Welcome in. Hope you guys, if you were on the Western side of the world, you got to see that solar eclipse today. If not, we're going to dive into some high yield cardiology.
That's going to be going through concepts from my guide. It's going to be integrating NVME style vignettes and disciplines from other systems as well. I did want to mention that we will be doing a giveaway at the very end.
And so be sure to look out for that. This is a QR code. If you guys want to scan it now, I'll also come back to it at the end. So my cardiology guide, we're going to be giving away a few of these copies to some lucky winners. So stay tuned for that.
This is who's on the team in our Discord. So I'm really, really fortunate to have Fahad and Khaled as mentors in our Discord community. They just matched to dermatology and ophthalmology at the University of Miami. And so...
So... It's been quite a busy time for them with the match and whatnot, but super excited for them to start their residencies in this upcoming spring and summer. They're great mentors. They run weekly webinars similar to this, covering everything from MCAT to step one to step two, applications, residency applications, etc. And so if you're looking for any support across any of your journey, both for these exams, but also for interviews, advice, etc., I highly, highly recommend.
that you guys check out our team and as well as our as our discord so this is today's um kind of lecture topic and path we're going to follow we're going to start off with everyone's favorite with embryology then we're going to go to cardiac physiology vascular physiology electrical conduction do some pharmacology aortic pathology hypertension heart failure cardiac microbiology and we're going to end with shock so Our first NBME style question everyone. I want everyone to go through this with me and answer in the chat. So we have a 3,900 gram newborn who's delivered via uncomplicated vaginal delivery at 38 weeks gestation by a 3-1-P1 mother.
The baby's prenatal screening was significant for genetic abnormality. Early after delivery, the newborn appears bluish in the lips and extremities while pulse ox reading on room air is 83%. Echo shows a common overriding vessel arising from both the right...
and left ventricles. An abnormality in the development of which of the following embryological structures is responsible for this newborn's finding? All right, everyone.
Everyone in the chat box, let's answer this question. I've seen lots of Cs, and if you are seeing C, you are absolutely correct. So this is truncus arteriosus.
Now, I will be going through the other answer choices as well. But first, I just wanted to do a bit of an integration here. So the kid presented shortly after birth with this bluish cyanotic features, right? There's a mixing of blood. There's a right to left shunt in the heart, right?
One of which is our truncus arteriosus. And an easy way to remember your five cyanotic heart diseases, guys, is your five Ts. And conveniently as well, you can think of it in a numerical fashion, okay? So for one, the first T, you're going to think what we just discussed, truncus arteriosus. there's a common overriding vessel so typically right in the heart's development you'd expect the pulmonary trunk and the aorta are going to divide and the neural crest cells are actually responsible for this process but guys in something like the george syndrome right something like other neural crust cell abnormalities there's going to be a problem with this and you get a common overriding vessel if you get a common overriding vessel then you'd expect to have mixing of blood which is what we saw with the child for two we have transposition of our great vessels.
You can think to switched vessels. So your aorta and your pulmonary trunk are swapped in where they should be. So typically, right, your aorta should come off the left ventricle, pulmonary trunk off the right ventricle.
In this case, they're swapped. And guys, really, really important to know that this is associated with a mother with diabetes. Okay, so I want you to remember that association. Mother with diabetes with transposition of great vessels.
For three, easy. Try is three. you're going to think of tricuspid atresia as the name implies there's an absence of a tricuspid valve reminder your tricuspid valve is between your right atrium and your right ventricle you don't have a if you don't have a functioning tricuspid valve then your right ventricle right is not going to develop properly in terms of its musculature and you're going to get this floppy weak right ventricle okay i also want to just tie in something really important guys what exposure what drug can can affect the mom prenatally that can also affect the trachea spit valve everyone in the chat what drug exactly if you're saying lithium you're absolutely correct and what is it called what is the condition called ebstein's anomaly you guys are phenomenal so In this case, right, look out for a mother with, you know, some sort of bipolar or for any reasons taking lithium. And what's going to happen is it's actually going to cause a malformation of your tricuspid leaflets.
It's going to displace into the right ventricle, and it's going to cause a tricuspid regurgitation. So look out for those signs as well when it comes to the tricuspid valve. Next is Tetralogy of Fallot.
Reminder, Tetra is four. you can also think of it because there's four main signs and you can use mnemonic prove. Now I want you to understand all of these, not just memorize the prove mnemonic.
Pulmonary stenosis. If we get pulmonary stenosis, guys, right, what is that going to cause? Well, your pulmonic valve, right, is to the outflow of your pulmonic trunk and your pulmonic circulation, right?
So if you get pulmonic stenosis, you might've seen in Uro questions or when you're going through your studying, this right ventricular outflow obstruction. with tetralogy of fallacy because it makes sense right your pulmonary if you're getting severe pulmonic stenosis you're not properly pumping out the right side of your heart into the pulmonic circulation and so you're going to get this pulmonic stenosis and outflow of tract obstruction secondary to that right your right ventricular hypertrophy so what did we just talk about pulmonic stenosis you're not pumping blood forward through the pulmonic circulation now the right ventricle has to work harder and harder because there's building up pressure right in this right ventricle so you're going to naturally get a right ventricular hypertrophy, right? And this is going to cause, right, on x-ray, a classic boot-shaped heart, which is why you see that, right?
So I really want you guys to understand and not just memorize, oh, boot-shaped heart, oh, right ventricular outflow, contractive obstruction, but if you know pulmonic stenosis, if you know, you know, because pulmonic stenosis, we're going to get right ventricular hypertrophy, it allows you to kind of make these connections. The other features are an overriding aorta and a BSD. Now guys, a VSD is one of your most common septal defects of the heart, and it's going to classically cause this pan-systolic murmur. And I want you to contrast that with something called an ASD, right, your atrial septal defect.
And I remember ASD with a split defect. So ASD, a split defect, because you classically get a split fix-to defect. And really important, guys, both the VSD and ASD are going to be associated with your trisomy 21. And so just look out just look out for those but again vsds are super super common tp the apvr guys uh is our last cyanotic heart disease and you can remember that with the five letters and essentially your pulmonic circulation right is draining back into the right side of the circulation where it's deoxygenated right that's not good we want it to to return back to the left side um and so again this is going to cause mixing of blood and cyanosis so I wanted to make one more integration with heterology of follow, and that is with something called pet spells, which I'm sure you guys have seen and heard about.
But essentially, under physiological stress, under environments of physiological or psychological stress, this is going to cause a hypoxic environment. And when there's hypoxia, we're going to increase the amount of blood being shunted across our heart, so the right to left shunt. This is bad though, right? We don't want lots of right to left.
mixing. And so this is going to cause the cyanotic baby. And what they do to combat this is they squat. And why do they squat?
Integrating some physiology here, guys. When we squat, we increase our systemic vascular resistance. If we increase our systemic vascular resistance, we're going to increase our resistance to flow. So we're going to actually decrease that right to left shunt.
That's going to decrease the mixing, and that's going to hopefully alleviate the symptom. And so if you see anything around tet spells, squatting, boot-shaped heart, right ventricular outflow tract obstruction, guys, you're going to be thinking tetralogy of fallacy. Coming back to DeGeorge syndrome, I want you guys to have this integration in mind.
I want you guys to have syndromes on the USMLE always in mind. So particularly with the vignette we just saw, DeGeorge syndrome is going to be integration to your truncal abnormalities, okay? Remember the CATCH-22 mnemonic, cardiac abnormalities.
abnormal faces, thymic aplasia, and thymic aplasia, you're going to look out for a kid with recurrent T cell mediated infections, right? So that's going to be viral fungal infections, okay? Left palate hypocalcemia, which will often present with seizures or tetany.
And then remember your 22 Q11 microdeletion guys on the 22 chromosome, super, super high yield. Now, I just wanted to also integrate the embryology of the heart with the adult structure. Similarly, coming back to the vignette there.
There's a couple of little memory tricks that I have in my guide that might help. The truncus arteriosus, the TNA helps you remember the pulmonary trunk and the urinary arch. So truncus, you know, the two outflow trunks. Bulbous Cordis, I think a bulb is smooth. So this is the smooth parts of the ventricles.
The left horn of the sinus venosus, I think coronary sinus, so sinus venosus with coronary sinus, and then the right horn with right atria. So just a little bit of some memory tricks. Often the USMLE will test little factoids like that.
So be on the lookout and have that memorized. Now I wanted to come back to something super, super high yield and integration here. Failure of what embryological mechanism guys is related to degeorge think about your pharyngeal derivatives okay is it a failure of your third and fourth arch pouch or cleft i want everyone in the chat to answer this pouch really really good reminder everyone guys that your pouch is going to be coming from your endoderm your cleft is going to be your ectoderm and your arch is going to be your mesoderm okay really really good um for everyone There. Now, let's move on to some cardiac physiology. A cardiologist is studying the physiological regulation of blood pressure during strenuous exercise in periods of high metabolic activity.
He is interested in how quickly blood flow delivered to the peripheral arteries is affected by adaptations in the cardiac cycle. A pressure volume tracing from cardiac catheterization is shown in one study participant. Which labeled point in the diagram would correspond to the start of ventricular healing? Everyone, when you're ready, put your answers in the chat box.
Yeah. If you're answering A, you are absolutely correct. And what we're going to do in this next slide, everyone, is we're going to slowly go through the physiology of the cardiac cycle, and then we're going to go into some pathology and how that can relate, because often this is how the USMLE tests it, okay? So I want everyone right now to imagine they are inside the left ventricle, okay? Everyone imagine you're inside the left ventricle.
Above your head, you have the mitral valve and you have the left atrium, right? And then next to you, you have the aortic valve and the aortic outflow tract, right? Everyone imagine they're right in the left ventricle because that's what this pressure volume loop pertains to.
As you can see, on our y-axis, we have pressure. In our x-axis, we have volume. Each cycle that you just saw on that previous slide is going to represent one cardiac cycle, both systole and diastole, okay?
We're going to start off with point C here. Now just follow along the axis of that, everyone. Our volume is at a max right now, and our pressure is at a minimum, right? And so what this means is our ventricles are actually full, okay?
If our ventricles are full, our mitral valve, which is above us, right? The left atrium just filled us all up, and we're going to be closing off the mitral valve now, and we're ready to essentially pump, right? And so this is also going to be known as your end diastolic volume, right?
Diastole just finished. our ventricles relaxed, they filled up, everything's happy, mitral valve closed, okay? Now, Frank Sterling, we know all the types of mechanisms, right?
When they detect stretch, okay, now we're ready for contraction. If we're ready for contraction, what's going to happen? We shoot up and our pressure increases. But why doesn't our volume change, everyone? Well, we are in a closed system, right?
Our mitral valve and aortic valve at the moment are closed. So just very simple physics, right guys? If we have a closed system, and we have increased pressure inside that system, well, what happened, right? Our volume didn't change, but we made the area smaller, right? And so ventricles contracting against fixed volume, we're going to have increased pressure.
So what is this known as? This is called isoventricular contraction. Exactly, Amar. Very, very good.
This is where most of your oxygen demand is. All right. So what's going to happen, guys, is this pressure is going to build, build, build, build, build, build, build, right? until a point where what happens your aortic valve hop opens because your left ventricular pressure is going to oversee that of your aortic pressure so now your aortic valve pops open and we are ready to eject this blood out to the body okay so what happens well we get this phase called systolic ejection okay systolic ejection is important and we're going to reach a peak it's going to come down And what happens?
Our aortic valve eventually closes because again, the pressure between the aorta is now less than that of the left ventricle. Now what can we expect? We can expect our ventricles to relax, right?
And now the opposite of what we saw on this right side is going to happen, right? We're going to get this isoventricular relaxation. So what happens?
Well, our aortic valve is closed. Our mitral valve is closed. We just finished systole, right? We just ejected our blood out and now we're ready to fill back up. So our ventricles are relaxing and now we reach this point here where we have both a low pressure and a low volume.
That signals the mitral valve to snap open. N-systolic volume would be here because what is our N-systolic volume? We just finished the cycle of ejecting blood out, whatever remains in our, because we don't eject it all out, right?
That's what your ejection fraction relates to, guys. We don't eject all the blood out in every cardiac cycle. As you can see here, there's a little bit of volume still left, and that's our N-systolic volume. And guys, actually, N-systolic volume, sorry, if you subtract your N-diastolic volume from your N-systolic volume, that's your stroke.
volume, which makes sense, right? How much was in their ventricles when it was maximally full, and how much was left at the end of systole. This is how much you ejected, that's your stroke volume, okay? And then finally, guys, as coming back to our question, right, A was the start of our ventricular filling, right?
Because here, our mitral valve is open, right? Our aortic valve is closed, and blood from our left atrium is coming into our left ventricle, and we are filling here, okay? So that's... the cycle in its entirety. Good job to everyone who selected A.
Now, I wanted to come to this because this is often how it's going to be tested. Reminder, guys, what did we say these two points were? We said that this was our end diastolic volume and this is our end systolic volume. So I want you guys to think now how increased preload, increased afterload, and increased contractility can affect these loops, okay? You can just memorize what they look like, but if you understand what we just went through with the physiology, then this is a piece of cake.
Okay, let's think about increased preload first. Okay, what is increased preload? It's increased amount of blood volume back to the heart, right? Increased venous return, more blood is filling up the ventricle. Okay, what did we say our end diastolic volume was?
It's how much blood is being filled up right before we eject. We have more preload, if we have more blood, we can expect our end diastolic volume to go up. Okay, well, it shoots over to the right here.
Pretty simple, right? Our loop is going to shift over to the right, right? Increased width, and what did we say?
Our end diastolic volume is here, our end diastolic volume is here, we increase the width. Because our end diastolic volume subtracted by our end systolic volume is our stroke volume. So if we get an increased width of our loop here, we're going to have an increased stroke volume.
Okay. Now, increased afterload, as we can see in orange here. Well, what is afterload?
That's increased. I want you guys to think afterload with increased resistance to contraction. So think of something like an aortic stenosis, right? Now, if we have increased resistance to contraction, so let's say we're trying to eject all this blood out, but there's a high resistance.
Well, not... all that blood is going to come out, right? Less of that blood is going to be ejected.
So in our, when we talked about our end systolic volume, because I told you guys that a little bit of blood will still remain in the ventricles, right? Well, when we have increased afterload, more blood is going to remain in the ventricles. So what happens?
We increase, look, it shoots to the right. We increase our end systolic volume, right? More resistance that the part has to pump against, which makes more blood left in the ventricle after each contraction. What did we just do?
We decreased our width here. If we decreased our width. our stroke volume is down.
Okay, guys. Now, finally, with the red line here, increased contractility. So what is increased contractility going to do?
Our blood is, our heart is actually going to be able to beat and pump out more blood effectively than normal. So if we're able to pump even more of that blood out, then we'd expect our end systolic volume, right? We're gonna have less blood in the ventricle, right?
We're doing a really, really good job of pumping out that stroke volume. So there's gonna be left in the ventricle. to end.
So what happens? Look, it moves to the left. Our end-systolic volume moves to the left. And if you just want a really fast way of memorizing this on the exam too, guys, watch this, okay?
We said preload is the green. Look at this. It's the shape of a P. If you want A for increased afterload, it's the shape of an A, right? And then if you draw a C, you can draw a C all the way across like this for contractility.
So if you're really stuck and you're sweating on the exam and you have no clue what I just talked about, maybe you can fall back on that. but I do think it's important to understand. And if you just gain, you know, if you just understand this basic physiology, I'm sure you'll be just right.
All right, vascular physiology, everyone. 91-year-old male patient calls the emergency paramedics to his home because of severe chest pain that started 30 minutes ago. The paramedics obtained an EKG, which is notable for acute ST segment elevations in leads of E1 to 4. The paramedics quickly administer sublingual nitrate.
rapidly acts to decrease the patient's chest pain within five minutes which are the following accurately characterizes this drug's mechanism of action responsible for relieving this patient's chest pain all right guys take a look at the answer choices take a second if you need it everyone stay active engage on this session i want everyone participating this is how you get the most out of it i'm seeing tons of d's come through and if you're saying d you are absolutely correct so in this case guys we are thinking D. Now, I wanted to do this integration here, and we saw subliginal nitrate being administered, i.e. nitroglycerin, and let's go through just the pathophys and the physiology by which this works, okay? So D was the correct answer, but let's understand why.
So what nitroglycerin is going to do is it's going to cause systemic peripheral vasodilation. If we cause systemic vasodilation, right, that's going to cause more blood to pool in our peripheries. That means there's going to be less blood, right, and less force essentially coming back to the heart. And if we understand the principles of myocardial wall tension and contraction effort, we have decreased preload because our blood is pooling in our peripheries. We can put less strain on the heart, and that's going to cause less O2 requirement essentially.
And what... angina is and what the system uh how we combat this of course is giving nitroglycerin decreasing the o2 requirements um which can relieve symptoms now it's really really important to understand something guys here with nitric oxide and i want everyone in the chat box to put in what type of messenger pathway nitric oxide works via everyone in the chat box Yeah, really, really good everyone. If you're putting CGMP, second messenger system, stick with GMP, you're absolutely correct. Very high yield.
Again, guys, just a tip for the USMLE. Oftentimes, questions aren't going to be perhaps as straightforward as these first order questions. I could have given you the exact same stem that you just saw and said, what messenger system does this work for you?
And, you know, we could have CGMP and PAMP and the other receptor tyrosine kinases as well. So just make sure you understand and can integrate that across your biochem as well. And I have a little memory trick for the cyclic GMPs, and that's the Ns for cyclic GMP.
So we talked about nitric oxide, but also pay attention to natriuretic peptides like your ANP and BNP, right? These are when the heart is in states of like something like heart failure, right? and this is going to promote your natural recess right your salt wasting through the urine and the water follows so what enzyme now everyone in the chat box breaks down cgmp everyone in the chat box what enzyme breaks down cgmp phosphodiesterase you're saying phosphodiesterase you're absolutely correct and How this is going to all tie back into things, guys, is some of the drugs we can also administer.
So if our phosphodiesterases break down CGMP, and our CGMP is responsible in the case of nitric oxide, right, for this basal dilation, then in cases such as pulmonary hypertension, right, we can administer a PDE4 inhibitor like riflumilast, right? Or we can administer PDA5 inhibitors, right, like sildenafil. for erectile dysfunction.
Now, lung has four letters in the name. Another body part has five. You might be able to remember the receptors that way.
I think it's pretty self-explanatory, but reminder guys, if we inhibit the breakdown of phosphodiesterases, right, we're going to get less CGMP breakdown and we're going to have more effects in terms of our vasodilation, right? Both for erectile dysfunction and for pulmonary hypertension. And just coming back quickly, guys.
to the other answer choices here. A is actually correct, but this is a more minor mechanism by which nitrates are going to work. We talked about D, how that's obviously correct. B is going to be correct in the setting of norepinephrine, right? Remember your alpha one.
And then indirect venous vasodilation via L type is going to be your non-dehydropyrmidines. Remember those work on the heart. Okay. We're just going to put her on ahead here, guys. and move on to our next topic.
But before we do, I just wanted to let everyone know, all 163 of you, thank you guys for tuning in, that our Discord hosts webinars like this on a weekly basis. As I mentioned in the beginning, we have two really, really great mentors, Fahad and Khalid, who help support me in running these webinars. We do everything from, as I mentioned, MCAT and USMLE prep. similar to these webinars, but we also do everything from interview, applications, how to build a study schedule. time management etc we also have just a great community of like-minded individuals um you know various chats in there we have resources that we all share with one another we have exclusive pdfs for the discord so uh feel free guys to save this and come back to it um at the end again we are going to be doing a cardiology webinar uh cardiology sorry giveaway at the end as well all right i'm just gonna take a sip of water and then we are going to move on to electrical conduction.
So everyone, let's read. 27-year-old female graduate student with irritable bowel syndrome, constipation predominant form presents to the emergency department due to increased nausea over the past three days as she prepares for her final exams. She's given ondansetron to treat her symptoms but feels lightheaded over the next few hours. An EKG is obtained that shows polymorphic ventricular tachycardia, which in the following find is expected on this patient's EKG. I want everyone in the chat box to answer.
All right, so I'm getting some mixed answers here, but that's all right. The answer is B. If you're saying D. we're going to come back to the difference between a greater than qrs of 0.2 seconds 0.12 seconds versus a lesser than 0.12 seconds but you guys were really really great in the sense of getting that the it's an irregular rhythm so let's move on to some integration here so when you have a cardiac rhythm guys of greater than 100 beats per minute so it's tachycardia or the qrs that's greater than 120 that is your wide complex tachycardias okay so What I'm going to do here, guys, is I'm going to have an EKG strip, and I want you guys to tell me what you see. So does anyone want to name this one for us in the chat box?
If you're saying torsades, you're absolutely correct. What we just saw in the question, right? Guys, very buzzy, this polymorphic shape, as you can see here. Okay.
You're going to be associating things, guys, with your long QTs. right? Drugs that can cause long QTs are those that decrease your potassium, magnesium, and calcium ions.
We're also going to get into the drugs such as ondansetron, right? That can cause QT prolongation. All right, let's keep going.
What's this one here? Yep. VTAC.
Great. If you said VTAC, you're absolutely correct, guys. essentially those lower chambers are being too fast your qs is going to be wide bizarre independent irrespective of the p waves you can't even discern p waves it's just this messy line um look out for structural heart disease as it relates to vpac next this one guys b fib very very good V-fib is when the heart beating is not in a, the heart sequence is not in the correct order.
So V-tach is your ventricles are just going crazy. V-fib is the incorrect order in which signaling is occurring in terms of the sequence. And I want you guys to think of this one as your very, you know, fatal immediate management, right? With your CPR and defibrillation, the ventricular rate, rapid, chaotic, indiscernible.
And finally, guys, we have our congenital long QT syndrome, which the USMLE does love. And there's two phenotypes you guys need to know. That's your Romano-Ward syndrome and your D'Aurel-Lange syndrome. Okay.
Now, I think of the Roman Empire dominant. And that's why I remember Romano-Ward syndrome is the autodominant phenotype, the pure cardiac versus D'Aurel-Lange is your autorecessive, okay, which is going to present also with a sensory neural deafness. So just be on the lookout for long QT, everything greater than 440 milliseconds.
in your males and then 460 in your females. Now, to contrast that with the question, guys, because a lot of people were split between your QRS greater than 120 milliseconds versus less than. In cases when it's less than, we're going to get our narrow complex tachycardias. And guys, think about this. If your QRS is not prolonged, that means the beat, right, the electrical conduction is actually originating supraventricularly, right?
where it's normally supposed to be coming from. Okay, so I want you guys to keep that in mind. If it's originating from the ventricles, it's slower, right?
Because the ventricular rate is naturally slower than the atrial rate of depolarization. So be on the lookout for that. Again, with torsades, this is going to be a wide complex rhythm.
But let's go through the same sequence, guys. What is this one here? everyone in the chat box so it looks like afib but oh yeah i see it's a couple psts yeah that so this is actually your paroxysmal super ventricular tachycardia you have normal atrial and ventricle rhythms as you can see here but the p waves are very very um aberrant and sudden and onset and a key thing here guys is going to be you always want to attempt with this one, your Valsalva maneuver, before you just go straight into your IV adenosine.
And I just want to make a little integration here. So Valsalva maneuver, right? It's essentially like when you're straining on the toilet, imagine, you know, you're forcing air against a fixed, a closed system, like a fixed glottis, right, is what they typically say.
When it comes to Valsalva, I want you to imagine this. You're increasing, right, the pressure inside your thoracic cavity. This is going to increase the pressure on your baroreceptors.
If you increase pressure on your baroreceptors, that's going to increase your vagal tone, right? Your PNS. That's going to slow conduction through the AV node, and that's going to decrease your heart rate. So oftentimes, patients that are coming to this sudden paroxysmal supraventricular tachycardia, you're often going to attempt this vagal maneuver before you just go straight to the IV adenosine. Okay, so stay on the lookout for that.
The other integration I wanted to make, guys, here with your Valsalva is how it relates to murmurs. So what did we say the Valsalva does? Increases interthoracic pressure. If we increase our interthoracic pressure, right, this is actually going to decrease blood back to the heart, right?
Because we're compressing on, you know, your inferior vena cava, etc., the vessels that return back to the heart. So you're going to get decreased blood flow back to the heart. You get decreased blood flow back to the heart. You're going to get a decreased preload.
If you get decreased preload, then you're going to have a decreased intensities of your murmurs. Because what are murmurs, guys? Murmurs are turbulent blood flow.
If we have less amount of blood, then we're going to have decreased murmur intensity. Two exceptions, guys. You can't forget.
I want everyone to pay attention right here. So I just said, if you decrease preload, you're going to decrease the intensity of all your murmurs except two. And you need to know these two.
Mitral valve prolapse and hokum. Okay? If you know those two exceptions to the rule, you'll get all the maneuvers and murmurs down.
Okay? Also, you can remember... that right-sided murmurs increased by inspiration left-sided murmurs expiration but knowing you know which maneuvers like leg raise and squatting and all salve and all these different uh maneuvers how they relate to physiology and how they take back into the pathology of the murmurs guys super super high yield okay if you guys have any questions too more more in detailed questions i will answer those at the end we just need to uh get on with the presentation just due to time um This next one, I'll just go through quickly.
We have atrial flutter, classically your sawtooth appearance, right? Sharp zigzags. That's your rapid depolarization of your P waves.
Then here is your AFib to contrast that with paroxysmal supraventricular tachycardia, where you have an irregular rate in rhythm. So in paroxysmal supraventricular tachycardia, guys, we had a normal atrial and ventricular rhythm. In AFib, it's irregularly irregular.
So that's a way to differentiate the two. And also, guys, consider your CHADS-VAX2 score, right, your anticoagulant risk with AFib. Also, I got a question.
I believe I got a question on Step about this. Look out for your paradoxical embolisms, guys. So it's kind of like AFib and an undiagnosed atrial septal defect that only is detected later in adulthood.
You can get this paroxysmal paradoxical embolism, essentially, where it crosses. over the heart because there's still a hole in the heart essentially. So be on the lookout for that.
The presentation may not make sense to you, but then when you tie it back to the fact that they have an ASD, it does. So keep an eye out for that as well when you're going through your setting. And finally, guys, we have Wolff-Parkinson-White syndrome, which is classically associated with this delta wave. Okay.
Reminder that Wolff-Parkinson-White is this abnormal fast connection between the atria and the ventricle. This is something called the bundle of Kent. right it's a it's an accessory pathway and it bypasses the rate limiting av node okay and we get this widen qrs and shortened PR. Okay, so a very short PR interval here.
And we get this, we get a lower slope here of the upward delta wave, very, very characteristic of Wolk-Parkinson-White. Yes, the recording will be provided to everyone after. Now I want to finally tie this back into the question that we saw with our, of course, odds to point up here, right, our polymorphic tachycardia with our drug-induced QTs, long QTs. You can think of it as the A, B, C, D, E, F, okay?
In our case, we have antiemetics like ondansetron, but look out for your antiarrhythmics of class 1A or 3. Look for antibiotics like macrolides, antipsychotics, antidepressants, and antifungals like gluconazole as well, okay? Pharmacology, section five. We are just over halfway through, guys. Stay active, stay engaged.
We will be covering five more topics. Let's get into it. This is a two-year-old male with past medical history of obstructive sleep apnea and congestive heart failure.
His last ejection fracture was 40%, presents to his cardiologist's office with two days of palpitation. An EKG demonstrates a soft appearance, violence consistent with rapid atrial depolarization. What did we say that was?
Atrial flooding. Intravenous pharmacotherapy is initiated with a drug that acts on myocardial cells and is known to decrease the slope of phase 0 and 4, as well as prolong the root polarization time of the cardiac pacemaker action potential. the patient was likely treated with which of the following drugs everyone in the chat box when you're ready what do we think here seeing lots of d's guys phase zero and four of the action potential so zero as well and four what okay I'm getting a bit of mixed answers now. This is going to be a good one to go through.
I'm getting some mixed answers. That's okay. We're about to go through this. So the answer is actually guys, a verapamil.
We will go through this. I'll come back to all the answer choices and make sure you guys all understand this. Now guys, the key here is to understand our pacemaker action potential. This doesn't look like our action potential, right?
For a ventricular or myocardium, right? These ones have pace. they skip phase one and two.
There's just three phases here. Phase four, which is your funny current. So you remember funny current with phase four. It's characterized by this unstable resting membrane potential. And guys, we're going to go through all these channels here.
So we have our sodium channels here in red. We have our calcium type T here and our calcium type L in blue. We have our potassium up here. Let's go through this one by one and understand phase four and zero.
So the drug acted on phase four and zero. And so that means it has to somehow affect, you know, calcium, of course, is probably the most likely one because these are the ones that the channels that are engaged with both phase four and zero. Amiodarone affects your potassium, right?
But that's only up here. So let's go into this. So as I mentioned, guys, your funny current, your phase four is going to be characterized by this unstable resting membrane potential. You get a mixed influx of sodium.
and your T-type calcium channels, okay? Next is what's going to happen with this upstroke, right? We're going to get this rapid opening of L-type calcium channels influx, right?
Remember L for later because your L-type comes after the T-type, okay? And you're going to get this upstroke, and we're going to get this depolarization, crosses the threshold, and finally, we're going to get this repolarization, right? Potassium channels are going to activate, and they are going to efflux. and you're going to get this, you're just going to come back down to the resting membrane potential, and then you're going to get the cycle over and over and over.
Now, I want you guys to understand this is how it's implicated with our antiarrhythmic drugs. So what did we talk about with our calcium channel blockers, which is our verapamil, right? So let's go through this.
This is our regular one here. And phase four, which we said is here, is going to be decreased in terms of its slope. And then phase zero is also going to be...
prolonged okay so this calcium channel blockers they're going to affect phase four and zero that's something you need to know um they prolong repolarization that makes sense because our atrium is just going crazy we want to slow it down and so calcium channels are going to be uh very first line in that case what i want you guys to understand as well though is that your your calcium channel blockers right your non-dehydropyramidines these are actually going to be negative ionotropes which means that they're going to actually be really really bad heart failure so in in patients with systolic heart failure in particular these are contraindicated And just stay on the lookout guys, when you're doing cardiac pharmacology for your negative ionotropes, because those are always ones you're not going to want to select when it comes to first line treatments. Now, there's a fun naming rule. We said class four here, right?
Deltiazam with an I and V, to remember just how Deltiazam and Verapamil, reminded these directly affect the myocardium. We can contrast that to something like your dihydropyrmidines, right? Those are your dipene suffix.
that's going to also have effects on your vascular smooth muscle. Now, if we contrast that, right, I think a 10 of law was on that last slide for beta blockers. Your class two beta blockers, right, these are only going to decrease the slope of phase four depolarization, which is right here.
They're not going to affect phase zero at all. Beta blockers, guys, they're going to decrease your heart rate, and they're going to decrease contractility, right? A naming rule that everyone probably knows from my videos is... that cardio-selected beta blockers, right, they have beta-1 receptor activity in the heart, one heart, beta-1, is going to be your naming of A to N, right, perpanolol, etc.
O to Z is going to be non-selective, meaning that they also have beta-2 effects, such as perpanolol. If it doesn't have the classic olol suffix, so if it has alol or ilol, like carbadolol or labetalol, okay, these also have alpha antagonism, okay, so they're not selective. the only exception to this entire rule so if you just know these three rules you'll get it down pat with one exception and that is that natalol is non-selective so we said a to n right is going to be cardio selective the only exception guys natal so i hope you guys uh understand that there your pacemaker action potential and your and your myocardial action potential guys is different make sure you guys can look at both side by side and see the difference reminder that your class one and class three drugs, right? So your class one A, B, C, and urinics, and then your class three, such as amiodarone, digoxin, right?
Those are going to work on your myocardial action potential, okay? Not your pacemaker. That's why the correct answer here, guys, was the class four.
Now we're moving on to hypertension. 58-year-old female with a history of type two diabetes and hypertension presents to her primary care physician for a has been consistently elevated and today her bp reading was 160 over 95. lab and lab investigations reveal elevated serum creatinine levels consistent with stage 3 chronic kidney disease the physician decides to initiate antihypertensive therapy to manage her blood pressure which of the following antihypertensive medications is the most appropriate first-line choice for this patient everyone in the chat box i want everyone putting their answers in guys getting lots of a's some e's ease okay so we're getting a mixed but i'm getting lots of e's and a's the answer is actually going to be e um now here guys it's really important that yeah really really good marjana ace and arbs for type 2 diabetes are actually going to these are the ones that have been shown to have some renal protective effect and they can actually help slow the progression of chronic kidney disease. All the other options, guys, would be reasonable second lines, but remember that your ACE and ARBs are going to be first line, okay, in the setting of chronic kidney disease and slowing that progression. Okay, this is something you guys just need to know.
Now, I wanted to integrate the renin-angiotensin-aldosterone system here for a second because it's really, really high yield and understanding both the action of... um your ace inhibitors and arbs ties really really nicely into this so angiotensin we know is a protein that's made from the liver what's going to happen is renin from the kidneys right is going to convert angiotensin to angiotensin one angiotensin one is going to be converted to angiotensin two via the ace enzyme from the lungs ace is also going to have effect on breaking down something called bradykinin into its inactive peptides we're going to come back to this angiotensin two is going to act on the angiotensin one receptor and that's going to cause vasoconstriction aldosterone production salt and water retention all the things that we'd expect angiotensin to do okay now here's the integration guys what kind of drugs are going to block our at1 receptors that's our arbs we just went over these these are our sartans remember the sartan stuffings okay these are going to have very similar clinical indications as our ace inhibitors but be on the lookout guys these ones don't have a cough okay And so. A stem or vignette might give you a patient that has been on an ACE inhibitor, is experiencing this cough, and it might ask you which one to change to, and it would be an R because they are similar in their indications as well as their mechanisms.
The only difference, of course, is the cough. And why? We're going to come back to Bradykinin in a second. ACE inhibitors are going to inhibit ACE.
These are our PRILs. These are first line of patients with hypertension and heart failure, and then... guys, look right here, answer to our question, patients with hypertension, diabetes, protects against diabetic neuropathy, there wasn't an ACE inhibitor there, but there wasn't ARBs there, and again, they have the same clinical indication, okay?
Now, the side effects of our ACE inhibitors are really, really high yield, guys, and we're going to come back to cough and angioedema because that's related to bradykinin, but remember that these are teratogenic. How are these teratogenic, guys? Remember renal dysgenesis, remember ELO.
legal hygeminos, right? They affect the renal systems. Other things you can get, proteinuria, renal impairment, as we just mentioned, itching, low BP. Let's come back to cough and angioedema here. So if we block our ACE enzyme, right, we're decreasing the conversion of angiotensin 1 to 2. So we're going to get more angiotensin 1. But we're also blocking the conversion of bradykinin to its inactive peptides.
And I want you guys to understand two important integrations here, okay? Bradykinin. is actually going to be a peptide, okay, that induces sensitization of our airway sensory nerves, okay, via our adapting stretch receptors and our C fibers, okay?
They release neurokinin A and substance P. This is going to cause smooth muscles to constrict, and it's going to cause bronchoconstriction, which is why we get this classic cough with our ACE inhibitors. Now, the second fold, guys, is that bradykinin is also going to cause edema. Okay. In a, in a very, very similar mechanism, guys, this is going to cause swelling and edema through your substance P and your neurokinin A, which is why you can get both the cough and angioedema.
Now on the USMLE guys, I want you to be able to differentiate hereditary angioedema and ACE inhibitor induced, uh, and, uh, yeah, ACE inhibitor induced essentially, uh, angioedema. So hereditary angioedema guys reminder is going to be a defect in your C1 complement protein. Okay.
Now, this can be triggered. Hereditary angioedema can actually be triggered by someone who takes ACE inhibitors, because what you're doing is you're increasing bradykinin and its effects. And because you don't have the complement C1 pathway, you're going to be more susceptible to the effects of bradykinin.
Okay. Now, on the topic of complement, I just want to do one more quick integration here. Remember, guys, so complement, we said C1 is going to be decreased, defective, right, in our hereditary angioedema. Now in post-structococcal glomerulonephritis, we're going all the way to renal for a second.
Reminder, that's your type 3 hypersensitivity. I want you to remember the threes. C3, our complement 3 protein, is low in PSGN, and it's a type 3 hypersensitivity.
Okay? This is because in PSGN, we get a selective activation of our alternate pathway. Our alternate pathway, again, guys, our C3 is implicated.
So things like C4 and the other complement proteins in PSGN are normal. That's because, guys, the classical and lectin pathway... are not implicated in PSGN.
So PSGN, guys, high 3 hypersensitivity, C3 low, because you get selective activation of your alternate pathway. Hereditary angioedema, C1 deficiency, okay? Radikinin, going to be responsible for cough, going to be responsible for swelling and angioedema, okay?
I hope everyone understood that quick integration, because it's super, super high yield. All right, quick water for me, and then we're going to move on to myocardial infarction and heart failure. So, 62-year-old male, history of hypertension and smoking presents to the emergency department one week after experiencing a myocardial infarction. He complains of dyspnea, on-exertion empathy, on auscultation, a holosystolic murmur is heard at the apex, radiating to the axilla, and coarse crackles are heard over the bilateral lung fields.
Which of the following complications is most likely to have occurred as a result of this recent myocardial infarction? Everyone stay active, stay engaged. We are getting towards the end here.
Everyone put... their answers in the chat box please we've got 150 of you guys which is absolutely amazing if you're saying d i'm seeing lots of d's yep you're absolutely correct yeah if you're saying d you're absolutely correct here we have a papillary muscle rupture now we're going to be doing this active recall oh we're going to be doing this active recall um little thing here. What I'm going to get you guys to do is I have macroscopic findings on the left-hand side, and I have microscopic on the right-hand side.
And we're going to have our timeline, our post-MI timeline from zero to 24 hours, all the way to two plus weeks post-MI. Okay. I want you guys to tell me what are the macroscopic and microscopic findings we're going to see throughout this timeline.
So macroscopic, what can we expect to find guys in the first 24 hours? Everyone in the chat box. Yep.
If you said ventricular arrhythmia, you're absolutely correct. And this is actually, guys, going to be the most common cause of death post-MI. And it's within the first 24 hours. Look out for an SVT, cardiogenic shock. This is going to be your most common complication and death in post-MI patients.
Okay. Now, what about our microscopic findings, guys? Tell me about those. What's going to happen in your first 24 hours?
So we're not going to get, yes, yes. So neutrophils, not yet, but coagulant necrosis and reperfusion injury, yes. Okay. So in our first four hours, yeah, in your first four hours, you can actually see nothing or you can get these wavy fibers and then you're going to start getting this coagulant necrosis, right? Keep in mind, guys, reperfusion injury, right?
That's super high yield here. When your, when your cells dies, when your mild. Cardio cells die. They're going to release calcium This is gonna cause myosin and acting to stay stuck in bound on each bound on to each other, right? So there's this contraction state, right?
You can get something called a contraction bandic process So look out for that, but you guys are absolutely correct when it comes to your issue is most Susceptible to reperfusion injury right the superoxide radicals As well as you're gonna get that initial coagula necrosis and the loss of the loss of nuclei. Okay, what about One to three days. Microscopic. Everyone in the chat box, what can we expect to find? One to three days.
Post MI macroscopically. Yes. Really, really good. If you guys both, I see, I saw both post-infarction fibrinous pericarditis and I saw papillary muscle rupture, which is what we saw in our question, guys. Our papillary muscles, right, those are responsible for holding our leaflets of our mitral valve together, essentially.
If we get a rupture of those, right, then we get these floppy mitral valves and mitral leaflets that's going to cause this severe mitral regurgitation, which can lead to shock and pulmonary edema. Okay? And reminder, guys, that our posterior medial rupture is most common, and that is supplied by the PDA.
Now, what about microscopically, guys? What are we going to find one to three days post-MI? Now... we have neutrophils.
Exactly. One day you can think neutrophils. Okay. Neutrophils are coming in.
These are our first innate cells to action. Okay. Now let's move on. Three to 13 days.
What is going to happen macroscopically? Really, really good. If you're putting free wall rupture.
Yep. You're absolutely correct, guys. And things like a cardiac tamponade, right? When you get a complete rupture of and this is when your structural changes are going to be most common guys right it's now been three to thirteen days and you're you're attend essentially the whole wall is is uh prone and susceptible and so look out for signs of tamponade when do the free wall rupture that's the highest tested one there and then what about microscopically what can we expect to find macrophage good and you can think of it like this guys one day neutrophil one week macrophage okay is a good approximation of when that happens.
And we're going to start getting this loose collagen deposition. Now, finally, guys, two weeks post to months, what are we going to get macroscopically? Yes, Dressler, very, very good. Yeah.
So you can get a true ventricular arrhythmia, really good athera, as well as your Dressler syndrome. So guys, contrast the two of these. Post-infarction fibrin is pericarditis.
You're going to get that. pleural rub, right? Your classic signs of pericarditis, chest pain, pleuritic chest pain, but that's going to happen very shortly after the MI.
If you contrast that to something like weeks to months after, this is actually an autoimmune-mediated process with Dressler syndrome. And look out specifically, guys, for your persistent low-grade fever for Dressler syndrome. That's going to be the way to differentiate post-infarction fibrinus pericarditis from Dressler, is your persistent low-grade fever.
Okay, guys? And finally, two weeks post, I think I saw a couple people put it in there. you're going to get your contracted scar, right?
Collagen, fibrin deposition, really, really good. If you said scar, fibrin, yep, really, really great, everyone. So we're going to move on to our next question.
Everyone, stay active, stay engaged. We're almost to the end. 45-year-old male presents with progressive dyspnea on exertion and fatigue over the past several months. His medical history is significant for alcohol abuse. An echo demonstrates global left ventricular dilation and systolic dysfunction with an ejection fraction of 25%.
Which of the following clinical findings would not be associated with this patient's clinical condition? Which of the findings would not be associated, everyone? When you guys are ready, put your answers in the chat box and we will go through this one.
So we're getting a mixture of D's and E's and often confused, which is completely to see all the time, but that's okay. We would not expect to see an S4 sound because your S4 sound, guys, is more implicated with something like A, your stenosis, a problem with ventricular compliance, right? Your S3 is going to be your filling problems, like a dilated cardiomyopathy. but we're going to get into that, okay?
We're going to come back and do a full breakdown on S3 and S4 right now. So in that patient, right, we said they would expect to see an S3 sound, but we wouldn't expect to see a S4 sound. Well, that was a classic presentation of a dilated cardiomyopathy, which was triggered by chronic alcohol use, which is one of the secondary causes of dilated cardiomyopathy.
But I want to first understand the physiology between dilated and hypertrophic cardiomyopathy, because that's going to help us understand our S3 versus our S4 sound, okay? So in states of volume overload, okay, we're going to get this eccentric hypertrophy, right? Our sarcomeres are added in series. The S3 sound, I always, this is super easy, guys, just remember these little tricks in your head, they will help for testing.
S3 has three syllables, heart failure, and you'll see with S4, hypertension is four syllables, to help you remember. it's something like heart failure right this volume overload state you're gonna get this s3 this s3 is this rapid ventricle filling right it happens in early diastole okay and e looks like three if you want to remember that one that happens early diastole if we contrast to s4 that's something due to ventricular compliance right reduced ventricular compliance that's going to happen in late diastole okay but we're going to first go through dilated cardiomyopathy because that's what we saw in our patient we're going to look out for signs of heart failure with volume overload in the systolic dysfunction right we saw that ejection fraction be severely reduced there this is either idiopathic or there are family um association and links to the ttn gene which is a sarcomeric protein the titan gene okay clinical findings we're going to expect to see the s3 systolic regurgitation murmur and classically this balloon-shaped heart all the vests all the ventricles right are dilated thin walls expanded and weak Um, you can expect to see this really, really big art on, on x-ray this, this, uh, classic balloon appearance that they call. Okay. Now, if we contrast that to an S4 sound, which we were briefly talking about, you can remember S4 with four syllables, hypertension, pressure overload. What is pressure overload going to do?
That's going to cause our, our myocardium to add in a parallel fashion, pressure parallel. Okay. So we're going to cause a stiff non-compliant ventricle.
It's going to. it's going to create this s4 sound happening in late diastole okay i want you guys to think of ari stenosis i want you to think of things like hokum i want you to think of things like cortication of the aorta infiltrative diseases like amyloidosis right apple green refringens um these are just buzzy words and associations to keep in your head but that's all s4 s3 that we just talked about you're going to be thinking what dilated cardiomyopathy you're going to be thinking what micro regurgitation okay with your s3 gallop So hypertrophic, as we said, we're going to get this really stiff, non-compliant ventricle. We've talked about this. I want you guys to make the association with a young athlete, sudden death, family history of sudden death, you know, from the ages of the teens to 20s, early 20s.
Hypertrophic cardiomyopathy. Keep that in mind, guys. Very, very strong familial autodominant link with the myosin protein, right?
The S and B myosin proteins. And then as we said here, guys, we're going to get this S4 sound. And We want to keep in mind those associations, okay?
Now, cardiac microbiology. Everyone's favorite, I'm sure. We have two sessions left, and then we are going to end this off with our giveaways.
So stay tuned for that. Stay active for these last two questions, okay, guys? 45-year-old male with a history of mitral valve prolapse presents the urgent care center with fever, chills, and rallies. reports undergoing a dental procedure and coloscopy two weeks ago. On exam, the patient has a diastolic murmur, best appreciated at the apex, blood cultures are obtained, and empiric antibiotic therapies initiated, results from peripheral blood cultures are taken from this patient, and they'll most likely show which of the following findings.
So this is really integrating, guys, our microbiome here. What do we expect to see? Fawad, Andrew, Neha, Renad, Amar. Really, really great, guys, if you are putting B.
And I think I saw someone put streptococcus viridans, which is absolutely correct. And that's going to be your gram-positive alpha-hemolytic optogen-resistant cocci. Now, just a little point, guys.
The USMLE will often not just test straight up, you know, strep viridans, group A strep, strep bovis, you know, staph aureus, etc. They will put what you can expect to find on peripheral smear, and they expect you to know that. So. this is this is a really really easy way that they test this and so make sure to just have that um kind of flow chart and your alpha beta and gamma hemolytics all straight okay that's just something you need to row memorize for this exam there's great sketchy things my guide my guide hopefully helps as well i'm gonna i'm gonna put a slide after this um that you guys can come back to but just going through them right um this first one here step pneumo we got strep beard ends here uh c is our group race trap D is our epidermis, right?
Think of prosthetic heart valves. And then E is going to be, that's not associated with endocarditis. So let's go through the gram-positive classification system. Let's spread it up between strepto and staphylococcus, okay?
We were on this side of the flow chart. You have your alpha, beta, and gamma. We went down this chart, right? We said it was alpha, and we said it was optogen-resistant, and that's our viridans, okay?
I put these little key buzzwords down here, guys, to help you remember. So again, if you're a veer dance, you want to think dental procedures. Strep pyogenes, think rheumatic fever in the setting of renal disease, right?
Think of post-streptococcal glomerulonephritis, right? Remember, we came back to that one, type 3 hypersensitivity, low C3, normal C4. I said that. Strep agalacticae, right? Think in your newborns, neonatal sepsis, pneumonia, right?
Non-enterococcus species is going to be related to your strep. bovies and your colon cancer or current gigu procedures thinking of your anterococci this is going to be differentiated by whether they grow in uh 6.5 sodium chloride right and then on our staphylococcus side we divide it further into coagulates positive and coagulates negative remember staphylococcus classically with our injection iv drug use affects our tricuspid valve don't try drugs everyone try with your uh effects drugs affect your tricuspid valves um Staph epidermis, we said, was our prosthetic heart valve. So look out for a patient with severe or chronic aortic stenosis, recently got a heart valve. Staph epi likes to colonize there.
And saprosidicus is more related to female UTI. All right. Really, really good, guys, for those of you who put this viridans one, alpha hemolytic, optogen resistant. But let's move on to something.
high to rheumatic fever and rheumatic heart disease because it's super super high yield and we're going to remember the mnemonic the mighty disease i want you to think of the m's okay there's a lot of m's here but first it's understand the sequelae the rheumatic fever classically going to present in a kid often in a developing country right where they don't have access to certain vaccines etc two to three weeks post group a strep infection you're going to classically see your jones criteria right joint heart nodules erythema marginatum and your sydenham choria, your involuntary movements. I want you guys to look out for increased anti-structolysin O and your anti-DNA ACE B, and as well as characteristic Ashoff bodies. Okay, this granuloma with a giant cell, super, super high yield. Okay, now untreated rheumatic fever or chronic rheumatic fever or chronic recurrent bouts of rheumatic fever can really lead to something called rheumatic heart disease.
And this has a tendency, and I remember coming back to the B. right? Coming back, sorry, to the M with the mighty disease. I want you to remember that it affects the mitral valve, okay?
It is caused due to a type 2 hypersensitivity due to molecular mimicry, which is the antibodies to that M protein that cross reacts with your self antigens, okay? So remember the mighty disease because it affects the mitral valve early, you're going to get regurg, late you're going to get stenosis, you're going to get this commissure of fissures, right? In terms of that fish mouth appearance of that valve due to the autoantibodies too.
the M protein, okay? Molecular memory is the pathogenesis there. And I briefly touched on the Jones criteria for your rheumatic fever.
That's going to help you remember joint manifestations, apart with your pancarditis, nodules, erythema marginatum, which is that rash with a ring margin, and then your sydney hemorrhoea, guys, involuntary rapid movements. If you see any of this, think of your rheumatic fever. Now, in the chat box, everyone, what is going to be your first-line treatment for rheumatic fever? And we definitely want to treat group A strep, pharyngitis, and skin infections.
very, very promptly because we don't want it to progress to a rheumatic heart disease. Exactly. Penicillin V. Yeah.
Penicillin is absolutely correct. Yes. Really, really good.
Yeah. And from Jane, you can use the from Jane as well. Yeah. That's another one. Yeah, exactly.
Penicillin G. Yeah. Very, very great. So I want to move on now to shock. This is our last part of the the presentation so we're almost there um stay active stay engaged we're going to be doing the giveaway and we are going to get this down pat all right this is really really important guys because it integrates lots of physiology so 35 year old female presents the emergency department with acute onset dyspnea urticaria and hypotension shortly after receiving iv antibody on examination she appears anxious with diffused wheezing and widespread hives her blood pressure is 80 over 50 heart rate is 130 and respirate is 28 beats per minute which is the following sets of physiologic measures would be expected in this patient last question everyone let's end it off strong i want to see all i want to see every single person on the stream put in their answer here there's no wrong answer today Okay, I'm getting mixed.
I'm getting lots of B's and D's. If you said D, you're absolutely correct. And guys, we're going to slowly go through this one by one. This is probably the most important slide in this presentation. So everyone pay attention.
Okay. All right. So when it comes to shock on the USMLE, you're going to want to first identify the low hanging fruit.
What does that mean? What is the primary physiological disturbance in these types of shock? Okay.
So Let's understand some variables first, okay? Pulmonary capillary wedge pressure, right, is going to be a proxy for your left atrial pressure. That is super, super high yield, guys. Our PCWP, okay, i.e. our heart preload, the left side of our heart, right, is going to be a proxy for our left atrial pressure. Our mixed venous content, guys, is going to be related to oxygen extraction.
So you've probably seen SVO2, right? This is your mixed venous oxygen content. And I want you guys to really, really understand this concept because it's going to help us go through the chart, okay? In settings of shock, there's increased metabolic demand, right? The tissues are frantically wanting oxygen.
They're trying to uptake oxygen as fast as possible, right? Think about it. At the tissue level, if our tissues are busy extracting as much oxygen as possible, right? Then that means that the venous blood coming back is going to have a lower oxygen saturation, right?
And so I want you to understand that... SVO2, okay, and O2 extraction are inversely related. Meaning in settings of shock, when we have high oxygen extraction, right?
We are gonna have a low SVO2 because our tissues are taking all that oxygen away so that that venous blood coming back is gonna have a low O2 percentage, okay? I hope you guys understand that because that's an easy, easy way to make sure that you guys get these questions on your step exams, okay? So make sure you understand SVO2 and...
pulmonary capillary wedge pressure as a proxy for left atrial pressure, okay? Now, what we're going to do, guys, we're going to do a little exercise. I'm going to have the type of shock, and we're going to go through the arrows, okay? So, hypovolemic shock, classically due to hemorrhage, dehydration, burns, trauma, right?
What is going to be our primary variable affected out of these ones here? Primary disturbance, guys. Absolutely correct if you said...
if you say cardiac output you are also correct but your pcwp is directly going to be linked to that cardiac output of course so think of you're going to have low right you're going to have a low preload because there's going to be less blood available if you have low preload right left left atrial pressure with our with our pulmonary capillary red pressure what we're going to see we're going to see a low cardiac output as well right low preload low cardiac output now In settings of low perfusion, guys, what do our vessels do? They clamp down, and we're going to increase our systemic vascular resistance. Our afterload, guys, is a measure of our systemic vascular resistance. So we're going to expect, right, that our afterload is going to increase, okay? Because again, vessels clamp down in settings of low perfusion, increase systemic vascular resistance.
If we have increased resistance to flow, we're going to have increased afterload. Now, guys. i want everyone in the chat box if you guys were just listening to what i said about mixed venus content here what could we expect our mixed venus content or svo2 to be here is it gonna be high or is it gonna be low very very very good everyone you guys are all listening if you said low again settings are shock guys we're gonna have it we're gonna have all that o2 extraction right high metabolic demand our tissues are gonna demand that oxygen extract that oxygen less o2 saturation venous saturation through the heart so we're gonna have low very good you guys all paid attention let's move on cardiogenic shock myocardial infarction heart failure arrhythmias left heart dysfunction guys what's our low hanging fruit here cardiac output everyone is staying engaged amazing yes so our heart's not pumping properly right low cardiac output low cardiac output what's that going to cause guys we're going to cause that to back up in the left atrium We're not pumping out blood forward, you know, back up in the left atrium.
What did we say our PCWP is? It's a proxy of our left atrial pressure. That's going to go up, right guys?
Again, in the same sense, our vessels are going to clamp down in low perfusion states. Our SVR is going to increase and we're going to have an increased afterload. And you guys got this concept down.
Our SVO2 is going to be low. Now, distributive shock, anaphylaxis, sepsis, right? This is what we saw in our vignette that we just saw, right? The hypotension, the wheezing.
Um, look out for other signs of atopic features, right? Um, very, very good. I want you guys to tell me what is the low hanging fruit here? Afterload. Exactly.
Systemic vascular resistance. You guys are absolutely correct. If you said that we're going to get a severely decreased afterload. Keep in mind, guys, let's talk about the two. We have septic shock and we have anaphylactic shock and septic shock.
It's our cytokine mediated, right? Our cytokines like IL-6, IL-1, PNF-alpha, right? These are going to cause a rapid vasodilation systemically, right?
Decreasing our systemic vascular resistance, decreasing after them, okay? This low systemic vascular resistance, guys, is actually going to trigger our heart to start pumping. You know, it's going to trigger it to start pumping as much as it can. And we can actually get something called high output cardiac failure, okay? And so we're going to get essentially...
Our body needs the blood. Our body wants the blood. It demands the blood.
So our heart is going to sense that. And it's just going to pump everything out from the heart. And it's going to cause this high output cardiac failure. Okay.
And so we're going to expect to see a really, really high cardiac output. Our preload is going to be, our PCWP is going to be lower, of course, because we're pushing so much through the forward. Okay. Now, guys, if you guys, if you guys are listening.
You might be able to answer this next part with the SVO2 here, but it is a little bit of a complicated mechanism. Do you guys want to guess what our SVO2 is going to be here? Amara's saying hi.
Benny's saying hi. Really, really great if you are saying hi. Let's understand this, guys.
Okay? Everyone stay with me. We're just to the end here.
If you have a high output cardiac failure, right, you are putting so much perfusion from the arterial capillary vein. uh interface right that your tissues don't even have time to extract the oxygen so because we're pumping so much right and your your oxygen your your tissues don't even have time to extract this oxygen well what did we say seo2 is directly related to o2 extraction so we have left extraction because it's just pumping so fast through it right we're gonna have an increased mixed venous oxygen saturation coming back to the heart okay so you guys got that really really down really high yield to understand those integrations We talked about septic shock. In our case, we saw an anaphylactic shock right to the IV antibiotic.
Keep in mind that's a type 1 hypersensitivity, right, guys? IgE mediated, mast cell degranulation, right? That's going to cause the same profile that you see here. And the edema, and specifically with the anaphylaxis, is going to make that O2 extraction difficult. So the edema, right, too much fluid in that interface is going to cause...
um difficulties with extraction and cause an increased mixed venous content now finally guys i wanted to end off with something called cardiac tamponade which is a form of obstructive shock But most importantly, guys, I want you to think about this for a second, okay? Cardiac tamponade, as we mentioned, and I this back into a concept we were talking about with our free wall rupture, right? Our structural change post MI, right? In that three to 13 day mark, we're going to see three common features, an increased JVP, muffled heart sounds, right?
And hypotension. So I want you guys to imagine a bunch of fluid around our heart. Imagine in the pericardial sac, right guys?
we would have this non-compliant heart. If fluid is surrounding the heart, it can't pump, it can't fill properly, we are getting a non-compliant heart. And if we can't expand during diastole, right, then our end diastolic volume is actually decreasing, okay? Remember we talked about end diastolic volume and end systolic volume?
Well, if there's a bunch of fluid, imagine just a bunch of fluid around the heart, it can't expand fully. So it's not gonna blow up with volume as much. It's not gonna fill up with volume as much.
So our end diastolic volume is actually gonna decrease. Our stroke volume is hence gonna decrease. and our blood pressure is going to decrease. And that's where there's a really important integration, guys, pulsus eridoxus. And that is a greater than 10 millimeters of mercury decrease in your blood pressure, okay?
Now, let's understand this physiology, and we're going to end it off on this note, okay? So in normal conditions, right, guys, when you inspire, your diaphragm pushes down, your lung volume increases, and your intrathoracic pressure decreases. This causes that negative pressure, right, to increase venous return.
and increase right ventricular filling. In tamponade, right, we're going to have a backup and more blood coming into the right atrium, right, which is going to put more blood into the right ventricle. Now, we said, what does the right ventricle want to do? It wants to expand. But there's fluid in the sac, so it can't expand.
So what does it do, guys? The right ventricle can't expand outwards because there's fluid around it. So it actually expands inwards and compresses the left ventricle, okay?
It expands immediately to the septum. and actually using a compressed left side of the heart. This is going to decrease your left ventricular volume.
And this is why we see this exaggerated decrease in blood pressure drop, guys, with Paul says paradoxes. So my goal, guys, to explain all these mechanisms is not just to memorize this stuff, but to actually understand it. Because once you understand it, it should become so much more easy. And it's not just you going through a thousand tedious Anki cards where you're not, you know, thinking. And it just, you know, you forget it the next day.
When you actually understand the pathophysiology or the mechanisms behind this stuff, guys, this is the way to learn. This is the way to integrate. This is the way to instill all these things into your long-term memory, okay? And classically, guys, I want you to look out for this QRS alterends, which is this alternating, essentially, amplitude of your QRS complexes on ECG, because they could also give you that. So with that being said, guys, we have reached the end of the presentation.
Thank you guys so much for all being so active and engaged. Sorry about a little bit of the mix up in the beginning. We will be posting this recording again, scan this QR code to be entered for cardiology giveaway.
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Peace out, everyone.