between the atria and the ventricles. And you slow it down. It's really slow through that AV node in order to allow time for the ventricles to fill after the atria has contracted. Cool. But basically, it also makes it like susceptible to damage or to problems. What happens in third-degree block is that the atria and the ventricles are beating independently of each other. That's what was happening in, in the case of our, our guy in this vignette. The AV node doesn't conduct signals between the atria and the ventricles. And it's usually because of ischemia.

Deb, can you basically, what that means is that the AV node is out, right? Here's the SA node is going, that's beating the atria, and then the basically the ventricles are then depolarizing, but they are independent of each other, and as we'll see, the ventricles beat in, beat at a, at a much slower rate, which is problematic for your cardiac output. Your atrial heart rate is determined by the SA node, and the ventricular heart rate is going to be set by the ventricular intrinsic pacemakers, which are a lot slower.

Deb, can you tell us if I were to remove the SA node, would the heart stop beating? Why or why not?

I guess the heart would not stop beating because there are still other firing points like the AV node and even the Purkinje fibers or His or His-Purkinje, sorry, sorry, the His-Purkinje system or even the ventricles. But it just would not go through the normal transduction pathway because if the firing would not be delayed in the atrium or delayed in the AV node, because the AV node,

Perfect. So, in other words, it's not ideal, but yeah, the heart would still continue to beat. Kind of cool. There's a backup system. If my, if the original pacemaker of my SA node stops working, I have other pacemakers. The rhythm, instead of it being sinus, now the rhythm is going to originate in other parts of the heart. Excellent.

Hadra, what's the order of the parts of the heart that would take over pacing if I remove the SA node and why?

If we remove the SA node, the AV node would start, would take over the rhythm next. And then if, if we also remove the AV node, the ventricles themselves would take over the rhythm.

Yeah. Actually, interestingly enough, the atria would take over first, and then the AV node, and then the ventricles. Yeah, there's a different sort of intrinsic rate of depolarization, which again, is set by the phase four, just like it is in the SA node. Typically, again, the faster things take over fast, cuz you'll reach threshold faster.

Joyce, I just said this. What, what phase of depolarization would determine the pacemaker rate?

Four.

Great. All right. That was a gimme, so let's give you another one. Why would the atria take over pacing of the heart first if I remove the SA node? Like, why wouldn't it be the AV node?

I don't know.

Think about it. What determines who is going to reach depolarization first? The, the atria or the AV node? And why?

The atria because the SA node is located in the atrium.

No, but it all has to do with the phase four depolarization. In other words, remember the heart rate is determined by what aspect of the phase four depolarization?

The slope.

The slope. Yeah. In other words, right, another way of thinking about the slope is how fast or how slowly do I reach the threshold at which the, the voltage-gated calcium channels are going to open. In other words, if my atria have, which has a fast intrinsic rate, my atria or my ventricles?

The atria.

Great. What does that mean about the slope of their phase four depolarization?

Sharper, or it's faster than that of the ventricles.

Perfect. Yeah. Exactly. So, in other words, what is going to determine the pacing of my heart? Is it going to be my atria first, or is it going to be my ventricle?

So, it would be the atria.

Yeah. Exactly. They have the fastest slope. The atria is the fastest slope of their phase four depolarization, which means they're going to reach depolarization threshold first, which means if they start the action potential first, they're going to depolarize the rest of the heart before the other pacemakers have had the chance to reach their own threshold. Does that make sense?

Yes.

Perfect.

Luis, why is third-degree heart block bad then?

Because the ventricles are going to be, or the, yeah, the ventricle myocytes are going to be contracting, are going to be contracting independent of the atrial rhythm. Therefore, the patient is going to be bradycardic, since the, the ventricles have the, the slowest slope phase four to reach the, the threshold. So, the patient is going to be bradycardic and possibly symptomatic.

Very good. Yeah. Almost usually symptomatic. I don't want to say always.

Good. Why are they being independently? Because the AV node is not going to receive all the electrical stimulus from the atrium because of that dissociation between the atrium and the ventricles, and, and yeah, the block is basically in the AV node. The ventricles are going to be, will be independent from the sinus rhythm.

Perfect. Yeah, exactly. My guess is that a lot of you guys hadn't really thought about like, why is third-degree heart block bad. Wasn't until probably late med school, early residency where it really hit me. I was like, "Oh, you have ventricular bradycardia. Oh, that's going to be really bad for your cardiac output." But again, this is, I want you to start, I want you to correct my mistakes. I want you to start thinking about these concepts sooner and applying them, using them as your eyes to see literally the same landscapes but in a new way. That's the key to getting these questions is to be able to recognize the concepts behind them. That's true for Step One questions. That's true for shelf questions. That's true for Step Two questions.

Luis, that was awesome. That was great. The ventricular intrinsic gated repolarization, super slow. Yeah, exactly. Because your heart rate in that's basically determining your heart rate. That's awesome. Great.

Marielle, what is the pulse of this person? If you were to feel their pulse, what would it feel like and why?

It, it looks erratic.

Yeah. What are we looking at? This is something they could share in your test. This is something they could share in your test. Particularly Step Two, but even Step One. Can someone walk us through? Can

Someone walk us through? What are we looking at?

Yeah. What are we looking at? First time I saw this, I was like, "What?" And then when when someone points it out, you're like, "Oh." Oh, yeah. You want to give it a shot?

>> Yeah. Can I ask you? You are asking about the heart rate.

>> The pulse. I'm asking for the

>> I I really I'm not sure that I'm saying is right or wrong, but I'll try. Basically, I think we try to determine the RR intervals like the how many block between how many blocks comes.

>> Yeah.

>> And then from there, if there are like almost like there are seven blocks are coming in there. Yeah. So, we'll divide 300 by 7 and we'll get like 42 something.

>> Perfect. Yeah. In other words, super low.

Let's let me point out the key elements of this cuz again, it's like one of those it's like one of those like magic eye puzzles. Like once you see it, you're like, you can't unsee it. But until you see it, you're like, what the heck is this? These are the P waves. This is a Pwave. This is a Pwave. This is a Pwave. You can see there should be a Pwave here, right? You see it's basically a P that's buried underneath a TE. It looks funny, but this should be a Pwave. This is a Pwave. This is a Pwave. There's presumably a Pwave here. The QRS looks a little little more funky. This sort of blip is probably the part of where the Pwave is. Pwave wave Pwave Pwave Pwave Pwave Pwave Pwave.

Now, in other words, the the Pwave intervals, if we think about this, as Chadv was saying, as 300 divided by the number of big boxes, it's one big box, two like three big boxes, maybe like around 100, one, two, three. Yeah, pretty fast each algorithm. But if you look at the QRS intervals, this is QRS. This is QRS. This is QS. This is QS. This is QRS. This is QS. This is the Juki heart block because you can see the atria are the the the P waves are progressing or I guess here that has its own intrinsic rate and the QRS's have their own intrinsic rate. Pretty cool. Yeah, you can do 300 divided by the big boxes. But yeah, the rates about 100. There's about seven boxes between cures the ventricular rates which again fits at rates a little high. Presumably that's because this patient's probably hypotensive. Their sympathetic tone is probably very high. I wouldn't be surprised if they had really they were essentially tacocardic, right? Their they have atrial tacoc cardia but their v their ventricle is not makes sense why the atrial rate be that high. Cool. Does that makes does that make sense to you guys?

Interestingly I actually had a student once who had 32 heart block. I was like no that's no way. you're like, where's your pacemaker? But apparently she just she didn't have she's like the first person I've ever met who has surgery heart block that did not have a pacemaker cuz typically the treatment for a third degree heart block or even Mobitis to second degree heart block is to have a pacemaker cuz again you will become like if your heart rate suddenly dropped to the 40s and you couldn't augment it like when you stand up or any other time that you would need to augment your cardiac output that's going to be a problem. face.

Why are the atrial and the ventricular rates different in third of your heart walk?

>> Because they are beating independent of each other.

>> Perfect. Sure. Both. Yeah. But what's like why what explains such a big difference in their rates then? Because beating independent doesn't necessarily mean that the rates would have to be different. But why are they different?

>> The conducting system in the atria is faster and smaller than the one in the ventricles.

>> Yeah. Yeah. The intrinsic pacemaker rate. Yeah. Yeah, the atria they're driven by their intrinsic rates rather than being all driven by the SA node. The SA node drives the atria. The ventricular rate is going to drive the ventricles.

Why then Nicole would someone have syncaby with vary heart block?

>> My guess is because the atria and ventricles are not contracting like in an orderly fashion that they're not getting enough cardiac output.

>> That's like no. Again, I want you to use the concepts that you know in order to explain this. The next step is to figure out which concept to use. But when in doubt in a cardiology question, you should always think about which equation.

>> Map. Map equals cardiac output times resistance.

>> Yeah. Perfect. Or times TPR. Good. Which also equals what?

>> The heart rate times the stroke volume turns TPR.

>> Perfect. Now tell me, why would someone have syncopy with their DPR heart block?

>> Because it is affecting their stroke volume.

>> It actually not really. Their stroke volume actually would be pretty high in this case cuz they'd have a monster preload.

>> I'm not sure. Why are the atrial and the ventricular rates different Nicole?

>> Because they have different intrinsic rates between the atria and the ventricle.

>> So what's the ventricular intrinsic rate?

>> It's a lot slower than the atria.

>> Great. If I What determines my pulse? What determines my So in that equation map is cardiac output* TPR which equals heart rate time stroke volume* CPR. What actually is determining that heart rate? Which rate are we talking about?

>> The ventricles.

>> Yeah, the ventricular rate. Now tell me why would someone have syncopy with thirdderee heart block? because they are relying on their ventricular rate which is a lot slower. I'm not sure

>> you're right. So what

>> they're just not getting enough beats per minute. It's reducing their overall cardiac output.

>> You're asking it as a question. I want you to I get the impression that you have you're not thinking about MAP equals cardiac output CPR every time you stand up. You have not made this a part of your thinking that this is just like something that you're recalling when asked on a test. Okay,

>> you can do this, but I want you to I want you to tell it to me as an answer, not as a question.

>> I think that because they're relying on their intrinsic ventricular rate, the their heart or their ventricles are beating at a slower pace and there is less beats per minute and less cardiac output

>> which leads to what?

>> A decrease in MAP because they're not getting enough blood to the brain. There's cerebral profusion. Yeah, the cerebral profusion pressure equals MAP minus ICP. And when the MAP decreases, the profusion pressure, the cerebral profusion pressure also decreases.

>> Boom. That was good.

>> Thank you.

>> Again, I want you to think about this in terms of I want you to use this as a way to see the world. I really like just like with the the what vessel thing, you can use this as a as like basically new eyes to see the world because again almost all cardiac questions can come back to this, right? map is cardiac time DPR which equals heart rate time stroke volume* CPR. If my ventricular rate is only 40 if my heart rate suddenly drops to 40 hugely low then my cardiac output is going to go low. My cardio output is down my map is down my C treatable profusion pressure is down I'm going to get brain hyper profusion that's going to lead to syncopy. Cool perfect nitia what is the typical treatment for third degree heart block and why why would that make sense?

>> No I believe it would be a pacemaker to the cardiac rhythm that we have the nodes. Ooh, that's not right the right answer. Why is that not the right answer? Think about it. That was like a system one answer. I think if I paste my essay node, what am I going to do? What's the problem in third degree heart block?

>> The main problem lies in the vententral rate being very slow.

>> If I paste my essay node, the main problem is that I I don't have conduction between my atri my ventricles. If I paste my essay node, what's going to happen?

>> That would create an independent rhythm in which would be independent of the ventricle rhythm. So I think that would be wrong. I understand that should be pacing the ventricular rhythm. Now

>> how would what does that mean to pace the ventricular rhythm?

>> Since we do not have any AB nodal conduction pathway, the the main pacemaker of the heart at the present moment would be the ventricles. If we put a pacemaker at the level of the ventricles, it would perhaps increase the ventricular rate.

>> Yeah. Yeah, exactly. It's just terminology. You wouldn't say that you would pace the ventricular rhythm. It just doesn't I'm not I don't think that makes sense. You would you say you'd pace the ventricles. But yeah, that's right. Good. Yeah, you'd paste the ventricles. You'd artificially pace the ventricles so that you're no longer bradaartic. Good. Pria, what blood vessel supplies the essay in the AV nodes?

>> I think the circumlex.

>> So, usually

>> is it right coronary artery?

>> Yeah, usually.

>> Sorry.

>> Yeah. Technically, right? Want to get really specific. It's about 60% of the time for this, about 90% of the time for the but for your test for test purposes, it's like almost always going to be the RCA. It's a but it's a pretty common thing. Puja, what are the inferior leads of an EKG?

>> 2, three, and uh AVF.

>> Boom.

>> Yeah. 23 AVF. Good. Sebastian, what artery feeds the inferior part of the heart? And what artery does this at least typically arise from?

>> The inferior part of the heart is going to be perused by the posterior interventricular artery and which a continuation of the right coronary artery.

>> In what kinds of people? right dominant

>> technically it's only right dominant people yeah the posterior descending or as you called it the posterior interventricular artery is a branch of the RCA at least in right dominant individuals good but then again this is I'm telling you the classic case because this is pretty common to see pretty common to see in a STEMI an ST elevation MI involving leads 23 and AVF why might a patient have sinus bradic cardia why would that make sense

>> right coronary arteries broke dead spy and because it's also supplying in node.

>> Mhm.

>> So if Senode will not function properly then be science cardia.

>> Boom. Yeah. Exactly. This is one of the like really tricky questions that they'll give you sometimes on step one or step two. And honestly this is the kind of thing that you have to be aware of in clinical practice too. Whenever you see an inferior MI you have to have your antenna go up and think oh man there may be a problem with some of the nodes either the SA or the AV node. And yeah, you can get inappropriate brada cardia. This is a very real thing. Yeah. The inferior wall remember is fed by the posterior descending artery which in right dominant patients arises from the right coronary. If I have an RCA thrombus, not only will I have an inferior MI because if I'm right dominant, it'll affect my posterior descending artery which feeds my inferior wall, but I can also get SA node eskemia which can give me sinus predicardia dysfunction of my SA node. Awesome. Well done. Again, you'll notice this is bolded because again I want you to be able to learn to make these connections. The way to do it is to practice it when you're not in a test when there's not time pressure that when you see it in a test well and then then make a pathophysiolog pathology start to see it in context and then ultimately when you're in your test when you see oh inferior MI someone is bradic cardia you'll you can intrinsically you can intuitively know what the connection is as opposed to what most people do which is see that completely gloss over it and then miss a large part of the question. Let's go back to Danielle. Danielle, would a lateral wall or an inferior infar be more likely to be associated with their degree heart block? And why?

>> I would think an inferior infar because but we just said that was since the right coronary artery supplies the SA node and AV node, but you would because you would have the brada cardia of the third degree block. Since the right coronary artery is supplying the SA node and AV node, then an inferior wall MI is usually a blockage of the right coronary artery that would cause the disconnect and the electrical impulse to the ventricles at the SA navy node.

>> Yeah. The idea is is that the RCA thromus assuming it's a right dominant individual, the RCA would give rise to the posterior ventricular which would feed the inferior wall, but it also gives rise to the to branches that supply the AV node. So if the node gets es schemic you can get to your heart. Good job. If I see eskemia in tooth and AVF what should I be concerned for? What kind of complications should I be concerned for? Again you'll notice all these are bolded because again these are things that show up a lot in bunas. I really want you to make cards on these. What do you think?

Eskeeia in the inferior leads which means that the posterior descending artery eskeeia the most concerned things would be the ab node nodal dysfunction which would lead to bradic cardia or heart block. Yeah and in the heart blocks the third degree heart block would be the most serious ones I guess.

>> Yeah. Essentially again the RCA gives rise to both to to the posterior descending artery but also supplies basically the or usually supplies the SA and the AV nodes. You can be concerned for right ventricular failure which will give you isolated heart failure. It will give you SA node eskeeia which can give you sinus cardiaard. It will give you a node eskeemia which will give you heart block. Yeah. Puja just says she had a question on this. Can you share the question or what was the context? Oh yeah, it was something with the guy coming in and they gave the the EKG and like he he basically passed away. The question was which of the following complications of an MI would also contribute to this patient's death and they gave some microscopic examination results and one of them was also papillary muscle rupture was like cancer and the patient had an MI an inferior MI basically and these were the things that like an inferior MI most likely predisposes to or something.

>> I see. Yeah, it's pretty common. I got to say like that using using 23 and AVF as a proxy for an RCA infar is super common and this shows up a lot. One of the ways we didn't discuss really much here, but one of the ways in which the we'll talk about this in a sec, but one of the ways in which this can affect you is that if you get right heart failure, you have to be really worried about dropping their preload because if you if if they go into right heart failure and then you decrease their preload, you're just going to make it worse. Like an inferior infar is one of the times when you actually don't want to give nitrates where you have to be really careful about giving nitrates because you can kill them because you'll make them hypertensive because you'll drop their preload too much because in right heart failure you're like say preload dependent because you need the right heart to get more preload that you can give more more blood to the left heart. Yeah, it's pretty pretty common. Hadra in a right dominant individual what would the pulmonary artery wedge pressure be if I had two three and AVF if I had an MI there

>> the inferior part of the heart is affected of the right the right uh heart is affected which means that it's like a right heart failure and there will be back of a backup of blood in the right heart and the right heart will have a difficult time pushing the blood into the pulmonary arteries and then the capillaries and then the veins in the left atrium. Left atrial pressure will will decrease which will decrease the pulmonary artery wedge pressure.

>> Boom. Yeah, exactly. Well done. Yeah, your wedge pressure is down. The reason is is because if you have a right sided MI, you'll have right heart economic failure. Your pulmonary flow is going to be down. Your left atrial pressure is going to be down, which means your right pressure is going to be down. Nice. Well done. Now, we're going to come back to the question again. We we just went through the trouble of going through and explaining every single line basically in this question and why it makes sense. It takes a while, you'll notice that it takes a while to do this. However, now that we've done it, I want you to read the question again and I want you to tell me what is the pathophysiological? How can you make sense of this? I want you to take a little bit of time and then I will call on someone at random or you can volunteer. Right.

>> This 63 year old man was born normal and he had he developed some sort of dietary and lifestyle changes which were not good for him and he developed hypertension and which he did not control was not taking his medication as such or and and he also developed diabetes malitis. Both of these chronic conditions affected his arteries and it caused some sort of inflammation and because of that it led to deposition of proteins or this arterial sclerosis and that's what led to him having a block and he had

>> let's actually be clear technically it's actually the atherosclerosis. Arteros sclerosis just means your arteries are hard. Athero is the plaque is like the fatty. So it's actually atherosclerosis that would give you a heart attack. Just having stenosis in and of itself doesn't mean that you're gonna have a heart attack. What actually leads to the heart attack?

>> Yeah, it's the atherosclerosis. That's basically when he develops fatty streaks at a very young age and that leads to deposition of

>> It feels like you memorized it. What is but like what exactly is the the cause of the MI? What's different about an MI versus just before the MI?

>> The rupture of a plaque.

>> Very clear of a plaque. The plaque rupture is which causes what?

>> Dislodgement of the it it causes the thrombus.

>> Exactly. Right. So the fatty material has like tissue factor and other stuff in it but causes a big clot, a big thrombus. Great. Which causes what in this case?

>> It causes a block. Movement of the thro thrombus causes a block. Becomes like an emblei and causes a block. Again, it's not really an emblei. I used to think that. I used to think, oh, there's like a plaque rupture and it was it's not doesn't really I think it's actually mainly like inside you. It's right where there's a clot. I used to think there was like, oh yeah, maybe it's like some rupture somewhere and it like goes maybe that happens a little bit, but really it's just it ruptures and then boom, immediately there's like a clot.

>> It's like the rupture leads to an inflammatory process response or

>> No, it's not it's not inflammation. It's just

>> cl formation. Yeah. Because of that he develops fainting episodes because there's decreased perfusion to that area of his heart because of the thrombus in the clot. Here it is the right side

>> which causes what?

>> Which causes him to have a decrease or or a change in the Rwave rate.

>> Why?

>> Because the ventricular rates are decreased.

>> But why?

>> Because the AV node is not functioning.

>> Why?

>> Because there's a block in the supply to the AV node. Good. Because why? Asking this because this is the level of detail that I want you to think about this at.

>> No, I really appreciate it because I miss out all of this. It's because the right coronary artery gets blocked.

>> Yes. Aththeroscerosis in the right coronary. There was a plaque there. The plaque ruptured which caused a thrombus. That thrombus caused the eskeeia to you said the AV node which causes what?

>> A decrease in the ventricular heart rate. The conduction.

>> But why? I mean like describe what does that mean? So like what what condition are we talking about here though? Syndrome, right? Third degree heart block. Just got third degree heart block which leads to what?

>> He has a decrease in his blood pressure.

>> Uhhuh. Why? Again, that was really good. That was really hard to do. Really hard to do. What I want you to work on though is I want you to you mentioned Regina earlier that it's really hard to make these like really small detailed connections. I This is I want you to go through these vignettes and I want you to I want you to look at all of these connections. You can use them. I've already made them for you. And same thing with the mentors. They've given you these connections. They've made them for you. And I want you to make more of these concepts automatic because I get the sense that you that's what I did honestly. Like I I memorized, oh, fatty streaks are the first thing that you see and there's this inflammatory process and there's macrofasages muscle cells or like blah blah blah. I could drone on, but there was like no real understanding behind it on my end. When I listen to you talk about some of these things, I get that sense that you've memorized the words, but you don't really understand the concept behind them. The approach I want you to take, and this is true for all of you guys, is I want you to slow down and I want you to actually learn the concepts to the level that you can see the world with them. Use them as your new eyes to see the world. Cuz that was pretty good. But I think that the more that you do that, the the faster you'll see these connections. Danielle, I want you to walk us through the end. We've gotten Martina got us really far. we have doesn't take good care of his body develops diabetes hypertension atherosclerosis of the RCA leads to a plaque that ultimately ruptures that leads to a thrombus actually let's do Joyce actually I want you to tell us that leads to a thrombus in the RCA now tell us why does he have syncable episodes

>> the thrombus causes a decrease of blood supply to the right ventricle then you're decreasing stroke volume which means you're decreasing cardiac output which means are decreasing.

>> That works except that that's not what the EKG shows us. That that could explain it. Right. Yeah.

>> Again, let's we're going to try and move past the confirmation bias and try to look at so try to evaluate all evidence and see does it fit with our idea.

>> The RCA also supplies blood to the to the AV node and with the thrombus in the right coronary artery. You have eskeeia in the AV node which means then the heart uses the ventricular pace which slows and because of the eskeeia to the AV node the SA node and the AV node have independent rates. So the atria and the ventricles have independent rates.

>> So why would it be syncopole and be

>> right the ventricular pace is slow. It's 20 to 40 beats per minute. And because the heart rate is slow, that means your cardiac output is low, which means your mean arterial pressure is low. And that results in decreased cerebral perfusion pressure.

>> Boom. Perfect. I can tell that you've made that the last part pretty automatic cuz that just flowed off your tongue. You're like low cardiac output low map low pressure. In other words, hopefully you've been practicing that, right? when you stand up at least some of the time. Hopefully, when you're on your side rotations, you're thinking about cardiac physiology.

>> Yeah, definitely. Yeah.

>> Yeah. Hopefully. I can tell you're at least doing it some of the time, but I can also tell that this other stuff is new like something about the rates are different and the essay and the ventricle and right in other words, now the key is to bring this the new concepts up to snuff with the old ones. That was pretty good. That was pretty good. Does someone want to give does someone want to see if they can do that or do it faster? Walk us through, right? Give us like the try and predict what the sum or tell us what the summary statement is going to be.

>> Just a summary of the overall pathophysiologic knowology.

>> Yeah. If this were a timed test, if this were like your real test like what how quickly and how like the big picture stuff, how could you do it?

>> I would just say that with his hypertension and diabetes, it's poorly controlled. He that predisposed him to cardiovascular disease. He developed an atherospherotic plaque that ruptured which developed into a thrombus in the RCA and that decreased the blood flow to his AV nodes or his AV node and then he developed third degree heart block which resulted in the heart relying on the intrinsic ventricular pace which decreased heart rate decreased his blood pressure and then decreased his cerebral perfusion pressure.

>> That was pretty good. That was that's maybe a little bit more than I would have given my summary but that was that was it was still pretty fast. If if I had given it, I probably would have said something like honestly I probably would have said RCA infarct, AV not eskemia, thirduki heart blocks, symptomatic bracardia. Like you can tell I skipped a lot of steps but because I've already gone through those steps in my head like I I can I know that if I needed to I could fill in the gaps but again in a time setting you have to be practical. you can't like sit there and as much as I would love for every single time under tests for you guys to go through like heart rate is low, credit card output's low, map is low, like I I recognize you won't be able to do that for literally every single question. If you're doing an card, you better believe that you should do that. But that was actually really good. I'm impressed. Yeah. I want to ask you, let's wrap up. I don't think we have time to do any more questions, but we can certainly wrap up. My goal with this is to show you what happens when you a master the concepts behind it that you can start to see those concepts a little bit more automatically and b what happens when you make a pathophysiological chronology that when you see the question the second time or the third time or the fourth time once you've made a card and you've repeated this whole a number of times that it starts to just become more automatic. You start to see it and it's like those like magic eye puzzles. You just you can't not see it. I don't know, Nicole, what what was your impression because that was that was pretty good actually. I was

>> just my impression of like the scenario

>> or of your ability to answer it like of your ability to answer this or like thinking to the future if you were to do this more, how much would this what would be the effect on your ability to interpret questions and get more questions, right?

>> I definitely obviously it would help a lot more. I haven't really understood like the progression of atherosclerosis to essentially something like syncopy as well as I do now. It was hard for me to make the connections at first, but once I made them, it seemed like it was pretty easy to see the whole picture of what was going on.

>> Yeah. Yeah, I think that's generally true. How about other people? What what your impressions or just overall impressions? Like how does it feel to do this? I think it really helps me to put abstract concepts together because I think that in first aid or yeah in first aid all of the concepts have their own little box. This sort of ties all of them together instead of learning and and memorizing them as individual things to see it in in the system that I think makes it stick a lot better.

>> Yeah, totally. Yeah, there's very good evidence behind making abstract things concrete and concrete things abstract. I think that's there is a department of education study they looked at basically like big picture like they looked at what are the educational techniques that have the strongest evidence that was one of the things that had the strongest yeah makes total sense perfect other people

>> I it actually made me realize that I I forgot what the term you were using what you were calling it but from I was thinking back to like when we first started this session I was really stuck on the idea of poorly controlled hypertension and then I was like immediately thinking left ventricular hypertrophy or like you know something along those lines of how completely wrong I was and then when like you said but it doesn't correlate with the EKG and I was like crap like you're right I completely do that where I just need to like pull myself together and just go read the whole thing you know thing that I need to really work on is what this made me realize

>> that's good I think the concept you're talking about is anchoring

>> yeah anchor on a particular diag Oh that's that's a really good point yeah because our assistant one can also sort of like our intuition right our intuitive answer can lead us down the wrong path too and that happens a lot because often times when you see poly control hypertension you're right like control hypertension you're thinking LV you're thinking it's it's really easy to anchor on that and to think oh maybe this is LVH and then you're thinking oh that would actually explain sync could be potentially there are certainly ways that you can do that the problem is that then we have the confirmation bias and then we start to then you ignore why the why like why are they bradic because LVH wouldn't explain bradic cardia certainly wouldn't explain symptomatic bradic cardia and and then the EKG totally doesn't fit is that yeah that's it's really common that that's one of the things that I I I like about the papers because it forces you to make sense of all the sentences and it helps you cuz because then you're stuck trying to explain what like the EKG like oh I can't do that it becomes a lot more clear like when we're about to go down the wrong path or not before we get to the end of the path and we realize oh man I have no idea what's going on other impressions how about you

>> yeah yeah when I was going through the question I realized that I completely ignored the EKG and I was just thinking about the rest of the scenario. I think if we keep on repeating these scenarios, similar scenarios on the test are going to look familiar and I think we'll do better.

>> Yeah, totally. Yeah. Yeah, cuz it's cuz it's kind of in in fairness I set you up for this. I in the past I gave you literally like I think our first vignette was one where they it was a guy with long-standing diabetes that had orthostatic and it makes sense. You're like yeah it makes sense that you would latch on to that. The problem is that you have to have the flexibility to recognize when the scenarios vary and I agree. I think if the more scenarios my goal with this with this was to show you that there's lots of different scenarios that can lead to the same symptoms and like a PE could lead to these symptoms a right-sided MI can lead you to these symptoms autonomic neuropathy can lead to these symptoms like a lot of things can give you hypertension and particular static hypertension and being able to recognize that and knowing all of these different scenarios gives you more flexibility gives you more lateral thinking that you can transfer between as opposed to just seeing the buzz word like poly controlled hypertension anchoring on that and then you're just stuck Initially when we did these there was a lot of emphasis on going like one sentence at a time and putting the pieces together but in this scenario I was trying to do that and when I do that I do get trapped in this like you're saying anchoring and I do dig my heels into something that I'm thinking just based off of the first two or three sentences. By the time I get to the last sentence like in this case would be the EKG. I would just I I would glaze over that almost because in my mind I already have a decision. Is it better to maybe read the entire scenario first before we sort of

>> That's a fantastic question. You're saying if I think about every sentence, sometimes it leads me down the wrong path. Maybe I shouldn't think about every sentence and I should just read everything first and then try to put it together at the end. The problem is that for particularly for the longer the vignette, the harder that is to do. And oftentimes I'll I was writing I'm in the middle of writing a like a lesson on this, but basically how you think of the first sentence affects how you think of every single other sentence after that. I guess what I would say is that the best thing that you can do is not it's really how it is that you prepare before you go into the test that matters. It's like those like those coaches that say like championships are won in practice not in or games are won in practice not in the actual game itself. I look at question interpretation the same way. If you're if you find yourself anchoring on one diagnosis and not being able to generate other ideas, it's not really a problem of how it is that you're thinking about the question at the time. It's really a problem with your preparation leading up to doing the question. In other words, the more pathophysiological chronologies that you've generated, the more flexible your thinking will be. Where you are right now, I would I actually don't like doing sentence by sentence analysis, not doing sentence by sentence analysis. I think it matters much less than making sure that you can generate a clear path of physiological where you can connect all the details because if you can do if you can do the latter in other words if you can generate the path of physiological it will be a lot easier to analyze the question the next time you see a similar question. Puja what are your thoughts?

>> I mean like you just said you know how you read the first sentence will affect how you read your second sentence and third sentence and you know so on and so forth. So for me, as you can tell, like for the past few sessions that we've had with you or the other tutors, like this has been my biggest concern because I do keep getting trapped into this where I read the first sentence, I think it's something and by the end of the vignette, it's like completely something else and I don't catch on to it because I'm still that first sentence.

>> Exactly. So I guess what I would say is that it's two parts. It's like we said in the first lesson, you we're trying to improve your intuition. In other words, you're trying to train your system one. That is how that's why we're doing the path of physiooies. In other words, if your first sentence like if your intuition was right, then everything else becomes a lot easier. That would be in an ideal world. Your first intuition is going to be right. But what you're asking is is well, it's not an ideal world. Sometimes my first intuition is like, sure, I'm working on training my first intuition, but what happens when my first intuition is wrong? That's where your system 2 comes in. You have to generate the pathophysiological knowologies for every sentence as you're going. It has to fit. In other words, if you read the third sentence and it doesn't fit with the idea of LVH, then you need to change your story. You need to recognize then that you need to change your story because if you ignore the bradic cardia and you keep going, that's now on you. Does that make sense?

>> Yeah, that makes sense.

>> It's a two-part process. You have to improve your system one, you have to train your intuition so that your natural your gut instinct when you read a sentence is right more often. But then you also have to trust but verify. think yeah my system has told me that this is LVH but also let's see if I can make that fit with the vitals I can make that fit with the respirations and the blood pressure but I actually can't make it fit with the pulse oh I don't know brada cardia but brada cardia could certainly explain the low blood pressure maybe there's like a reason that he's bracartic in other words I'm starting to open my mind to other ideas I'm not anchoring on one diagnosis and then I read the next sentence and I'm like oh we have third degree heart block here that would totally explain the low pulse and the low blood pressure and could also alternatively explain the feeding episodes because they would be syncable from low certifics that it's cardiac most likely. This is known as unheralded syncopy. Unlike vasovagal syncopy where you're like diaphoretic and get like faint beforehand, this is there's no warning. Typically, you see that more in cardia. I'm thinking something cardiac and again which fits with his age coronal hypertension diabetes mellus again I'm thinking cardiac risk factors there's again like I'm I have a pretty open mind though because there's a lot of as you saw there's a lot of reasons why card coronary disease could lead to hypertension pulse is low now it's pretty specific it's either essay not eskemia or aviono eskemia most likely right because but in other words I didn't anchor here part of this is learning to not anchor early on or to see a buzz word until I think something but it's hard to do I would say the easiest the most straightforward thing to do at your stage is to make good pathophysiologies because it'll give you more options because the difference when I read a question and I think when you're reading a question is that I have like probably I could generate five or six ideas pretty quickly of how diabetes hypertension could lead to syncopy and exertional diseir or easy fatigue ability right whereas because you don't have the pathophysiological knowledge knowledge it's a lot harder for you to generate them on the spot you're kind of stuck right you like you go with the one thing that you're like I know LVH this must be LVH or oh I know autonomicopathy this must be autonomic the difference is that I have many more pathophysiologicalities at my fingertips this week I just have more yeah just more experience but again the question is how can you gain that the way to gain that is to do more pathophysiological anologies does that make sense

>> yes thank you

>> perfect guys thank you very much this was very fruitful we will I think we've got another session next week cardio just went from your weakest block to your most predictable. Next, you need the practice system to lock it in. In my UWorld complete guide, I'll show you the exact phase byphase approach top scorers use to crush their shelf and step two with 260 plus performance.