DIP Episode 134 - USMLE Step 2CK Rapid Review Series 12 (IM-Cardiology)

Okay, welcome. My name is Divine. I am a resident. This is episode 134 of the Divine Intervention Podcasts. And in this podcast, I'll be continuing our rapid review series for the USM list of two exam with a focus on internal medicine. So what if you get a question about a patient, you know, that had like a RISMI and then they tell you, so let's say this person had the MI like 12 hours ago. And then they tell you that the patient suddenly becomes unresponsive and dies. What's the likely cause of death in that patient? I hope you're saying V-Fib. Remember V-Fib is one of the most, is essentially the most common cause of death in the first 24 hours after an MI, okay? That's something I heard that the MBME expects you to know. And if a person has V-Fib, how do you treat V-Fib? What do you do first? What's always your first step? You would want to go ahead and start chest compressions, right? You want to go ahead and if you're essentially following your ECLS algorithms, you'd want to go ahead and start chest compressions. And then after studying the chest compressions, the next thing you want to do is you want to proceed with trying to defibrillate the patient, right? Remember defibrillation is the option that you explore for two arrhythmias only, right? One is V-Fib and the other is a person that has V-TAC with no pulse, okay? So pulse less V-TAC, okay? Under those circumstances you consider defibrillation. Remember, another info defibrillation is unsynchronized cardioversion.

And then you can then begin to mix and match things like giving like a mixture of like epinephrine, like every four minutes and then you give a mutator, right? So it's like epinephrine and then give a mutatorone. And then after the mutatorone you give epinephrine again. And remember, right? Immuterone is a class, is a class three anti-rhythmic, right? It's a potassium channel blocker. And remember, there is essentially two uses classically for epinephrine on NV Me exams. You can use it for arrhythmias, like again, like V, basically for ACLS, like AC-STELY, you can use epinephrine for that, P, you can use epinephrine for that V-Fib, P, P, P, S, V-TAC, you can use epinephrine for those, right? We remember that epinephrine is also the drug of choice in the treatment of an aphylactic shock, okay? Now, what if you get a question about a patient that, you know, they tell you that this patient had like a RISNMI and then this patient has bilateral crackles when you're trying to like oscultate the lungs and the person is profoundly hypotensive. What kind of shock is this person in? I would hope you're saying like a cardiogenic shock, right? So if a person has an MI, right, they're gonna have death of their death of their cardiac amiosites. And if those cardiac amiosites die, right, they would not have adequate contractivity, right? So they can go into like, for it, heart failure, right? So they were going to essentially a cardiogenic shock.

So the thing is, again, on the MBM, you just don't want to like, because again, right, this scenario I brought up is an easy enough scenario, right? But the thing is the MBM, I think of it as a derivative test. If any of you have some kind of like investment background, you understand what I mean by a derivative. I used to do investments back in the deep, but that's a different story. But the MBM is a derivative test. And if you're thinking about derivatives, right, they would not necessarily ask you about cardiogenic shock, right? Cardiogenic shock is what's going on. But they will ask you some concepts that are related to cardiogenic shock, right? So for example, they could easily make up like 20 different questions about this. I mean, let me run through a few scenarios, right? So they could ask you things about like endastolic and all that endastolic volumes, end systolic volumes, or end systolic pressures and all those things in cardiogenic shock, right? Obviously, for a person has cardiogenic shock, right? The heart will be full with blood because things are backing up. So the endastolic volume will be elevated, right? And if the endastolic volume is elevated, the endastolic pressure will be elevated as well, right? And if a person has cardiogenic shock, right, they would have a decreased ability to send blood forward out of the heart, right? So the astrovolumes will be decreased. And if the astrovolumes are decreased, right?

That will also tell you that the ast systolic blood pressures should be decreased, right? And if the ast systolic blood pressures are decreased, right? Again, they're essentially thinking that, okay, these people have a decreased cardiac output, right? And since these people are sending out less blood with each contraction of the left ventricle, their end systolic volumes are also increased. Remember, the difference between your endastolic volume and your stroke volume is your end systolic volume. So if your end systolic volume goes down, your, sorry, if your stroke volume goes down, then your end systolic volume should go up, okay? Again, these are all hymodynamic parameters you want to know with cardiogenic shock. And if you think about it in cardiogenic shock, right? Again, if the heart is not pumping blood forward out of the left ventricle, right? You'll have backup of blood in the left itchium, right? And if, again, if you're having backup of blood in the left itchium, what will be trove your left itchial pressures? You'll be elevated, right? Remember, your left itchial pressures are a surrogate for your pulmonary capillary which pressures, right? So if a person has cardiogenic shock, their left itchial pressures will be, they will have elevated left itchial pressures, they will have an elevated pulmonary capillary which pressure, okay? So and this person, I am explaining that this person has like crackles when you're scooting along, right?

So obviously this person has a pulmonary edema, right? But the thing is this person has a pulmonary edema from a cardiogenic sauce, okay? They have a cardiogenic pulmonary edema, right? Cardiogenic pulmonary edemas tend to be associated with elevated pulmonary capillary which pressures. Contrast that with a situation like ARDS, where people have pulmonary edema because they have increased the vasculoprimability, that is an example of a non-cardiogenic pulmonary edema, so in that those circumstances those people who's left itchial pressures will actually be normal, so one classic tell, tell finding on end being of ARDS is that the person's pulmonary capillary which pressure is less than the magic number 18, okay? Again because it's a non-cardiogenic pulmonary edema, so what are some other things that can cause pulmonary edema in a person that recently has an MI, right? You want to think about things like a mitral, like flush mitral regert, right? If they have like a papillary muscle rupture, for example, right? Because again if you rupture a papillary muscle as the hardest contracting those people will have like essentially like just floored back flow of blood from the left ventricle to the left chitrim and then obviously to the pulmonary veins and then to the lungs, right?

So they'll have a pulmonary edema with that and then remember that people can also have like an interventricular septal rupture as well in the setting of a recent MI, they will likely describe that as a person that recently had an MI and then the person has a holosistolic murmur that's heard best at the left churnal border, okay? If you see those kinds of situations think about an interventricular septal rupture, right? And then your friends at the MBME can also give you a question about a person that again has a recent MI and then they tell you that this person starts completing of severe abdominal pain and they tell you that when you pulpit the abdomen like the person like screams out in like just ridiculous amounts of pain, blah, blah, if you see those kinds of scenarios I would hope you're thinking about like an acute mesenteric ischemia, okay? Remember when a person has an MI, right? The heart doesn't work as well as it should, if the heart doesn't work as well as it should, right? The heart on is almost like quivering is not contracting appropriately, right? So those people can form clot, right? And that clot can cause an acute ischemia of some organ in the body, like the bowel, right? Especially like if you send off that clot, it flexes off in an embolic phenomenon and goes on to close the super-mesenteric artery, remember? The super-mesenteric artery is the most commonly occluded vessel in acute mesenteric ischemia. So those people have occlusion of the SMA, right?

And they can have an acute mesenteric ischemia from that. Similar presentation can also be again, recent MI severe acute onset leg pain, right? I would hope you're thinking about acute limb ischemia. Are you seeing that this is essentially the same concept? You're just substituting out the middle letter, oh, if it's the bowel, it's mesenteric ischemia, or if it's the limb, it's limb ischemia, okay? Acute mesenteric ischemia, acute limb ischemia, right? Those things classically arise in people, at least on MB Ms, in people that have like some condition that mix them from clot in the heart, right? So like in the left page, I'm like if a person has like heart, if a person has like a recent MI, another classic one on exams is a person that has a history of ephab, okay? So those are things you want to keep in mind, right? And right, there are ways you can, you shouldn't, hopefully you do not confuse acute limb ischemia, or acute mesenteric ischemia, with the more chronic forms of those diseases, right? So like a chronic mesenteric ischemia, for example, will not be a problem that has an acute onset, right? There'll be something where along the lines of, oh, this person, anytime you eat, they have severe abdominal pain, and it gets better when like a few hours after eating, right? If you see that, because think about it, if you eat, you are working out your abdominal muscles, right? You need to use your abdominal muscles to digest food and all that stuff.

So if you have a ischemia, right? Your muscles are working more when you eat, your abdominal muscles are working more. So there'll be more need for oxygen and blood, and everything like adequate blood supply to your bowel, right? So under those conditions, it's almost like engine of the heart, is this is just more like engine of the bowel, okay? So the person has engine of the bowel, right? Because people that have like stable engine, when they rest, they don't have any chest pain, but when they start exercising, they have chest pain, because when they start exercising, they place more demand on their cardiac myocytes, so they then begin to have like activity and use the ischemia. That's kind of like the same thing with chronic mesenteric ischemia. The person has activity induced, basically 18, so activity induced bowel ischemia, okay? So those are things you want to keep at the back of your mind on exams. Chronic limb ischemia is essentially peripheral arterial disease, right? Okay, now what if they give you a question about a patient that has like, no, how to recent MI, and then this person's blood pressure is like 80 over 50, the person has like JVD, and then they show you an EKG. And you notice that you have a tokyrish complex, then one that's really tiny, tokyrish complex, one that's really tiny. If you're seeing that in succession, what are you thinking about? I would hope you're thinking about like a ventricular free-water rupture, right?

Remember, ventricular free-water rupture can cause cardiac tamponat, right? Because if the ventricular free-water ruptures, all that blood will essentially pull in the in the pericardium, right? And that can squish the heart. So they can give you like a bextriate presentation in a patient that is recently post MI. If you ever see something like that, then I really want you to think about, I really want you to think about a ventricular free-water rupture. And again, it tends to happen a few days after a person has an MI, right? And one thing I'll just go ahead and say here is, if a person had a recent MI, you don't want to put those people on steroids. I mean, if it's obviously something that you really, really need to find. But in general, putting a person on steroids is not a great idea, right? In the setting of a recent MI, because that can impair like one healing, right? And that can essentially make it harder for them to recover from the myocardial infraction, right? So again, ventricular free-water rupture can present as cardiac tamponat. You have the triad of like the GVD, more food heart sounds and hypertension, right? And one thing I want you to keep at the back of your mind, right? Is that again, there are many things the NVME can use to tell you that a person has more food heart sounds. They can make your life easy and say, oh, the heart sounds are distant on our scotation, right? But they really do that.

Other things they can do is they can give you like electrical alternates. Remember, electrical alternates is a surrogate for a person's heart, essentially, dancing in some kind of fluid, like in the setting of a cardiac tamponat, right? So those people under those circumstances, right? Like because the heart is dancing in fluid, whenever the heart comes close to the chest wall, right? The EKG will record a strong signal, they'll get a big nice, fat, QRS complex. But when the heart dances away in the fluid away from the chest wall, right? They will have a decreased amplitude of the QRS complex because the EKG lead will capture less in the way of electrical activity, right? And then, so electrical alternates is one surrogate. Another surrogate they can just give you is like a low voltage QR, like a low voltage EKG, right? Again, if a person has a low voltage EKG, that means that the person's heart, like the EKG leads are not capturing enough. So because there is, they're not capturing enough electrical activity because there is something in the way between the ventricle, right? And the EKG leads, right? Like fluid, for example, or it could be like fibrosis or like deposition of like some substance like amyloid, for example, those conditions are all associated with low voltage EK Gs. So those are high old things to keep in mind.

And then, remember if a person has, like again, like an MI and they have this cardiogenic shock, what should be true of their systemic vascular resistance? It should be decreased, right? They should have a, oops, sorry, it should be increased because think about it. If a person has a decreased cardiocopal because they have cardiogenic shock, right? Those people's blood pressures go down. If their blood pressures go down, then the body says, like the body says, hmm, I need to maintain, elevate, I need to maintain blood pressures, right? So the way your body would choose to maintain those blood pressures, right? To keep like your profusion going is that your blood pressure, your body will go into like extreme viso construction. And that would increase the systemic vascular resistance, okay? Now, what happens to the central venous pressure if a person has cardiogenic shock? The central venous pressure should go up, right? Again, remember, the central venous pressure is a surrogate for right-itre pressure, okay? Contrast that with the pulmonary capillary wedge pressure that is a surrogate for left-itre pressure, right? So if a person has cardiogenic shock, fluid is backing up in the right-itre, right? So the endastolic volume, if you may, of the right-itre will go up, right? So the endastolic pressure will go up. So the CVP, the central venous pressure should go up, right? And again, it should make sense that the right-itre pressure is called CVP, right?

Central venous pressure because where do all the veins of your body with the exception of the pulmonary veins draining to? That's the right-itre. Okay, good. Now, what if they give you a question about a patient that, you know, had like a recent MI and then they tell you that the other patient, you know, went for re-vascularization and then they tell you that this patient starts complaining of chest pain again. What is the best lab marker for this patient if you want to detect reinfaction? I would hope you're thinking about CKMB, okay? I hope you're thinking about a CKMB, right? Remember, CKMB is the troponian, right? If a troponian arises, it sort of takes a while for it to die down, right? So if a person has a reinfaction, you want to go ahead and check the CKMB on that those circumstances. Okay, now, what if they give you a question about a patient that had, like, you know, had a recent MI that would go to percutaneous coronary intervention and then they tell you that this person, that the person's creatinine has started rising and then they tell you that this person, they show you like a picture, like a really gross picture of the person's toes and you notice that the person's toes are like blue and the person has like this netted, like almost like mat-like lesion on the low extremities. What are you thinking about on that those are circumstances? I would really hope you're thinking about a cholesterol embolization syndrome, okay?

Collestual embolization syndrome, that is something your friends at the MBML have to test a lot, right? So if a person gets PCI or some kind of like vascular procedure that could potentially dislodge cholesterol from a vessel, right? That cholesterol can shoot all around the body, it can begin to cause like embolech phenomena in different organs, right? So classically on MBML it will present as like renal failure so the person's creatinine will begin to rise. But other things that can happen is it can begin to do that, those cholesterol crystals can begin to embolize like vessels in your distal extremities, right? So it can cause something called like a like a Bluetooth syndrome or those people can have like like the net-like skin finding on the distal extremities that I was talking about is levidoraticularis, okay? Those are all things that can pop up and exempts in this setting. Now what do they give you a question about a patient that has a recent MI? And then they tell you that this patient is a convener of chest pain and then they tell you that when you listen to the chest you hear like a scratchy sound in systolean and in diastole. What are you thinking about? I would hope you're thinking about like a post-infraction pericarditis, right? A post-infraction pericarditis, right? Remember people after an MI they can have a pericarditis that happens like a few days after the MI or a few weeks after the MI, right?

So the one that comes up a few days afterwards is the post-infraction like the Fibranos pericarditis, the one that shows up weeks later, right? That's your dressless syndrome. Remember dressless syndrome arises from arises from an autoimmune phenomenon. Okay, right then again I'm essentially describing pericarditis, pericarditis, right? So like chest pain, we're seeing when you lie back, better when you lean forward, right? And on an EKG, right? I would really hope that you remember that those people can have, those people can have ST elevations everywhere, right? Remember normally if you have ST elevations, it should be in a territorial distribution. But if you're having ST elevations everywhere, it doesn't seem to be obeying any vascular territory. Then under those circumstances, you want to really think about, you really want to think about pericarditis, right? And then also remember that pericarditis can also be associated with like PR segment depression on an EKG, right? And then some other high yield things you want to keep at the back of your mind with a pericarditis, right? There's many other things that can cause pericarditis, right? So they can give you a person that had like a recent viral operator infection and then they have like the classic classic pericarditis symptoms, right? Viral UR Rs can cause pericarditis. In fact, they are probably the most common cause of pericarditis in the US, right?

Now other things that can cause pericarditis, they can give you a person that has renal failure, right? Renial failure, those people can have pericarditis. Euronea can cause a pericarditis, right? Another thing that can cause pericarditis is the person has like radiation therapy to the chest, right? They can classically give it to you in a person that, for example, had a heath of like breast cancer and they got radiation and then they are completely in a chest pain or a person that has like a lymphoma and they got radiation to the chest, right? And then they're completely in a chest pain, right? If you see those kinds of scenarios think about pericarditis being the inciting cause, right? And then some other things they could also test with that, right? Remember, if a person gets radiation to the chest wall, that increases the risk of what? That increases the risk of thyroid cancer, right? Especially, papillary thyroid cancer. Remember, the biggest risk factor for thyroid cancer is a prior history of exposure to chest, I mean, to radiation for the like, the chest, the neck, the head, okay? Those are high old things you want to keep at the back of your mind. And then what if they give you a question about a patient that, you know, they, they come in with chest pain, relating to the joe so classic MI symptoms. And then for the person's chest pain, you give them nitroglycerin and then the patient suddenly becomes unresponsive. What are you thinking about?

I would really, really hope you're thinking about a patient having an RC infarct, right? So like ST elevations in like two, three VF, right? So why did the patient become unresponsive after you give them nitro for their chest pain? It's all right, side dead infarction, right? Remember, people that have right side dead infarcts, they are very, very preload dependent. So if you give them like nitroglycerin for like their chest pain, remember, nitroglycerin is a vino dilator, right? So that would decrease preload. If you decrease preload, those people can going to like just very like almost like a low volume shock like real quick, right? And then they can die, they can die relatively quickly. So before you start throwing out drugs for a person that has an MI, you better make sure you've looked at the EKG if not you can get into trouble relatively quickly under those circumstances. The way you actually treat right-sided MI is to give the person fluids, right? Just to keep you a preload up. Okay, now what if you get a question about a patient that this doesn't necessarily relate to the scenario I'm thinking of in my head, I'm not really really really to an MI. So okay, I think I guess I'm going to maybe go ahead and stop here. Yeah, this other topic is should best make it sweet to another podcast. So I'll talk about it in another podcast.

Really in this podcast, I just really wanted to hit the complications of an MI really hard because MI is a thing you're going to see on your NV Me exams, you're going to see on your step two, CK exam. And as I do at the end of every podcast, I'd offer one on one tutoring for all the USMLA exams, right? So step one, two CK, two CES, step three, the preclinical medical exams, third year shelf exams. If you're an internal medicine resident, I do tutor for like the IBIM board exams, right? And the entry in exams. And then like college students, I tutor essentially every pre-med subject. And then I do offer like one on one advising or like I guess consulting for like Eras applications, Amca's applications. So if you're like a med student applying to residency, I'm currently working with a ton of people in that process with Eras coming out next month. So if you need advising for any of those things, don't be afraid to reach out to me and I'll be more than happy to point you in the right direction. I do it on a one on one basis. So if you reach out to me through the website or send me an email at divine intervention podcasts with an SADN.gmail.com. So have a wonderful rest of your day. I will see you in the next podcast. God bless you. Thank you.

Ventricular fibrillation (V-Fib).

Chest compressions and defibrillation.

It is used for arrhythmias (ACLS) and also as a drug of choice in hypovolemic shock.

SVR increases because the body attempts to maintain blood pressure despite low cardiac output.

Beck's Triad: JVD, muffled heart sounds, and hypotension.

Holosystolic murmur heard best at the left sternal border (LUSB).

Electrical alternans or low voltage ECG.

Class III anti-rhythmic; potassium channel blocker.

Cardiogenic has elevated PCWP; ARDS typically has normal PCWP (< 18 mm Hg).

CKMB.

Superior Mesenteric Artery (SMA).

Viral URI, Uremia/Renal failure, or Radiation therapy to the chest.

Chronic presents as activity-induced abdominal pain (worse after eating); Acute presents with sudden severe pain.

Profound hypotension/low volume shock because the heart is preload dependent.

Class III anti-rhythmic; potassium channel blocker.

Cardiogenic has elevated PCWP; ARDS typically has normal PCWP (< 18 mm Hg).

CKMB.

Superior Mesenteric Artery (SMA).

Viral URI, Uremia/Renal failure, or Radiation therapy to the chest.

Chronic presents as activity-induced abdominal pain (worse after eating); Acute presents with sudden severe pain.

Profound hypotension/low volume shock because the heart is preload dependent.