DIP Episode 5 - Cardiology A (Physiology)

Okay, welcome. My name is Devine, I'm a fourth-year medical student. Welcome to a fifth episode of Divine Intervention. Today we're going to be talking about cardiac physiology and basically my goal today is to use different scenarios to describe cardiovascular physiology concepts. Your board exams classically love to test these in the context of analysis questions where they give you like a scenario and either give you like arrows or give you a scenario and give you like answers, right? And you have to reason through your understanding of the physiology to get at, to correctly answer many of these questions. So the goal today is to spend some time going over some common scenarios to buttress certain cardiovascular-fist concepts. And as I go through the scenarios, I will spend some time going over like whatever equations underlie whatever is going on. Okay? And as we go along, we potentially have other cardiovascular physiology podcasts. And if you spot any errors or you have any questions, feel free to reach out at divineinterventionpodcasts at gmail.com and I will try to put you through fairly quickly. Thank you. So slide 1 A. So where cardiac valves hurt best? This one's pretty easy. Okay? There are many nomonics that lie out there. There's like a department M and all physicians take money or whatever floats your boats. But basically the thing you should think about is the A in a department M stands for your eortic valves. You hear that right-oppersonal border.

The P stands for your pomonic valves. You hear that at your left upper sternal border. The T stands for your tricospit valves. You hear those best at the left lowest sternal border. And then the M stands for your mitral valve. You hear that best at the Apex. The Apex is defined as being in the fifth intercostal space in the mid-clavicular line. Okay? So where hurt murmurs hurt best? In general, heart murmurs mirror where the valves are hurt best. So most mitral murmurs are hurt best at the apex of the heart. Many eortic murmurs like eortic stenosis is hurt best in the right-oppersonal border. Many tried cross-speed murmurs are hurt best in the left-low sternal border. Some exceptions to those roads. And I'll sort of give you some background for this. In fact, I guess I'll just give two examples like eortic regearge and eortic stenosis like what they heard at the specific locations to sort of give you again some context for understanding this. But one thing I will say is eortic regearge. In fact, let me just let me talk about my reasoning first. So if we think about this, the left ventricle is on the left, right? It's on the left side of the heart. And the order takes off from the left ventricle. If you sort of think of it anatomically, it takes off from the left ventricle and goes right toward in the thoracic cavity. So a forward-floin murmur in the eortic valve like eortic stenosis, for example, should also flow right or it.

That is why eortic stenosis is hurt best in the right-opper sternal border. On the flip side, if you have a backward-floin murmur through the eortic valve, that murmurs that back-flove blood is from the from the order, right? Which takes off to the right back to the left ventricle. So that regurgitant murmur is heading backwards from the right side of the thoracic cavity to the left side of the thoracic cavity. That is why eortic regurgitation is hurt best at the left sternal border, okay? At the left sternal border. Like, think of it as more of the left-low sternal border. That's also where you hear hypertrophic cardiomyopathy pretty well. So the next question says a discussion of preload and afterload reducing manoeuvres, right? So talk about manoeuvres that increase preload and decrease preload and manoeuvres that increase afterload and decrease afterload. The preload increase in manoeuvres that commonly shop on exams are inspiration, right? So if you inspire, you decrease in throthoracic cavity, that increases venous return, okay? So a decrease in intra-thoracic cavity increases venous return. Another thing that could accomplish the same goal is squatting. When you squat, you compress, you cause venoconstriction and that venoconstriction. Remember your veins are capacitance vessels, so the hang on to blood, so when you venoconstrict, you increase venous return as well because you are decreasing the capacitance of your veins.

And we'll see some more things about that in the later slide. Another thing that could accomplish the same purpose is leg raise. When you raise your leg, excuse me, when you raise your leg, you again send more blood back to your back to the right side so those are preload increasing manoeuvres. Now, the big preload decrease maneuver you want to know is the valve solver maneuver. So in the valve solver maneuver, you basically close your mouth and try to blow out air, okay? That increases the intra-thoracic pressure because your pressure is building up because the air has no way to go because you're basically closed off your airway. And if intra-thoracic pressures go up, your venous return goes down because the pressure is in your right each arm increase. Normally the pressure in your right each arm is like zero. So if that pressure goes up a few points, then that gradient that encourages blood to flow from your veins back to your right each arm decreases. So let's assume the pressure in your veins are like 15 and the normal pressure in your right each arm is zero. But for some bizarre reason, you perform a valve solver maneuver and the right each arm pressure becomes five. That gradient goes from 15 to 10. And if you have a lower pressure gradient, if you're thinking about one of the laws we're going to talk about in a bit, a decreasing pressure gradient decreases flow. So the venous return actually goes down on that those are circumstances.

Now, the afterload increase in maneuver, the big one I'm going to mention here is hand grip, so when you shake a person really hard for some bizarre reason, you're basically clamping down on the radial arteries. For example, if you clamp down on the radial arteries, that decreases the radius when the radius goes down, the total preferred resistance goes up. So that increase in total preferred resistance increases the afterload. And if the afterload increases, we have certain implications that we'll talk about shortly. And then the big afterload decrease in maneuver, almost going to mention here is the administration of immunitrate. So immunitrate is a very powerful arterial dilator. And when you dilate your arterials, the venous rate, the afterload goes down, and the afterload goes down, you can sort of begin to imagine that drainage of the left ventricle would increase. So now that we've talked about those different maneuvers and the pathophysiology behind each, let's talk about the effect of these maneuvers and murmuring densities. So this is a classic head scratcher for many people and many people just say, you know what, I'm not going to bother to reason through this. I'm just going ahead and memorize it. The only problem is there are so many intricacies to this that if you have one misstepping on memorization, then you run into a lot of serious problems.

So it's just much better to try to understand, then on an exam, you can very easily reason through these scenarios relatively quickly, because they're actually pretty easy. So there are three different kinds of murmurs. So there's stenotic murmurs. So this is the way I'm grouping them. And grouping them is either being stenotic, as being regurgitant, or as being a special case murmur. And the two special case murmurs I will talk about are the murmurs of mitral valve prolapse and hypertrophic cardiomyopathy. I think if you group these ones, if you group these murmurs like this and know like a one big room for each kind of murmur, you're good to go. So stenotic murmurs, regurgitant murmurs, and special case murmurs. So what is the big construct you want to know for a stenotic murmur? A stenotic murmur will sound louder whenever there is increased flow across the stenotic valve. So increased flow across the stenotic valve makes the murmur louder. So what are the things that could increase flow across the stenotic valve? You could increase preload, right? Because if you increase preload, there will be more blood flowing. If you're bringing more blood to the heart, obviously more blood will flow through the valve. Another thing that could also happen is if you decrease afterload. So if you decrease afterload is like you're opening the roads that are distal. So that's stenotic valve so that there's more flow.

So an increase in an increase in preload or a decrease in afterload makes a stenotic murmur sound louder. If you remember that singular concept, you can reason through whatever you know, you know the maneuvers I just talked about a few minutes ago, then you can know what would increase or decrease the loudness of a murmur of a stenotic murmur. Okay. Now for the regurgitant murmurs, the constructs, the one principle you want to remember is that anything that puts more blood in the vessel or the structure distal to the regurgitant valve will make the murmur sound louder. So what do I mean by that? For example, if a person has mitre regurgitation, the involved valve is the mitre valve. The distal vessel or structure, if you may, is the left ventricle. Anything that puts more blood in the left ventricle will make the mitre regurgitation murmur sound louder. Okay. So anything that will increase preload, right? If you increase preload, you will increase your left ventricle in the stolic volume. You're putting more blood in the left ventricle in the process of filling. Another alternative is to increase afterload. If you increase the afterload, you are decreasing drainage of the left ventricle and if you decrease drainage of the left ventricle, there will be more blood in the left ventricle. If there's more blood in the left ventricle, as the left ventricle is contracting, there will be more feet stuck if you may to go back through the regurgitant valve.

So you have worse a worse name of the regurgitation across the mitrovove. So you get a louder murmur. So that's the big construct you want to know with regards to your regurgitant murmurs. And as an aside, the thing I will say is the same rules apply for a VSD. A VSD is basically a kind of regurgitant murmur. The only difference is that the regurgitation is not across a valve, it's across a septal defect. So anything that increases preload or increases afterload, just like we said for a mitre regurgit, for example, would increase the loudness of a ventricle septal defect. Now, the special case murmurs, they're basically just examples of either stenotic murmur or regurgitant murmur with a small twist. They do not be the general rules that apply to their closed cousins, like the stenotic murmurs as you see when I talk about hypertrophic cardiomyopathy or regurgitant murmurs as you see when I talk about mitral valve prolapse. So let's talk about the stenotic murmurs, the stenotic murmur closed causing special case first. That's hypertrophic cardiomyopathy. Again, it's a stenotic murmur with a twist. The big construct you want to remember here is that anything that increases the volume of blood in the left ventricle makes the murmur of hypertrophic cardiomyopathy sound softer. Okay? Anything that increases the volume of blood in the left ventricle will make the murmur of hypertrophic cardiomyopathy sound softer. Now, what's the pathophysiology behind that?

The thing is whenever you have an increased volume of the left ventricle that pulls the anterior mitral valve leaflet away from the left ventricle outflow tract. When you pull that anterior mitral valve leaflet away, you relieve the obstruction. If you relieve the obstruction, you have easier flow. If you have easier flow, you have a softer murmur. Anything that increases preload, an increasing preload will increase your left ventricular endastolic volume. Your left ventricular volume goes up or anything that increases after load will make the murmurs softer. The murmur of hypertrophic cardiomyopathy softer. Remember that the HCM murmur is heard best at the left sternal border. Okay? If you see me say left sternal border, just think of it as a region just above the left low sternal border. Okay? Now, the other special case murmur is the mitral valve prolapse. The murmur of mitral valve prolapse is a regurgent murmur again, but it has a twist. The construct you want to keep in mind, the one central principle you want to remember is that anything that increases the amount of blood in the left ventricle will make the murmur of mitral valve prolapse softer, not louder. Okay? Remember we said for mitral regurg, other regurgitant murmurs. Anything that increases the left ventricular blood volume will make the murmur louder. That's not the case for mitral valve prolapse. It actually does in fact make the murmur softer.

And I will encourage you to look at the diagram I have in the slide that will also sort of make that mix some more sense. You basically make the valve leaflets overlap better when there is more blood in the left ventricle and with that better overlap you have less regurgitation. So anything that increases preload or decreases or increases afterload will make the murmur of mitral valve prolapse softer. Okay? And remember the association of mitral valve prolapse with like Orozomo dominant polycystic kidney disease and Marfan syndrome as well. Okay. So now that we've talked about those constructs you should be an expert on these murmur maneuvers. If you just know what murmur what maneuvers do to preload an afterload. So next slide. So how does the murmur respond? So this is just me trying to torture you a little bit more but just to really make sure you have this concept of how does the murmur responds to an afterload increase very between mitral regurgitation and mitral valve prolapse. Okay? So again if your afterload increases there will be more blood in the left ventricle. More blood in the left ventricle makes a mitral regurgitation murmur louder because there is more feedstock to regurgitate across the uh upper and valve.

But in mitral valve prolapse more blood in the left ventricle makes the murmur softer because by having more blood in the left ventricle you have better overlap of the malposition if you make the malposition mitral valve prolapse and by having better overlap you have less regurgitation. Now the next one says how does the murmur responds to a preload increase very between a erotic stenosis and hypertrophic cardiomyopathy. If you have an increase in preload you have an increase in the left ventricle and the astolic volume that will make the murmur of erotic stenosis louder because you have more blood, more turbulence across the stenotic erotic valve. On the off side that you have if on the off if you have a rather if you have an an increase in preload for hypertrophic cardiomyopathy. Again that will also increase the left ventricle and astolic volume but by having that increase in volume you basically move the anterior mitral valve lymphly that's a big buzzword you want to remember you want to remove you basically remove the anterior mitral valve lymphlet away from the left ventricle out flow tract so you relieve the obstruction so because there's no more obstruction the murmur doesn't sound as loud anymore. So an increasing preload makes the murmur of hypertrophic cardiomyopathy sound softer.

And again the descriptions of those murmurs are the same they're like systolic ejection murmur, crescendo, decretescendo pattern that is literally the description of HCM anniotic stenosis but one the response to preload can help you make that differentiation too. The region where those murmurs are heard best will also help you make that differentiation. We say that the murmur of erotic stenosis is heard best at the right upper sternal border but the murmur of hypertrophic cardiomyopathy is heard better at the left sternal border. Okay again that's region that's just above the left lower sternal border if you may.

Okay so slide two so keyword number two right so heart rate changes with hydrolyzing administration right so if a person takes hydrolyzing hydrolyzing is a powerful arterial dilator right so if you dilute the arterial so what happens to your systemic vascular resistance you should go down because remember your arterial are resistance vessels so if the SVR goes down your borrower receptors for example your borrower receptors are the cardiac sinus descents a lower blood pressure and when descents a lower blood pressure you have a decreased firing of those borrower receptors that decreased firing activates your sympathetic nervous system in the in the brain okay and as you activate that sympathetic nervous system you have a big sympathetic discharge okay so you release more neuropinephrine for example and that neuropinephrine can go and act on beta-one receptors and that will increase the chronotropy of your heart because you're increasing the speed of conduction through the AV node okay so your heart rate actually goes up when you administer hydrolyzing that's why classically to that's the concept known as a reflex stagic cardi to reduce the chances of that happening if you're giving a person hydrolyzing you could also give them a beta blocker okay like my toporolone for example to blunt the reflex stagic cardi effect you get from the borrower receptor response okay now the initial management of a relatively stable patient who has a narrow complex regular tachyritmia so if you see this buzzword narrow complex regular tachyritmia what are you thinking about well I hope you're thinking about an SVT a superventricular tachycardia okay an SVT the if a patient is relatively stable the first step in management is to do some kind of vego manoeuvre okay some kind of vego manoeuvre remember the construct I said with the first scenario I said that whenever you have decreased firi

ng of your borrower receptors that causes an activation of your sympathetic nervous system if you massage a person's carotids for example that's one kind of vego manoeuvre okay or you perform a valsalva right or remember valsalva increases intra thoracic pressures so that can also sort of compress on your carotids if you may compression of the carotids causes increased firing of your borrower receptors okay and if your borrower receptors in the carotid sinus firemer okay that will cause the decrease in the sympathetic response and then increase in the press and pathetic response that increase in the pressing pathetic response through most carinic receptors can slow down conduction through the EV node and break the super ventricular tachycardia okay and while we're on this remember there we have borrower receptors the aortic arch for example is a kind of borrower receptor okay although it's also a chemoreceptor and an easy way to remember that is just remember your AB Cs okay aortic arch that's your A has borrower receptor function that's your B and chemoreceptor function that's your C okay so ABC aortic arch borrower receptor and chemoreceptor and the chemoreceptor remember the aortic arch is outside the center nervous system so the chemoreceptors that exist in the aortic arch annunas peripheral chemoreceptors and remember that that chemoreceptor information is released through crinion of 10 you'll dig a snurf okay that's a commonly tested board concept now your carotid sinus your carotid sinus you'll find it around your carotid arteries close to the bifurcation that's primarily a borrower receptor okay in fact it's probably the more sensitive borrower receptor that we find in the body okay that's the thing that explains what the difference in areas I talked about with taking hydrolyzing or massaging the carotid vessels now your another receptor related to all this bus

iness we're talking about is the carotid body the carotid body is more chemoreceptor and an easy way to remember that is just remember like ordering a CBC so carotid body chemoreceptor CBC okay so it's a chemoreceptor and because it's more place more in the center nervous system remember the carotid spas through traverse the neck and begin to go into the head think of them as being more your actually think of those as also being peripheral chemoreceptors think of those as being peripheral chemoreceptors it so happens that they're actually central chemoreceptors in the medallas so I don't let's speak on that okay so your chemoreceptors if your pH goes down or your partial pressure of carbon dioxide goes up or your partial pressure of oxygen goes down right so again think about this if your PO2 goes down you'll become hypoxic if your hypoxic your PCO2 go up if your PCO2 goes up remember CO2 is an acid and hydride if you're thinking back to college chemistry and that CO2 dissolves in water and in your bloodstream if you may and lowers your pH so all those things indicative of hypoxia and that hypoxic response is usually usually usually followed by an increase in your parasympathetic discharge I mean sorry in your sympathetic discharge okay your sympathetic discharge and increasing your sympathetic discharge can cause like hypertension for example okay when increasing your cardiac contractility increase your heart rate and things like that so now that we understand these different receptors let's talk about the brain's response to ICP increases okay so if your intracranial pressure rises um you begin to compress on the vessels that feed the brain okay you begin to compress on your cerebral vessels and when you compress cerebral vessels the profusion of the brain begins to go down which is not ideal so what do I mean by profusion of the brain there's this equation that rel

ates the cerebral profusion pressure I believe you'll find this in the neurochapter first aid to the minaterial pressure and your intracranial pressure so your cerebral profusion pressure equals your map your minaterial pressure so basically your blood pressure minus your intracranial pressure so if you have an increase in your intracranial pressure and your minaterial pressure is staying constant your cerebral profusion pressure begins to go down you can begin to run into trouble like cerebral ischemia and ultimately like infarction which is not ideal so one way your body responds to that increase in ICP is to try to increase your map because by increasing your map your CPP your cerebral profusion pressure will go up okay so you have a massive sympathetic discharge in the setting of an increase in ICP that massive sympathetic discharge um increases your cardiac contractility and basically makes your blood pressure go up okay and remember if you also have a very good sympathetic discharge if you're listening a lot of neuroprinephrin you're acting on alpha one receptors that we find on blood vessels that alpha one effect on blood vessels will cause viso-constriction that will increase systemic vascular resistance and that will increase minaterial pressures okay so you get an increase in blood pressure so that that means you get a hypertension and again that's to increase your CPP but that increase in blood pressure right as that blood pressure increase right so think of this as like time-lapse events you have that initial sympathetic discharge because you have ischemia of the brain increase the intra-cranial pressure because you're compressing on your cerebral vascular that hypertension will be sensed by your borrower receptors for example at the credit sinus when your credit sinus senses those increased blood pressures okay you have a massive you have increased firing

of your borrower receptors if you have increased firing of your borrower receptors you have a massive parasympathetic discharge okay and that massive parasympathetic discharge can slow conduction through your AV node if you may in fact if you're thinking of this with regards to the pacemaker potential you're actually decreasing the slope of phase four of the of the essay node opotential and if you decrease that slope you have a brady cardia okay so we said that the first thing that happens in the setting of increased IC Ps you become hypertensive that's step one and if you really want to be like super super nitpicky about this you actually get a tacky cardio as well initially initially initially but when your borrower receptor response kicks in the predominant effect that happens after that you have the initial hypertension is the brady cardia because you have that massive parasympathetic discharge in phase two if you may of this response so if you think about it what is the thing I mentioned in if you said oh a person has brady cardia a person has hypertension and let's just tag tag on irregular respirations with this what is this triad chord well I hope you're thinking of this as the cushioned striad of increased ICP okay the mechanism behind the irregular respirations have not exactly been worked out but the brady cardia hypertension actually do make sense and fact if you remember me saying that the massive parasympathetic discharge is what causes the brady cardia that can also sort of help you remember why you have uh uh uh peptic ulcers in the setting of increased IC Ps right so cushions ulcer um cushions ulcer uh is the kind of peptic ulcer you get with high ICP because again if your ICB is very high um your borrower receptor response causes a massive parasympathetic discharge through cranial nerve 10 um remember your parasympathetic system can activate g cells g

cells in the in the GI tract and those g cells when they activated by gastroreleasing peptide right you make more gastrin and one of the things gastrin could do is gastrin could go and talk to your parietal cells it could stimulate them through CCKB receptors um to release more um to release more acid okay and if you have hyperacidity you could get ulcers remember another thing that uh g cells do right after the secret gastrin that gastrin can go and activate um enterochromophine like cells those cells can release histamine histamine can hack achthona histamine H2 receptors in the GI tract and again that can cause a parietal cells to release more acid okay so that's the potential pathophysiology behind a cushing's ulcer okay so those are the different responses of the brain to increase this in intra cranial pressures now question three uh debutamin and cardiac alpha right so how does debutamin work?

debutamin is a beta one agonest okay so because it's a beta one agonest it will increase uh your cardiac contractility okay so that's a that's an i-notropic effect it also increases your heart rate that is a chronotropic effect okay so your cardiac alpha to go up because your heart rate is going up and your stroke volume is also going up because your cardiac contractility is going up with debutamin now the effects of merinon and cardiac alpha right so merinon how does merinon work?

merinon is a phosphodiester is three inhibitor it inhibits pd 3 and phosphodiester is we already know that this is the enzyme that breaks down cyclic AMP to AMP okay now let me teach you a quick construct here and increase in cyclic AMP causes contraction of cardiac muscle the mechanisms I'll let you go over that on your own I'll talk about that in the later podcast but the big construct here is an increase in cyclic AMP causes cardiac muscle contraction and increase in cyclic AMP causes smooth muscle relaxation so big cyclic AMP increases cardiac contractility big cyclic AMP causes smooth muscle relaxation so if a person takes merinon pd 3 inhibitor and cyclic AMP levels go up what should happen to the cardiac output it should go up because your cardiac contractility is increasing okay now the systemic vascular resistance in these people should go down and again the reasoning behind that is again remember your blood vessels are all lined by smooth muscle so if you cause smooth muscle relaxation because of elevated levels of cyclic AMP you have a vasodilation that decreases your systemic vascular resistance okay and if your cardiac output increase with merinon what's happening to your systolic blood pressure it's actually going up your systolic blood pressure is a proxy for your cardiac output in fact whenever you get any mbm equation or whatever that talks about systolic blood pressure just always ask yourself this scenario that was described to me what happens to the cardiac output if the cardiac output went up your systolic blood pressure should go up okay and on merinon we said your systemic vascular resistance is going down if that is going down what should happen to your their stolic blood pressure it should go down okay so again think of your their stock as of your systemic vascular resistance as being a proxy for your systolic blood pressure so any mbm equation

you get that talks about oh what happens to your systolic blood pressures just reasoned out in the context of SVR whatever happens to SVR will be what will happen to your systolic blood pressure so when you're taking merinon you exert in a positive and anotropic effect on the heart but on the flip side you're also decreasing the SVR okay so your systolic blood pressure is rising positive inotropy your stolic blood pressure is falling because of the viso-dialectory effect of merinon in fact some physicians refer to merinon as an ionodilator for this express reason so if your systolic blood pressure is going up and your stolic blood pressure is coming down what's happening to your pulse pressure remember your pulse pressure is your systolic blood pressure minus your stolic blood pressure your pulse pressure is actually going to increase on merinon okay you can also observe the same effect if a person is taking isoprotarinal isoprotarinal is a beta one and two agonist okay back to vidin but beta one receptors you have an increase in anotropy you have an increase in cardiac output just like merinon does and then back to vidin beta two receptors you cause a viso-dialectory because remember again beta two receptors a GS coupled okay they're kind of G protein coupled receptor if you activate that beta two receptor GS is activated you have an increase in agonylatesyclase activity your cyclicky amp activity goes up okay and we said big cyclicky amp because it's smooth muscle relaxation okay that is why you get decrease in SVR where you activate beta two receptors now and on the flip side again if you activate beta one receptors those are also GS coupled you increase the clk amp so you get more cardiac contractility and if you want there to take that to like a very if you want to want it to keep making analogies with that if a person is pregnant is in labor you want to delay yo

u can give a beta two agonist because as it so happens your myometrium has a ton of smooth muscle okay so give a beta two agonist you activate GS coupled receptors your cyclicky amp levels go up so you cause relaxation of the smooth muscle in the in the uterus again if you also want there to take this even further to your respiratory system for person has a history of asthma okay you give them a bit or a lot but it is a beta two agonist okay by giving a beta two agonist like our butter all you are a cyclic you activate a GS coupled receptor your cyclicky amp levels go up the smooth muscle in your early relaxes and you get a bronchordialation if you want to make one more analogy right I promise before we go into the next it if you gave a person a theophilin right theophilin is a phosphodilistries inhibitor if you give a phosphodilistries inhibitor your cyclicky amp levels will go up if your cyclicky amp levels go up again smooth muscle relaxation you get bronchordialation okay so hopefully these different examples so to reinforce that concept for you now next question says calculating cardiac output right so there's many ways to calculate cardiac output one way the easy one is cardiac output is heart rate times stroke volume that's easy to remember right so if you increase your heart rate or increase your stroke volume your cardiac output goes up end of story now the other equation that is somewhat less intuitive but if you really thought about it it's actually intuitive is your credit is the fixed principle equation where your cardiac output is equal to your VO2 and your VO2 basically means your oxygen consumption so it's equal to your VO2 divided by the difference in auto saturation between your veins and your arteries okay so cardiac output is equal to VO2 your oxygen consumption right so that's a direct relationship your cardiac output is directly proportional to y

our oxygen consumption that should make sense if you're consuming more oxygen because you're exercising you have to increase your cardiac output to meet that demand right so that's easy now in the denominator on the other side of that equation is the difference in auto saturation right so if you are reasoning along if you're reasoning along with me you can see that there is an inverse relationship between your cardiac output and the difference between your auto saturation your arteries versus the auto saturation your veins right so again think about this if your cardiac output is low right if you're just thinking purely mathematical before we go all heart curve physiology here if your cardiac output goes down the difference in the auto sets between your veins and your arteries should go up now why does that meet any sense the reason that makes sense is that when your cardiac output is low your tissues try to get more efficient at extracting oxygen from whatever blood is coming from the arterios because they're like my cardiac output is low I don't know where my neck where when my next blood supply will come so let me just try to take as much oxygen as possible right so if you're saving up more oxygen there'll be less oxygen left at the end of your veins that are sending the blood back to the heart okay that is why hypoxia actually let me hold that secret back I'll talk about that in an upcomming slide actually okay so a decrease in cardiac output makes your tissues extract more oxygen okay and if you extract more oxygen the amount of oxygen you will see in your vein will be much less than the oxygen you see in the arterio compared to a more high cardiac output state okay now and in a later later podcast we'll probably talk about why you have a decrease in the oxygen tension between your arteries and veins so like that difference is decreased in a person that is septic

in a person that is septic they have a very high cardiac output right the cardiac output is high if you're thinking in terms of fixed principle you can see why that arterial oxygen versus venus oxygen difference is much smaller but that's a more advanced concept we'll talk about that later okay let's move for like a nice uxx okay now the main arterial pressure so how do you calculate the maps right so there are many many ways of calculating your main arterial pressure there are many many ways of doing that right so the equation that will probably help and I'll flush this equation out some more in a later slide is that your p is equal to your q times r okay p equals q times r so the q whenever they're referring to the cardiovascular system is your cardiac output the r whenever they're referring to your cardiovascular system is your total peripheral resistance okay so your main arterial pressure is equal to your cardiac output times your total peripheral resistance now another formula for main arterial pressure is just a formula that relates your systolic blood pressure and your systolic blood pressure the thing is the heart spends more time in the asten right so two thirds of you the two thirds number goes with your dbp a one-third number goes with your sbp okay so another formula actually for your map is your one-third like one-third of your systolic blood pressure plus two thirds of a dastolic blood pressure and then a final formula is your systolic blood pressure plus I believe it's one-third your pulse pressure let me look this up I knew this uh when I was preparing this line now it's no longer there but let me just look this up easy to look up um so pulse pressure and map okay so let's look at the formula for this um formula okay yep so yep that was actually correct so your map is your dastolic blood pressure plus one-third your pulse pressure okay and again your

pulse pressure is the difference between your systolic your systolic and dastolic blood pressures okay and if you actually if you're more mathematically and you sort of work out that to thirds dbp plus one-third sbp you will arrive at this third formula okay so what is the one pediatric and one cardiac pathology that classically presents on exams with pulse pressure deviations okay in terms of the pediatric pathology um think so I guess I should modify this to pediatric cardiac pathology so pediatric cardiac pathology and one adult cardiac pathology that classically presents on exams with pulse pressure increases um the big pediatric pathology you want to know is the beaten doctor satiriosus okay it's a very specific finding on mbna exams and then for adults that's the odichriger education basically the construct I'll give you to easily remember this is whenever blood is flowing in so normally blood should flow in one direction okay let's just make that our construct if blood begins to flow in two directions I think of it as oh I'm creating a new blood vessel okay so if you may I'm creating more options for that blood that got into the order to flow and if you create more options you effectively decrease in systemic vascular resistance if your svr goes down your systolic blood pressure goes down so your pulse pressure gets wider okay so if you get any kind of mbmi question where a person has a blood pressure of like 110 over 40 that is a super wide pulse pressure think of if it's a pediatric question think of beaten doctor satiriosus if it's an adult question think about the odichriger education okay think about the odichriger in fact if you get an escoltation question and you see a white pulse pressure you probably don't need to burn time listening to the at least if you're short on time you can just very quickly say oh pulse pressure is wide it's one of these two p

roblems look at the age range they're good to go okay now three common mbmi strategies for increasing the cardiac output well this is relatively easy one strategy is you can increase the preload right so more preload will according to the Frank Stalin principle that's coming up on a later slide more preload increases your increases your endastolic volume and if your endastolic volume goes up your stroke volume will go up okay another strategy is to increase the contractility so if your endastolic volume is not changing at all when you just increase the contractility of the heart okay your cardiac output will go up as well because increased contractility will increase your will increase your stroke volume another thing that could make that happen is to also decrease your afterload whenever you decrease afterload your increasing drainage from the left ventricle okay so your stroke volume is going up so your cardiac output goes up and just as an addendum if you're thinking of I guess molecular strategies for increasing the cardiac output on your exam in terms of contractility the three molecular strategies are already talked about actually I've talked about most of them already if you have better one stimulation of the heart okay better one stimulation of the heart will increase cyclic amp you know cause increased contractility another thing that could happen is if you just increased cyclic amp through a backhand mechanism right by for example given a phosphodisteries inhibitor that increased cyclic amp will increase cardiac contractility another thing that could increase cardiac contractility is to increase the intracellular calcium okay so this is more what the joxin does okay the joxin increases your intracellular calcium and that increases cardiac contractility so those are three higher molecular strategies for increasing cardiac contractility or exerting if you make

a positive I know tropic effect on the heart okay so let's go to question four so these ones should hopefully go by a lot quicker so slight force says what does an increase in venous return due to the endestallic volume the stroke volume the cardiac output and the endestallic volume okay so if you have an increase in venous return right you preload is obviously going up if your preload goes up right you're putting more blood in the left ventricle your endestallic volume should in fact go up okay and according to the Frankstallian principle where if your endestallic volume goes up your stroke volume goes up right it means that as your ADV is going up from an increased preload your SV goes up okay and because your cardiac output is heart free time stroke volume and increasing stroke volume will in fact increase your cardiac output okay but as a nitpicky point your endestallic volume largely does not change according to the Frankstallian principle if your heart is working just fine because yes you put more blood in the left ventricle right so your endestallic volume is going up where your stroke volume is also going up proportionally okay and as your SV goes up proportionally your endestallic volume does not necessarily change okay although remember if because I can imagine if you're if you're like a very heart-courst physiologist you go say in divine yes what you just said is true body is true to a point and that is in fact true and that true to a point to be illustrated on the next slide because basically the Frankstallian principle is oh as you increase the length of sacrameres you're increasing the tension you're placing on those sacrameres as you increase the tension on you're placing on those sacrameres your you're actually squirting more blood out of the heart so your stroke volume is going up but if you look at the graph on the next slide that you have that prop

ortional relationship and then you hit a max where there is no more change anymore okay so there's a certain length beyond which your cardiac contractility doesn't I mean sorry I just want to be physiologically accurate here there's a certain length behind beyond which you've placed too much tension on your muscle on your sacrameres that they do not let out any extra blood okay so at that point your stroke volume will actually not actually not be increasing even if your preload is increasing right so if you put just way way way too much blood in the left ventricle yes your stroke volume will go up okay but at some point your your stroke volume will not go up in proportion to your endastolic volume so at that point your end systolic volume could increase marginally okay but I'll just say in general as your endastolic volume goes up from increase preload your stroke volume goes up and your end systolic volume generally does not change okay if you want to go to step one that's what you should take away but if you want to think even deeper about it at some point your end systolic volume actually begins to rise but that's not very relevant to our discussion today okay so this is the French style in principle so let's go to the next slide and talk about the relationship okay because your friends at the MBM love to touch on you with this so if you look at there are three graphs okay and I put my references in the in the last slide but there are three graphs here if you notice as the Venus return goes up okay your left ventricular endastolic volume should go up right and if your LVEDV is going up that should also make sense that your LVEDV should go up as well okay because more blood volume should increase the pressures in the left ventricle okay and as you notice as that is going up okay the stroke volume is going up that's the French style in principle and again the reasoni

ng behind that is as you put more blood in the left ventricle you're increasing the length of the left ventricle a placing more tension on the left ventricle and that increase intention as the left ventricle snaps back in the process of systole you're sending more blood out okay what notice that these changes are long one curve long one curve your friends at the MBM come for you to try to think about this in a relatively not prudent way what do I mean by that if you look at the second graph right you can see some so red is the normal curve okay you can see some black lines going above basically your slope is increasing and you can see some black lines going below basically your slope is decreasing okay those slope increases are at constant left ventricular endastolic pressures okay so if your preload is not changing one way you can make the slope of the French style in curve higher is by increasing contractility if you may so given a drug like the joxin or given merino for example okay those things if your your preload is not necessarily changing so if you're like oh my preload is being held constant but wait my stroke volume is increasing the reason your stroke volume is increasing is because your cardiac contractility is increasing so in that specific scenario your endastolic volume is not changing because your preload is the same your stroke volume is increasing okay and because your stroke volume is increasing your end systolic volume should go down okay your end systolic volume should go down so why am I making a force about this for the graph on the left okay for the very first graph on the left we said that an increasing preload increases your endastolic volume and because of that increase in endastolic volume your stroke volume is going up okay that is the French style in principle but your end systolic volume is not changing as a as a rough approximation okay

but if a person has a constant preload if the preload is not changing your endastolic volume does not change the only thing that can increase your stroke volume in the context of a constant endastolic volume is an increase in your cardiac contractility at least for purposes of this graph that I'm describing there are many other things that can do it but let's skip things simple here so an increasing contractility will increase your stroke volume in the presence of a not changing preload or you can say not changing endastolic volume or endastolic pressure okay that's a very important concept to understand and in those in those cases if you're edv staying constant and your SV is increasing it means that your ESV your end systolic volume should go down okay so in the French style in mechanism your edv is increasing your SV is increasing for your ESV staying constant contrast that with a constant edv let's say you're like oh I'm just increasing contractility another name thing to your preload your edv staying constant your SV is increasing so your ESV is coming down okay just one of those bizarre things that you want to make sure you understand okay so an increase in the slope of the French style in curve occurs it's not a French style in effect that increase in slope is an effect of an increase in your contractility as an example okay if you're decreasing the slope it's from a decreasing contractility right now you can give that if you're taking a class to an terrythmic like a better blocker or a class one terrythmic like your non-dihydroperidine calcium channel blockers like Verapamiland delta is it okay very high yield to understand these things and again graph 3 just shows this French style in thing I mentioned remember if you're looking at your pressure volume loops or the on the very left at the bottom you have your end systolic volume right because that's after is

o volumetric relaxation okay and then on the far right on the bottom you have your end systolic volume okay if you're increasing venous return right you see that red bulge you end that stolic volume goes up okay and because the width of the the width of the vertical lines represents your stroke volume your stroke volume goes up okay but if you notice because you're not changing because the only thing your changing is your preload your end systolic volume is actually not changing okay although that is not exactly true okay that is not exactly true but go with that approximation for your example okay so slide 5 what is the mechanism behind the peripheral edema observed with taking of hydrozene or a dihydroperidine calcium channel blocker okay so if we think of blood vessels right so blood vessels have blood vessels have we have like arterios that feed capillaries and capillaries then feed venous okay so it so happens that hydrozene okay and your dihydroperidine calcium channel blockers like amlodipine, phyloepine, clevidi-pin and all that fun stuff okay those drugs works very specifically by dilating pre-capillary arterios okay so the dilivate arterios that come before capillaries if you dilate those arterios that come before capillaries it should make sense that the hydrostatic pressures in your capillaries should increase okay and because again more blood is going to capillaries right so if you have an increase in hydrostatic pressures in capillaries right you have more extravacition of fluid if you think of the stalling forces you learn when you study renal an increase in your hydrostatic pressure in capillaries will cause more fluid extravacition okay so if we know that an increase in hydrostatic pressure causes an increase in fluid extravacition which causes a peripheral edema if you then make sense that whatever treatment strategy we employ should end to decrease

those hydrostatic pressures and we know that venous come distant to capillaries right so if we give something that's selectively dilated those venous we would draw more blood away from those capillaries will decrease the hydrostatic pressures in those capillaries and we could potentially fix the peripheral edema okay so it so happens that angiotensin 2 is a powerful constructor of postcapillary venous so if you give an ACE inhibitor which will decrease the angiotensin 2 levels or you give an ARB like low CYR10 which will block the angiotensin 2 type 1 receptor you would have dilation of those postcapillary venous or you have dilation of those venous you have a decrease in hydrostatic pressure and you can fix the peripheral edema okay now next slide slide 6 what is the pathophysiology behind the peripheral edema observed in a 30 year old female with a BNPR2 mutation right so I stole this from pulmonology okay if you see a 30 year old female with a bone morphogenic protein receptor 2 mutation okay I really hope you're thinking about pulmonary arterial hypertension okay pulmonary arterial hypertension remember your pulmonary arteries drain your the right side of the heart so if you have pulmonary arterial hypertension you have an increase in your right-sided heart pressures and because all the veins drain into the right side of the heart you have an increase in venous pressures and increase in venous pressures will cause more fluid externalization and then you can get peripheral edema with that okay so that's the pathophysiology there now next slide as blood flows through the vascular tree where do we record the biggest resistance for pressure drops okay so the biggest resistance slash pressure drops actually across arterials okay in fact that's why your tears are called resistance vessels so you're like hmm why is this true well this is true because arterials have a ver

y large I don't I do not see the largest I just say they have a very large cross-sectional area okay so like your yoder your yoder has like a big big big radius but you have just one in your you have millions of arterials okay so if you take all the redine of those individual arterials and add all of them up okay you have a very very big cross-sectional area okay and a very big cross-sectional area does in fact cause pressure decreases okay because again if you think to let's see what's the equation I'm trying to remember here so P equals q times R so P equals q times R if your resistance goes up right your pressures should go up that's one equation the second equation is an equation that relates to I believe Procels law where the the resistance in a vessel okay the resistance in a vessel is proportional to the viscosity multiplied by the length of the vessel divided by the radius of that vessel to the fourth power right so if a person has if you you are tiros if you take all the redine and add them all together the redine of your arterials are very large taking together okay and as that radius goes up because radius is inversely proportional to resistance to the fourth power the resistance goes down and from the first equation I mentioned if your resistance goes down right your pressures should go down as well okay so you actually have the greatest pressure drops across arterials because your biggest pressures like your arterials feel a lot of the like your beginning arterials if you may feel the pressures that are coming from your your order right so that's a very high pressure but after that blood has percolated all through those arterials you have a very big pressure drop because again you're going through a much wider cross-sectional area okay now so I've explained the path of physiology behind that and again that should make some sense because again you don't wa

nt to have super high pressures in capillaries so that you can have like a more harmonious exchange of nutrients and oxygen if you may okay you don't want your hydrostatic pressures to be so so high that those are the only pressures that are working at the level of your capillaries because if those are the only pressures that are working you have great feel like phenomenal filtration okay but the problem you're running to is you have very crappy reabsorption across those capillary walls okay so you want you don't want super high pressures in your capillaries you also don't want to block your capillaries and get peripheral adema okay so next slide what are the vessels with the largest right so I did not see the vessels with large cross-sectional areas now I'm asking about the largest okay the vessels with the largest cross-sectional areas in the cardiovascular system are your capillaries okay your capillaries have a very high cross-sectional area okay and if you go back to fancy college physics I know some of you will be like oh man I thought I would forget and drop all these things forever after I'm done with the pre-med well sorry that's not the case although we're not going into big detail here but if you remember your if you remember from college right like flow rates flow rates I call to your area times velocity okay so I already said that the area in your capillaries are very very big okay now if the area in your capillaries are very very big or that do to your flow velocity assuming the flow rate because remember your blood vessels and your heart they are all one continuous system in series right so the flow rate is equal everywhere so if the flow rate is equal everywhere and we said that capillaries have the biggest cross-sectional area what should happen to the velocity of blood flow in capillaries it should be low and again that is a good thing right because

by having that reduced velocity okay you have better flow I mean you have slower flow your capillaries and that slower flow your capillaries sort of gives you an off time to exchange nutrients gases and waste products okay but if blood is flowing way way way way way too fast you don't have that exchange of nutrients and oxygen and that is not ideal that is not what you want if you're human being okay so next slide what are the vessels with the largest capacitance in the cardiovascular system okay the vessels with the largest capacitance in the cardiovascular system well those are your veins okay your veins have the largest capacitance now what is the underlying pathophysiology the underlying pathophysiology behind that and I mean if you I'm sure you've taken some kind of histology class in Metzco if you look at the walls of veins on the microscopy versus the walls of arteries on the microscopy veins have very little in the well of elastic fibers okay and because they have very little in the well of elastic fibers that means they have very low elastants if they have very low elastants they should have very high compliance and maybe seeing divine wait wait wait for a moment what do you mean by that I thought that being more compliant meant I was more elastic that is what your friends at the MDM you want you to think do not think in that way okay elastants is not a measure of how stretchy you are okay elastants is a measure of how well you snap back after you've been distended okay so if something is very compliant it means that things distance very well if you're very good at distending it means you're very crappy at snapping back okay so any vessel or any structure that has very high compliance actually has very low elastants okay in fact compliance think of compliance as being equal to a change in volume or a change in pressure will make a bigger fuss about this when

I do some preliminary podcasts and if elastants is the reversal that it should stand to reason that elastants is a change in pressure divided by a change in volume okay so again because your veins have very little in the well of elastic fibers they have a very small elastants because they have a very small elastants they have a very high capacitance or compliance if you may okay and because they have a high compliance they have a very high capacitance because they can store more blood okay they can store more blood now so that's the underlying pathophysiology right so why do nitrates work in the setting of angina okay there is a nitrates work is nitrates have vino dilators okay vino dilators when you dilute veins okay you're increasing the capacitance some their compliance some more okay so you're retaining more blood in your veins and if more blood is being retained in the veins what happens to your preload it goes down if your preload goes down there is less blood that's in the heart okay because there's less blood in the heart that's in the heart you're not stressing the heart as much okay so you have a decrease in myocardial oxygen demand because it doesn't have to pump as much blood so your symptoms of angina are reduced okay it's not necessarily because you're dilating coronary vessels no that's not really the pathophysiology the pathophysiology is that because think about it right if you if you have um let's assume you're being paid uh fifty thousand dollars a year okay and you have a certain lifestyle with that and then let's say something bad happens in the economy and your salary plummets to like thin grand a year okay if you're any thin grand a year um if you were still trying to keep up with your previous lifestyle right so you're trying to keep up with the Joneses basically uh you sort of have a mismatch there you begin to have like painful living conditi

ons okay but if you adjust your lifestyle downwards like you move to a smaller house you buy a smaller car that consumes less gas then you you're pretty much fun even if you have a decrease in the flow of money towards you know uh you don't have any problems because your demand on that money has decreased so if a person has angina right they have stenosis of coronary vessels um if they try to same old same old for the heart like oh trying to leave at the normal flow lifestyle for the heart if you may the person will have angina right painful life conditions but if you decrease the demand of the heart for oxygen right even if you have minimal flow that minimal flow is just enough because you've basically like reduced the lifestyle expectations of the heart okay now what happens to the diameter or reduce of veins in the setting of severe blood loss well if you're losing blood right your cardiac output plummet okay if your cardiac output plummet your bar receptors are like whoa i'm not firing as much well if you're not firing as much remember i say that will cause a massive sympathetic discharge okay so if you're easy mourner i've been a friend uh you will clamp down on the alpha one receptors you find in venuals okay that will cause a venual construction so by doing that you effectively decrease in the compliance of your venuals or you could say you're increasing the last ends of those venuals and when that happens you're decreasing the capacitance so you're storing less blood in your venuals in your veins okay so you're sending more blood to the heart so you're preload increases okay so the radius of veins actually goes down in the setting of severe blood loss okay next slide why are veins more compliant than arteries um just explain that in the previous slide and the formula for compliance again is CVP right so compliance equals change in volume of a change in pressur

e okay now next slide okay so this one is kind of cool actually um it's just really annoying but once you get it down you'll be a maestro at understanding some bizarre things so that actually relevant to your step one exam um if you're going through this podcast you're basically going through the cardiology section of first aid for the USM and step one but i'm just trying to give you a context for many of those cardiac physiology concepts the outline in the textbook okay so why is high output heart failure feature venual that's one question it's a great question uh why would a patient with a jack two mutation have an increased risk of thrombotic events um so jack two mutation i hope you're thinking about your myeloper liverative syndrome like polycyclineia vera okay remember those people classically can get a hepatic vein thrombosis that can present as a borkiary syndrome so that's another question we have third question what is trough to the peripheral resistance and a patient with Walden strums macroclobolinein right so i remember this is an igm uh monoclonal proliferation okay um so why those the tip total perforations actually goes up under those circumstances and we're like why is that we'll talk about that in a bit uh 24-year-old female has only lentine hypertension with a flung brewery heard on physical exam right so this is the classic description of a fibromuscular dysplasia um uh and basically the last question is basically a leaking to answer all these questions what is the equation of pathophysiology that explains your responses to all these questions okay so uh let's talk about the equation and then we'll try to answer all these questions okay let's talk about the equation and then we'll try to answer all these questions so um have you really mentioned this equation already right so i said that there are two high old equations you want to know that basica

lly explain a lot of concepts relating to cardiovascular physiology okay one equation is the p equals q times r equation right so b q r that's an easy one to remember okay so if you do a substitution if you make you the subject of that formula uh your q which is basically like your flow through vessels is directly proportional to the change in pressure and inversely proportional to the resistance okay so q is equal to p over r okay so i hope you're still with me at the spot and then the second equation i said is that oh your resistance is directly proportional to the viscosity in a blood vessel and it's also directly proportional to the length in a blood vessel right so that should make sense right if you have more viscous fluid in a pipe uh it's much harder for that fluid to flow if you make okay uh if you have a longer pipe it's also much harder for things to flow right so you may be like uh divide that doesn't really make sense think about it let's assume uh uh you should not do this okay you should not do this well let's assume you're trying to steal gas from a person's uh uh trunk right and you use a very short pipe and you suck on the uh you know let me know use a uh bad example let's assume you're trying to get gas from your own car okay and you take a pipe and you suck on it you suck on the pipe and you try to get some gas out right if it's a short pipe you use the chances of you getting gas out of really high but if you're sucking out of like a big large hose like a lot of holes that's like I don't know like 20 feet long you're not going to get any gas out because you cannot apply enough suction okay so a very long blood vessel does not have enough suction so it's much harder for blood to flow through those vessels okay so resistance uh is directly proportional to viscosity and directly proportional to length okay but it is inversely proportional to radius to

the fourth power and because this radius has the fourth power going for it that should sort of tell you that that's probably the most important variable in this equation okay but if you understand these these equations right let's sort of make some parallels here right so the first parallel we want to make is why is high output hard failure a feature of anemia well if a person has anemia right what happens to the hemoglobin in the blood it goes down hemoglobin is a protein right so if the amount of protein your blood goes down okay what's happening to your blood viscosity well I hope you're saying that it goes down as well if your blood viscosity goes down according to that second equation your resistance should go down because those things are directly proportional and if your resistance goes down what happens to flow through your vessels it increases okay so if you have a constant increased flow in the setting or if your heart is constantly having to provide that increased flow because you have less blood viscosity you can have a high output hard failure in the setting of anemia right so this is a classic step one question classic medicine shelf question as well okay now the second scenario is why would a patient with a jaqtum mutation have an increased risk of thrombotic events well the magazine behind that is if a person has a jaqtum mutation for example right let's assume we have polycythemia there okay so polycythemia remember in polycythemia there you have a very high hematocrit but your ipo is actually low okay so don't mistake that with like an ipo secreting tumor like renal cell carcinoma you have high ipo but you also have high hematocrit with that polycythemia there has low ipo with high hematocrit okay so if you're making if your hematocrit is super high okay your blood becomes super super viscous if your blood is super super viscous the resistance in yo

ur blood vessels go up because those quantities are directly proportional and as the resistance goes up okay your flow comes down okay your flow comes down and if you really think about it if the flow or your kill through your blood vessels go down right are you thinking about vehicles trying it by any chance your she like steases hypercognizability and endothelial dysfunction so that is steases if you have a reduced flow of blood you have more steases of blood and because you have an increase in one of the factors in vehicle's triad you have an increased risk of thrombotic events okay so that's why you can get like a hepatic vein thrombosis with with with polycythemia there which classic Lyon exams presents as a botchiaris syndrome okay okay and yeah so what is true of TPR in a patient with water thrombosamacroglobellymemia basically the same thing with p-veera okay you have too much protein in your blood this in this case the protein is IgM okay so you have a hyper viscous blood so you have a big resistance you have a big resistance you have low flow okay so your TPR is going up the flow in your blood vessels are going up as well okay so I mean they're going down sorry okay they're going down and again because your TPR is going up right your cardiac output is going down because your blood has to work much harder to pump that sludge I mean your heart has to work harder to pump that sludge okay now if a person has a fibromuscular dysplasia right again the TPR goes up because their radii the radii of their renal arteries is going down okay so decrease in radius right is increasing the resistance okay so that decreases flow through the renal arteries okay and as you see on the later slide that has certain implications with regards to hypertension so slide 12 that is that later slide as it as it may happen so for the last patient in the preceding question what should be

true of flow through the renal artery even geography reveals 50% to noces right so this will be a conceptual mathematical question you could get on your exam okay so if you have 50% to noces detected on renal angiography in a person that has fibromuscular dysplasia okay your radius is basically being chopped up in half right and if your radius is being chopped up in half what's happening to the resistance in your renal artery remember your resistance is inversely related to your radius so that halving of your radius should increase your resistance to the fourth power okay so basically your resistance should go up to the by a factor of 16 right so remember two times two times two times two so two times two is four times two is eight times two is sixteen okay so resistance goes up by a factor of 16 and if your resistance is going up by a factor of 16 it should then stand to reason that your your flow through the renal artery should also go down by a factor of 16 okay your flow through the renal artery should go down by a factor of 16 okay so basically if you want it to be like I don't want to think through so many variables whatever happens to your resistance also happens to your flow I mean sorry whatever happens to your radius also happens to your flow so decrease in radius decreases flow okay decrease radius decreases flow but to the fourth power okay don't forget that addendum now as an aside if a person has renal artery stenosis right so what should be through the renal right so if they have stenosis of the renal artery the afran arterial is not getting enough blood flow okay low flow to the afran arterial will activate your joxtaglomerular part of your gg cells okay this equate more renal okay so your renal goes up okay one of the jobs of renal is to convert angiotensinogen from the liver to angiotensinone okay so angiotensinone levels do go up as well okay and th

en if you get to the endothelial cells in the lungs angiotensinone is converted by ACE and you're tensing convertin enzyme to angiotensin 2 so angiotensin 2 levels should go up as well okay if angiotensin 2 levels go up remember one of the functions of angiotensin 2 is to make its way to the zonal glomerulosa of the adrenal cortex when you activate that zonal glomerulosa you secrete more mineralocorticoids like outdoastro so your outdoastro in levels go up okay so your plasma outdoastro to renal ratio will be normal in a person that has renal adristinosis contrast that with a person that has a concentrum okay so an adrenal adenoma or adrenal hyperplegia secrete too much outdoastro your dose will be super super high that will raise your blood pressure that will negatively feed back at the level of the afran arterial so your secret less renal so your plasma outdoastro in renal ratio will actually be higher in concentrum okay and the analogous disorder in an older male will be renal adristinosis okay fibromuscular dysplasia is a cause of renal adristinosis but in order for they just call it renal adristinosis okay and the relatively high your locular finding here is AV-NIKEN right so NIK you can detect this on fondoscopic example I'll encourage you to look up a picture of this it's actually pretty striking when you take a look so if you see an old guy with unrelenting hypertension and the sale of fondoscopic exam reveals AV-NIKEN anterior venous NIKEN think about renal adristinosis okay that may be a question where they don't even tell you anything about the brewery okay but if you see AV-NIKEN old guy hypertension you really want to think about renal adristinosis with that okay now next question says a patient and I know this has gone long I apologize we will be done with this quickly this is the second to the last slide and the last slide is relatively not involved okay so

question 13 a patient undergoes an refractomy for the ZOMO dominant polycystic kidney disease remember ADP-KD has an association with mitral valve prolapse okay also remember it has an association with sub-ripe noiotemorrhages okay from ruptures of barianniurus in the circle of willis okay so so patient undergoes an refractomy for ADP-KD assuming sensitive measurements after surgery what is true of total perfor resistance cardiac output on heart rate okay and what is the underlying pathophysiology and how does this relate to resistance okay this is a very high opioid exam scenario okay in fact I believe you will find some like a one-liner mention of this in the nephrology chapter of your first deep book so let's talk about this okay but to talk about this we have to talk about resistance okay now if you remember back to college physics again don't type preventive list this should be fairly straightforward if you remember back to college physics if you have a pipe okay like one continuous path okay in fact let me write down my thoughts as I'm going through this to make sure I don't screw the sub because it's relatively easy to actually screw the sub okay so if you have one continuous pipe right the flow rate throughout that pipe is the same okay the flow rate is the same right so everything in that pipe okay is all going in series okay and if you remember if a person if you have resistors that have been arranged in series you get the total resistance by just adding up the individual resistances right so like if you have like three resistors and R1 is 1 R2 is 2 R3 is 3 and those resistors are all in series the total resistance will be 6 right you just add up all those numbers okay so if you notice the total resistance 6 is bigger than any of the individual resistances right so 6 is bigger than 1 bigger than 2 bigger than 3 okay so the total resistance is bigger than th

e resistance of any of the blood vessels that make up that that make up that singular system okay so if you're talking about like like if you're talking about like singular flow from the heart through the order to your materials to your capillaries to your venials to your veins and back to the right heart that's a series system okay that's a series system and that is also the same system that operates within a singular organ okay so singular organ so if you're just dealing with like I'm just dealing with the kidney or I'm just dealing with the lungs or I'm just dealing with the GI tract for example okay those are singular systems singular systems exhibit resistors that are placed in series okay but in the body if you're thinking about each of our individual organs sticking together those organs are actually all arranged in parallel okay all our organs think of them as being some kind of parallel circuit okay think of them as being some kind of parallel circuit so if you have a parallel circuit and think of each of our organs as being some kind of resistor okay and you arrange that parallel circuit you put resistors in parallel how do we calculate the resistance under those circumstances well if you're remembering college physics your the inverse of your total resistance will be the inverse is equal to the inverse of r1 plus the inverse of r2 plus the inverse of r3 and so let's use row numbers with this so it's like if you have three resistors right so like three different organs and r1 is I don't know like one r2 is two and r3 is three okay one over the total resistance will be one over one plus one over two plus one over three okay the common command in the mirror here should be six so in the numerator we should basically have six plus let's see blah blah blah plus one plus let's see so the inverse of r1 so 6 divided by 1 is 6 and 26 divided by 2 is 3 times 1 is 3 oo

ps sorry that's 6 plus 3 plus 6 divided by 3 is 2 times 1 is 2 plus 2 so 6 plus 3 plus 2 okay so that's 11 over 6 okay so the total resistance remember you have to flip the equation the ratio at the end that's 6 out of 11 okay that total resistance of 6 out of 11 is less than each of the individual resistances okay so are the total resistance is less than r1 or r2 or r3 so let me ask you a question now that we've done the math and talked about like how you can believe these resistances if you have resistors being placed in series when you add some new resistor what happens to the total resistance it should go up okay for a series circuit because again if you had like r1 r2 r3 1 2 and 3 and you add r4 which is four total resistance will go up okay but as you can see from the equation that we used for resistors that are placed in parallel if you added an extra resistor the total resistance actually goes down right so think about this so 1 over 1 plus 1 over 2 plus 1 over 3 let's say we add an r4 and make it 1 over 4 commanding on the internet should be 12 so that's 12 plus 6 plus 4 plus 3 right so we have 18 plus 4 that's 22 plus 3 that's 25 over 12 okay and then if you flip 25 over 12 that's 12 over 25 12 over 25 is a smaller number than 6 out of 11 okay so right 12 over 25 is a little less than 0.5 6 over 11 is a little greater than 0.5 okay so when you add a new resistor to a series of resistors already in parallel you actually decrease the resistance further okay so again that should potentially explain why uh because at materials and capillaries branch out a lot you have like very good decreases in resistance which decreases pressures what back to this example we're talking about we said add a new resistor to a resistance circuit in series total resistance goes up the corner to that is if you removed a resistor from that resistance circuit in series the total resis

tance goes down okay but if you're going for the parallel system if you add a new resistor we said the total resistance goes down we prove that mathematically on the flip side if you actually remove a resistor from a resistance circuit that is in parallel the total resistance actually goes up okay so it's like you're removing r4 uh you go from 12 over 25 to 6 over 11 so the total resistance goes up okay so I said that the different organs in the body they are basically arranged in parallel okay so if a person gets an effect in you're taking out one of their organs if you take out one of their organs and we already established that these organs are arranged in parallel okay that decrease in that that removal of one parallel resistor raises your overall total prefer resistance okay now if you want to integrate this with that bar receptor business we talked about that decrease in total prefer resistance right well sorry that increase increase sorry sorry sorry sorry sorry so you're taking out one organ but taking out an organ like a resistor that's in parallel so the total resistance goes up okay so you have an increase in total resistance so your TPR is going up if your TPR goes up okay you have an increased blood pressure that increased blood pressure will cause more firing of your bar receptors okay and if your bar receptors begin to fire more that causes a massive parasympathetic discharge as a response so your cardiac output should go down your heart rate should go down okay your heart rate is going down because through that parasympathetic discharge through your most carinic receptors you have a decrease in the slope of phase four of the essay note potential so your heart rate goes down okay and you also have decrease flow through your AV note okay and if your heart rate is going down remember that your cardiac output is heart rate times stroke volume as your HR go

es down your CO will go down as okay so that is the pathophysiology behind that thing this is one of those step one questions I can almost bet that many people will get rock okay don't be one of those people because you're listening to this podcast well I guess you read the first state page but at least you have your explanation behind that behind that factoid in first data and effrology okay so last question a 66 year old male with a 40 pack here history of smoking presents with severe abdominal pain and a blood pressure of 65 over 40 okay a pulsatile mass is about pitted on abdominal exam what is your diagnosis what is your diagnosis hopefully you know this is a triple A okay so an abdominal aortic aneurysm so what is the most commonly involved vessel in this process well it's the aorta okay the abdominal aorta okay the aorta is the most commonly involved vessel in this process and the last question is asking about the pathophysiology behind this observation so this is where we have to take a detour and discuss something known as the law of Laplace okay the law of Laplace basically the law of Laplace think an easy way to remember the equation is to remember TPR okay TPR TPR TPR to the prefer resistance so the T wall tension is equal to the the pressure times the radius of a vessel okay or you can remember the word okay all ladies are pretty right so P is in pretty R is in pretty T is in pretty okay so whatever floats your boat okay so if the radius of a vessel increases what happens to the wall tension the wall tension should also increase as well okay and if you look at all the blood vessels in the body what is the blood vessel that has the biggest radius it's your the order okay so because your the order has the biggest radius okay it should then make sense that it should have the biggest wall tension okay if it has the biggest wall tension as you have more and mo

re tension on that or more and more tension that wall could eventually balloon out you can get an aneurysm and if that aneurysm if you because think about it right it's sort of like bad in a set because as the wall of the order begins to bulge out more and more you actually place in more and more tension on the wall of that on the wall of that vessel it's sort of like a like a self-fulfilling process if you may and the more tension you please eventually you can sustain increased tensions forever that vessel can blow off and can get a triple A okay and remember that so that's the path of physiology behind the observation that the order is the most commonly involved vessel with regards to aneurysms okay and explosion of those aneurysms because again it has the biggest radius okay so that's basically just an illustration of the level of plus now the one thing I will say to that is smoking is the biggest risk factor for triple A okay so they may try to trick you on the example into picking hypertension as the biggest risk factor or like hyperlipidemia or whatever those are not the answers okay the answer you want to pick is smoking okay smoking is the biggest risk factor for triple A smoking is also the biggest risk factor for a myocardial infarction okay the biggest risk factor for an MI is smoking the pathology that has hypertension as the biggest factor is a is a is a is a eortic dissection okay eortic dissection occurs from having hypertension as a biggest factor okay so I know this was kind of long but I think we lost rid of a lot of very high yield concepts in this set and basically if you've gone through this the first state cardiac physiology at least many parts of it especially all those nasty equations should all make sense okay so make sure you understand this I promise you a pelf on your exam because these things are very commonly tested if you can reason thro

ugh these scenarios you should be well on your way to crushing your cardiac physiology portion of your step one exams okay I hope I didn't make any errors with this I think I tried to correct myself whenever I miss spoke but if you spot any errors or you have any questions again the email is divine intervention podcast at gmail.com just reach out to me and I'll be more than happy to either make any correction again I'm just a med student I'm not a professor um so I'm not perfect okay try to be perfect but I'm not okay so if you have any questions or you spot any errors just let me know and I'll be more than happy to help out okay so have a wonderful day and all the best on your exams thank you

A-P-T-M (Aortic at right upper sternal border; Pulmonic at left upper sternal border; Tricuspid at left lower sternal border; Mitral at the Apex).

The Valsalva maneuver (blowing out air while closing the mouth) or Squatting.

Increased preload OR decreased afterload.

MR gets louder because more blood flows back across the valve; HCM gets softer because increased LVEDV pulls the anterior mitral leaflet away, relieving obstruction.

AB Cs (Aortic arch = Baroreceptor and Chemoreceptor).

High hematocrit increases blood viscosity, which directly increases resistance.

Nitrates are venodilators, decreasing venous return and thus lowering preload, reducing the amount of blood the heart must pump.

Stenosis/narrowing of the renal artery, which increases resistance and decreases flow through that vessel.

The total peripheral resistance (TPR) will be less than the resistance of any single individual organ.

PDE-3 inhibitors (e.g., Merinon).

High hematocrit increases blood viscosity $\rightarrow$ Increased resistance $\rightarrow$ Decreased flow $\rightarrow$ Stasis and endothelial dysfunction $\rightarrow$ Thrombosis.

Resistance is inversely proportional to the fourth power of the radius ($R \propto 1/r^4$). Halving the radius increases resistance by a factor of 16.

Marfan syndrome and Orozomo dominant polycystic kidney disease (ADPKD).

Nitrates are venodilators, decreasing venous return and thus lowering preload, reducing the amount of blood the heart must pump.

Stenosis/narrowing of the renal artery, which increases resistance and decreases flow through that vessel.

The total peripheral resistance (TPR) will be less than the resistance of any single individual organ.

PDE-3 inhibitors (e.g., Merinon).

High hematocrit increases blood viscosity $\rightarrow$ Increased resistance $\rightarrow$ Decreased flow $\rightarrow$ Stasis and endothelial dysfunction $\rightarrow$ Thrombosis.

Resistance is inversely proportional to the fourth power of the radius ($R \propto 1/r^4$). Halving the radius increases resistance by a factor of 16.

Marfan syndrome and Orozomo dominant polycystic kidney disease (ADPKD).