DIP Episode 273 - The NBME and High Output Heart Failure (+ upcoming 2CK Course)

Okay, welcome. My name is Divine. This is episode 273 of the Divine Intervention Podcast. And in this podcast, I'll be discussing a topic that is very heavily tested on all the USMEL exams. Step one, step two, second, step three. And it's the topic of high output hard failure. So I guess I'll go ahead and title this podcast. High output hard failure. And the MBM Es. And just as a reminder, if you're interested in taking the step two CK course that's coming up soon, that's going to be on the 11th and the 12th of December from 11 a.m. to 4 p.m., Mountain Standard Time on both days. Go over like 700 concepts between OB-GYN, PEEDS, Surgery, Psych, Neural and Internal Medicine. And if you're interested in the MBME Testicking Strategies courses from 2 to 4 30 p.m., Mountain Standard Time. That's two hours behind this turn time on the 10th of December. All these courses are held via Zoom. So if you're interested, just shoot me an email through the websites like the Contact Me thin. And I'll respond to you relatively quickly. Okay, so high output hard failure. So this is something that again, many people unfortunately, a MBM Es don't understand. And the MBME understands that many people don't understand this. So they love to test this. And they tested it in many, many, many different ways. It's just one of those things that people don't pay attention to, but it ends up being extremely important on an exam. And if you look at the name, high output hard failure.

It literally tells you what this is. It's hard failure from chronically elevated cardiac output. So in this podcast, we're going to discuss like many of the different ways they go after this. We'll use keys presentations. Let me not call them keys presentations, but I'll call them like. Just like classic vignettes, classic disease scenarios where a person may have high output hard failure and the getting trouble. Right. So to set up this discussion, I think if you really think about it, if for example, you work out every day, let's say you're a very athletic person, you work out for like 30 minutes every day. You feel pretty good, right? But after you work out for like 30 minutes, you know, you're going to give your body some time to recover. The problem is if you work out for like 23 hours and 30 minutes every day, and then you maybe spend like a minute recovery and then go right back into working out, then remember that your body after a while will get tired and the person will die. That's essentially what happens in a person that has high output hard failure. For whatever bizarre reason, the common final pathway of all this stuff is the heart has to be providing elevated cardiac output for prolonged periods of time, these weeks, months. The thing you need to realize is ultimately the heart is a muscle and muscles can tire out. And when the heart tires out, then the person can go into hard failure. Okay. So that's ultimately the pathophys behind high output hard failure.

And I'll give you some more pathophysiology by using a different case scenarios. So like the first classic one, they can give you a question about a patient that has anemia. All right. You see a patient that has like a long standing anemia, especially like a micro city canemia, like an iron deficiency anemia from like I don't know like colon cancer or whatever. Those people can have high output hard failure, especially when it's a profound anemia because again, think about it. When you're anemic, what happens with the oxygen carrying capacity of your blood? It goes down. If the oxygen carrying capacity of your blood goes down, then your tissues are going to be very desires of oxygen. So they will keep asking the heart, we need oxygen, we need oxygen, we need oxygen. And the heart is like, I'm sorry, let me try to ramp up my output, right, so that I can have blood make more passes through those body body tissues. Right. So if you have more passes through the body tissues, well, to make that happen, you need an elevated cardiac output to support that. If the anemia continues for long enough, the heart will have a chronically elevated cardiac output. So initially, in high output hard failure, the person's ejection fraction is amazing. It's like 75% 80% like some crazy high number. But after a while, right, the heart will contract contract contract contract gets tired and then it will fail. And then the person's ejection version will then go down, right, it will then go down.

The person will ultimately then have a systolic heart failure. Okay. So that's how anemia can cause high output hard failure. How about like in a, what if they give you a question about a kid where there's concerns for like, I reach incompatibility or they give you a question about a child. And this child mom, you know, had like some kind of viral URI symptoms. And now this woman has polyhydram news, right? It want to think about like hydropsytiles. Remember hydropsytiles can be caused by many things. It can be caused by origin compatibility where, you know, mom has all these IgG antibodies against the origin of the gene that you know, destroy the federal red blood cells through the child into anemia. Or part will be 19. Remember part will be 19. Don't forget it's a single stranded in the virus in lots to infect red blood cell precursors. When you affect those red blood cell precursors, they are not going to be making red blood cells. So ultimately these, these two conditions I'm talking about are lituan anemia. Well, if you need to an anemia again, the oxygen carrying capacity of the child's blood will go down. The cardiac output will have to elevate in response. Basically whenever you're a hypoxic, right? Your heart starts racing. It starts racing for a reason. Remember heart. Cardiac output is equal to the heart rate thanks to stroke volume. So if you increase your heart rate, your cardiac output will go up.

So whenever there is hypoxia, just kind of think about it whenever like you're struggling to breathe, your heart is going to be racing, racing, racing, racing, racing. It's just a physiological response to hypoxia. So whenever a person has chronic tissue hypoxia, again, the tissues are demanding oxygen. So for the tiny blood that's in your body to again receive that oxygen, your cardiac output has to increase so that you can have blood make more passes through those tissues. So as the cardiac output again goes up after a while, the heart of the fetus will give away. The heart of the fetus will give away. When the heart of the fetus gives away, that fetus, you know, again, we'll have like that elevated ejection fraction initially. But after a while, the ejection fraction will go down. Then the fetus will go into systolic heart failure. When the heart stops working, remember everything will start backing up. So flora will start backing up in the upper extremities and the lower extremities and the lungs. So the child basically becomes a demeter. That's why it's called hydropsythylase. You have a hydropic fetus, hydromanian water. So you have a water field fetus because basically blood cannot be pumped forward. So the effective circulating volume is not great. Now what if they give you a question about a patient? The patient, you know, his heart don't fit very well anymore. He has all these cranial nerve deficits.

Has like painting one leg and you know, the tell you that, oh, they get a bone scan and the notice that like, listen, like he's left his left lower extremity really lights up on the bone scan. If you see that right, I hope you think about Pajet's disease, remember, classical in Pajet's disease. Those people's alkaline phosphatase is elevated, but pretty much every other lab will be fine. And don't forget that Pajet's disease is a risk factor for the development of osteosiracoma. So Pajet's disease, what's the big thing Pajet's disease? Again, remember, these people's bone marrow become very vascular. So kind of think of it this way. Let's say normally, I'm just making up numbers here. The heart needs to send supply blood to a million blood vessels. But because the person has Pajet's disease, they ultimately have like 10 million blood vessels in just the bone and bone marrow. So that's in addition to the 1 million the body has to service, right? So if you have so many blood vessels, again, your blood has to get into those blood vessels somehow, right? So the presence cardiac alcohol will increase because the bird, the body is like me and I got a send blood to these 11 million blood vessels, send blood, send blood, send blood. Well, again, ultimately, the heart can only work that heart or give it that elevated cardiac output for so long, right? Again, the heart is capable of increasing cardiac output, but it can do it transiently.

If it does it on a consistent basis for a prolonged period of time, that's going to be a huge problem, right? It's going to be a huge problem, right? So over time, again, the EF will be high at first, but then the EF will go down and then the person will go into heart failure. Okay? So that's how Pajet's disease can cause high output heart failure. What if they give you a question about a patient, right? And they tell you that this patient is stopped in the arm or something, right? And you know, they tell you that two, three weeks later, this patient has been having like shortness or breath. And in the tell you that physical exam, you can pulpit a pulsatal mass in that arm. If you see that, again, I want you to think about high output heart failure because again, when you have a stab injury, right? One thing that could potentially happen whenever you have been treating injury to a blood vessel. So they can make this question in the context of like a person being stabbed or they can make him the context of a person that had like a femoral line placed or the person got like cardiac catheterization. Remember, you need to do like a femoral puncture when you puncture the femoral vessels, right? Unfortunately, that can lead to the formation of an EV fistula. Remember an EV fistula is a direct connection between an artery and a vein, right? An EV fistula is a direct connection between an artery and a vein. So you're basically skipping the capillary end of the fins.

Now, there are two ways I think about EV fistulas, why they're potentially bad, right? The first thing with an EV fistula is, first and foremost, and this is the most important. By taking the capillary out of the equation, you're essentially taking gas exchange out of the equation. Because remember, gas exchange does not happen in arteries. Gas exchange does not happen in veins. Gas exchange happens in capillaries, right? So if a person has an EV fistula where you've taken the capillary out of the equation, then blood is literally going from artery to vein and is skipping the body's tissues. Because remember, it's at the capillary level where you have gas exchange between blood and the body's tissues. So if the capillary is at the capillary level, then the blood is flowing in your body. It's skipping tissues and not oxygenating tissues. So guess what? That person goes into hypoxia. When you go into hypoxia, again, the cardiac output is going to try to increase in compensation, that will ultimately lead to high-upor heart failure. Another way I think about it, that you know, it makes some sense for some people, is that in exchanging gases and nutrients and all those things that happen in capillaries, it's almost like the blood slows down in a sense, right? This is kind of like a good teleological explanation, like a decent way to just kind of conceptualize this in your head. It may not be fully accurate, but it will help you conceptualize this in your head.

And you're not going to be getting exam questions wrong because of this. Although that's why you see the first thing I explained was how an EV fistula leads to hypoxia, right? So the thing that happens in this circumstance, right, is, you know, as I just think of it as tissues and blood are exchanging oxygen, nutrients, waste between each other, the blood can slow down in capillaries, right? So the thing that happens is, although, if I'm not mistaken, if I'm remembering flow rates, the velocity of blood should be lower in capillaries, because they have a greater surface area combined compared to the other blood vessels in the body, but that's a different conversation. So essentially, right, you know, blood slows down in capillaries. I almost think of that blood slowing down in capillaries as time ticking for the hearts to like, whew, let me take a deep breath, let me relax from all my troubles, right? So if a person has an EV fistula, those capillaries are not there, blood does not slow down. The blood does not slow down. It's almost like the heart will be like, wait, I just send this blood out like a few seconds ago. How did it come right back so quickly, right? Because again, that slow down mechanism was gone. So again, the heart has to keep pumping, pumping, pumping, pumping, pumping, saving away. Yes, the AF will be great for a while, right? Well, that's for a season. After a while, the person will not be able to compensate anymore.

The person's heart will not be able to compensate. Remember, that's kind of like the same thing that happens in kidney disease. At first, when your kidney is not being perfused or, let's say your ifra and atrial is all jumbled up because of non-inzymatic like oscillation from diabetes. At first, your GFR is going to be really, really, really high, right? What the thing is, when you work so hard as an organ, you can do that for only so long, right? You'll keep compensating, compensating, compensating to injury. I mean, this is the whole basis of pathology as a discipline, right? So the thing that happens is when your body is subjected to stress, it tries to compensate, compensate, compensate, but you cannot compensate forever. After a while, that organ will give up and then go into disrepute and it will stop working, right? So the kidneys, right? Again, if you keep having hyperfiltration injury, I talked about this in the podcast on Stalin for six. That's a super high-yout podcast by the way to listen to all the USMN exams. But when the kidneys, you know, from that non-inzymatic like oscillation of the ifra and atrial, your glomerula, hydrostatic pressures go up, right? That will cause hyperfiltration injury because your GFR is going to be super, super, super, super high at the beginning, right? But again, as you keep getting subjected to those as your glomerular capillaries, keep dealing with those high pressures, high pressures, high pressures.

Over time, right, you'll stop functioning properly, right? And if you stop functioning properly, your GFR will ultimately decrease. Once your GFR goes down, then you're creating a stag going up, right? And then you're going to instigate your normal disease, right? So typically, so this is almost like a concept, the way the body works in general is to overcompensate, compensate, compensate. So it's almost like that person's organ is working better than good. But after a while, then that organ will completely fail, right? So that's why again, you want to always try to reverse the pathology so that you don't get to that point where your body cannot compensate, that organ cannot compensate anymore, right? Again, same thing here with with high upper heart failure, right? Again, at first, the name is almost like a misnomer, but the thing is, it's actually the high output that ultimately leads to the actual heart failure, right? So initially, you have the very high outputs, EF is 75, 80% of it will be like, wow, my heart is working better than good, it's not, right? It's working better than good, but the end result of that is something bad, right? So it's just something you need to watch, you need to watch out for. Now, another AV fistula question we can easily create for you on an exam is they can give you a question about a person that has like heart failure, stout symptoms or shortness or breath after getting a dialysis catheter, right?

So remember, before a person gets like, you don't just start dialysis on people, I mean, you can, in the ICU, where they can do like temporary dialysis in a patient's room by, you know, putting things like a gambrow or whatever. That's more for residents, we're not going to talk about that right now. But for like a person that's going to be getting like regular home dialysis or dialysis, where they go to a place like three times a week or whatever, the thing that will typically happen is you need to place, literally create some kind of AV fistula that matures, right? So you're literally creating an AV fistula to increase the efficiency of dialysis. Well, unfortunately, when you create that fistula, again, you're taking couplers out of the equation. So we have chronic hypoxia. We have no slow down mechanism that existing couplers has described. And again, the heart is going to work really, really, really hard for a while, but after a while, it can crop out. And the thing is usually people that have kidney disease, instead of no disease, you already have accelerated atherosclerosis. So those people's hearts are not breathed at baseline. And then you put that extra hit on an AV fistula, right? Again, these things all kind of explain why people that have an institutional disease, probably one of the most common causes of death in those people is cardiovascular disease, right? This is why a kidney transplant beats dialysis any day.

And any of this, they can literally ask you, ask you this as a question on an exam, right? Between dialysis and getting a kidney transplant, which one has the best morbidity mortality is going to be a kidney transplant. I'll tell you that right now, you can be on dialysis forever. After a while on dialysis, the person is going to die, right? So that's why dialysis is not always the most ideal situation because again, you need to create that AV fistula for the person. Again, that can begin to put a lot of stress on the person's heart that's, you know, not already good at is not good already at baseline, right? And then what if they give you a question about a patient again, still on this whole concept, I know, I know some of you are going to be like, wow, I didn't imagine that you can test higher, put heart failure in all these different formats, right? Again, if you pay attention here, you'll be good to go after all this said and done, right? But if you think about this, the give your question about like like a 25 year old guy, they tell you that, you know, he has a history, like a multi year history of maybe staxes, so all these nosebleeds. And then they give you a picture, they can show you a picture of his lips and his looks, we have all these black dots on them, or they can show you like a picture of his tongue. And the tongue can have all these red dots on them, right?

They can even tell you that all the person has had GI bleeds in the past, or they can tell you that the person has had episodes of him up to says, or they can tell you that this person has higher inefficiency andemia, right? Or they can tell you that, oh, this person is that died of a brain bleed, right? Like an epidural hematoma or some weird stuff like that or sub-rocknog hemorrhage. If you see all these things, I really hope you think about a genetic disease, right? And I hope you think about the disease called a hereditary hemorrhagic telangethesia. Remember, another name for that is Oslo Vibram Ducendrom, right? So how does that disorder work? Essentially it's an orzoid dominant disease, right? So it's heritable. And those people for whatever reason, they, they form a lot of evil formations, right? They form a lot of telangethesia. In fact, that's why it's called hereditary, right? Hemorrhagic, right? Bleeding telangethesia. A telangethesia is an abnormal blood vessel. It's basically an EV formation. You can remember an EV formation is essentially an EV fistula, okay? It's essentially an EV fistula. So again, when people have those EV Ms, depending on how big it is, again, that can ultimately cause problems, right? Because for example, people that have Oslo Vibram Duc, they tend to have pretty large EV Ms in the lungs, right? They tend to have pretty large EV Ms in the lungs. So in the lungs, they essentially have, again, the pulmonary artery will bring blood to the lungs.

Well, where does, where does that blood get oxygenated? It gets oxygenated in the pulmonary capillaries, right? So, if you have a pulmonary EVM, where blood is going from pulmonary artery to pulmonary vein, even if blood is returning to the left side of the heart, it did not get oxygenated, right? So it's almost like perfusion is happening, but oxygenation is not happening. Well, that's an example of a shunt, right? That is one nice way that your friends at the MBME, they can bring in some step one physiology into step two, seek step three. When a person has Oslo Vibram Duc syndrome, the primary pathophysiology behind their hypoxia, right, is from those EV Ms. And if they're going to heart failure, the primary pathology there is high output heart failure, right? So they essentially have shunt physiology. Shunt physiology is what happens in a person that has Oslo Vibram Duc syndrome, right? So again, ultimately those people can, again, the blood is not getting oxygenated, so they essentially have a shunt, they'll have chronic hypoxia, they'll elevate their cardiac output on a chronic basis, though ultimately they're too high output heart failure, right? And one thing many people don't give the lungs credit for. Those pulmonary capillaries that exist in the lungs, they are very tiny. They are very good at filtering things, right? They filter, especially all these clots or like bugs in the blood, right? I mean think about it when a person has a PE.

Where do you think people get PE's in? They get PE's on the pulmonary side of things. It's extremely difficult or extremely rare for you to find a patient that has pulmonary venous embolism, right? Usually people have an pulmonary arterial embolism, because those pulmonary capillaries are in the way, they are preventing that transit. So if you go, you know, God forbid, for example, the person has head injury hemorrhagic to the platycia, and blood is just zipping straight from pulmonary arterial pulmonary vein, right? Those people, they can actually have a DVT and get a stroke. So your friends at the MBM, they can actually give you a question about a patient having a, you know, history of all these bleeding, right? But then they get a DVT and then they get a stroke. And then they will tell you that, oh, they performed an echocardiogram and they did a bubble study, and they did not find any evidence of an ESD, they did not find any evidence of a PFO or a VSD or anything like that. If you see that, you want to think about those people potentially having a pulmonary EVM, that pulmonary EVM out formation, right? Again, that filtrate mechanism of the pulmonary capillaries is gone. So that plot that was a DVT can just go straight from pulmonary arterial pulmonary vein, and so giving them a PE, boom, you'll go to their heads and cause a stroke, right? In fact, those bacteria that are eliminated by the pulmonary capillaries, right?

Those bacteria, they can go to the person's brain and cause like an abscess, right? This is why people that have a slow way were on loose syndrome, they tend to get a lot of brain abscesses, right? And then remember, another thing that can cause an output heart failure, I mean, they can give you a question about a person that, you know, has been always has palpitations, has like panic disorder like symptoms, right? The person's heart rate is super elevated chronically, right? The person has hyperreflexia, the person has lead lag, the person has hyperglycemia. If you see all those things, right, you want to think about hyperthyroidism. Again, remember, when the person has hyperthyroidism though, it's not necessarily chronic hypoxia that causes the high output heart failure. The happen is, remember, thyroid hormone increases the placement of beta one receptors, right? On the surface of myocardial cells. Those beta one receptors, they respond very well to a benefit and not a benefit, right? So those people are going to have like a chronicly elevated heart rate. And that chronicly elevated heart rate will cause a chronicly elevated cardiac output. Again, if the cardiac output is high for so long, the heart can only hold on for so long, right? It can only hold on for so long, the person can go into high output heart failure from hyperthyroidism. That's why you need to treat a person that is hyperthyroid sooner rather than later, right?

And then don't forget that if a person has a berry berry, right? Berry berry. Many people have heard of dry berry, like people have heard of dry berry berry, they've heard of wet berry berry. So what in the world is wet berry berry? Wet berry berry is basically heart failure, right? Wet berry berry is basically heart failure, right? And the pathophysiology behind the heart failure and wet berry berry is high output heart failure. Remember berry berry arises when you have a thiamine deficiency, right? So I know some of you may be like, okay, divine. How does a thiamine deficiency give us to high output heart failure? Well, let me explain. Well, think about what with me here for a second. Going back to step one, remember that thiamine is a cofactor for a lot of energy metabolism, especially energy metabolism that comes after glycolysis, right? So for example, like the pyruvy dehydrogeny complex, right? It uses vitamin B1 thiamine as a cofactor. That's what. We know that in the TC cycle, right? The tricaboxylic acid cycle, the citric acid cycle, we use vitamin B1, right? For alpha-ketoglutarid dehydrogenase, right? And then remember also in the metabolism of in the pentose phosphate pathway. Remember, there is an oxidative phase of the pentose phosphate pathway, you know, that uses g6pd. But then there's a non-oxidative phase, right? That non-oxidative phase, the retinitin enzyme is transkytolis. Transkytolis uses vitamin B1 thiamine as a cofactor.

And it's also going down with the metabolism of, you know, branching amino acids like lucine, isolucine, valine. Remember, there's an enzyme that does that, right? Branching ketoacid dehydrogenase. That's the enzyme that's actually like not working right in a person with maple syrup, you're in disease. Branching ketoacid dehydrogenase uses thiamine vitamin B1 as a cofactor. So many energy pathways that are distilled to glycolysis use thiamine. So whenever you don't have, whenever you have a thiamine deficiency, those energy pathways, they are not going to work. And if they don't work, what's going to be the only source of ATP in the body? It's going to be glycolysis. Well, glycolysis is not good enough to support human function for long enough, right? So because that person is not able to generate enough ATP, again, the body's tissues are in almost like a state of chronic hypoxia. So again, what happens in response to that? The cardiac output is going to elevate, elevate, elevate. When the cardiac output elevates, they'll ultimately again, the heart can no work that hard for that long. So how will crap out after a while and then the person going to systolic heart failure, right? So that high output again will ultimately lead to a systolic heart failure. And then the person becomes a dimadocer everywhere. That's why they are called people that have berry berry, but they are wet. They are wet because they just have a dima. And they have that a dima from having heart failure.

And then don't forget if a person has a sepsis, a person goes into like really bad sepsis or like really bad septic shock. And they on the go cardiovascular collapse. Well, what is the mechanism behind the cardiovascular collapse in septic shock? Remember in septic shock, especially from like gram negative bacteria, you have all this inflammatory particles being released, right? Heastamine, bradykine, all those things, right? And those things lead to a decrease in systemic vascular resistance. Well, if your systemic vascular resistance goes down, well, the cardiac output is going to elevate, right? But again, the heart cannot take that hit for so long, right? So after a while again, the person can, the heart will then stop working. And then the cardiac output will go down. Remember in early septic shock, in fact, in general, for an MBM exam questions when the person has septic shock, the cardiac output is supposed to go up. Okay? That's the answer you should pick over time. For pressing a septic shock for a long enough period of time, the cardiac output is going to go down, right? That's essentially again, the person going into high output heart failure. Okay? Or if you think about it, if a person has a nephrodix syndrome, right? And they're going to heart failure again. What's the thing causing that heart failure? It's high output heart failure. All these things, if you notice, many of these things are just mechanism based, right?

If you understand the mechanism, you really don't need to memorize a lot of this stuff, right? Most of these things just make perfect sense, right? Because think about it. If a person has nephrodix syndrome, or if they have this thing called mini-trails disease, remember mini-trails disease is almost like the nephrodix syndrome of the stomach. Sometimes they call it a protein losing gastropathy, right? People lose protein through their stomach and then they poop it out. So if you're losing a lot of protein for whatever reason, because you have liver disease, because remember most proteins in the body are producing the liver, because you have nephrodix syndrome, right? So the kidneys don't work. I mean, the peanut protein, your kidneys, or your peanut protein in your... I mean, I guess your pooping out protein, this case in mini-trails disease, that's going to kill the oncotic pressure in your blood, right? If you kill the oncotic pressure in your blood, it would be good to maintain blood within your vessels, right? Within your blood vessels. And if you cannot maintain blood within your... because there's no oncotic pressure, you can keep fluid inside your blood vessels. Again, your tissues are not going to be seen a lot of oxygen, right? So your blood pressure will even go down, right? Again, from that decrease in oncotic pressure, so your heart is going to be like, okay, okay, let's try to keep maintain blood pressure here, right?

So your cardiac output is again going to crank it in a bit. If that happens, right? Again, that will ultimately lead to a higher up or lower failure. If you even think about a person that has like a protein malnutrition, like Quasiochor, if you don't eat protein, again, you're going to have nasty, nasty oncotic pressures in your body, you're going to be very low. Again, that can ultimately lead to a higher up or lower failure, just by the different mechanisms have described, right? So again, you just need to be careful with these higher up or lower failure questions on NBM Es. They're usually pretty classic. The things you can... you should usually be able to get correctly. Again, just understand the pathophys. Once you understand the pathophysiology, most of the many USML exam questions, you can see right through whatever the NBM is trying to write for you, right? And you typically also be pretty good at picking up on... picking up on... on whatever tricks that you're trying to throw in, although obviously you also need to be good at test-taking strategy, but that's a different conversation. So I think I'm going to go ahead and stop here. If you have... we show the best as you're studying for your exam, please subscribe to the podcast. It's an Apple podcast, it's an Google Play, although I think they now call it like Google Podcasts, and then it's also on Spotify, and then I also have the You Tube channel, Divine Intervention, USML podcast and videos. Please subscribe.

If you have any questions on any of the courses that I offer, the Step 1 course, the Step 2 CK course, the NBM and Testic and Strategy course, feel free to shoot me an email again through the contact button on the website. And then I guess in... Actually there are two things I want to say, and I will also make a post on Reddit about this stuff, especially for people that are in 30 years now or whatever. Going forward for future era cycles, the first thing you want to make sure you do is you want to make sure you have a Step 2 CK score. I'll just say this right now. One thing, because I do a lot of application advising with lots and lots of students, right? One thing that is that has kind of started shining through a lot of cycle, but is especially pervasive with this cycle is, many programs are no longer extending interviews to people that don't have Step 2 CK scores when the era's application opens, or they won't extend any invites to you after you've submitted your scores. So I'll just encourage you, before the guideline was, if you did decently well on Step 1, you can apply for era without Step 2 CK scores. That is still true. And no one is going to come out and tell you that without Step 2 CK scores, we won't send you an interview invite. They just won't send you an interview invite. So folks, please be careful of that. Just really, really be careful of that to be perfectly honest with you so that you don't get host for things that are literally beyond your control.

So just try to get your Step 2 CK done in time. I hope you don't have another COVID cycle, but you should really should be taking your exam by the end of July or the end of the first week in August to just be in a good situation so that you don't put yourself in a precarious position. That's the first thing, right? And again, I suspect that this is going to become more and more important as the years go by, right? We're really just not having Step 2 CK is you're not going to get any interview invites regardless of how well you did on Step 1. Okay, now, second thing I want to talk about is a is a life lesson, right? And my life lesson for today is gentleness. So what is gentleness? Gentleness is just a person being gentle, just having like a calm, cool, collected demeanor. Right? And many people think that gentleness is just a personality thing. It's not really a personality thing. It's it's smaller for life lifestyle choice. Really gentleness is a lifestyle choice because you can be gentleness in many different things, right? So it can be gentle in speech, right? A person that is gentle in speech when they speak, you can tell that these people are gentle, right? Because if you're the kind of person that you know just yells, yells, yells, yells, yells or response to people in an elevated tone, that's not being gentle in speech, right? So be gentle in speech, becoming your speech, right?

Like you don't have to yell, you don't have to elevate your voice to get the point across, right? And this is something that you know some people struggle with, especially when you're in a heated situation. And many of you think that, oh, heated situations are just situations where someone annoys you. No, no, no, no, even as a healthcare provider, when you're running a court or a patient is crashing and burning or the materials you have are not working as they should bring. Those things will cause you to get angry, right? Not that you just begin to retort at people, right? Again, just be gentle in speech. The thing is, you may be passing the right message across to people, when you pass it across in an elevated pitch, elevated tone, the message doesn't really come through, right? Just something you want to keep in mind. So I'll just encourage you, just be gentle in speech, be gentle in the way you approach life. The thing is when you approach life from a gentle perspective, one you become almost more observant of life, like things don't just slip by you, you're able to mentally keep track of many things, right? And just being gentle just reduces your stress levels, right? When your gentle is almost like you're telling the world, it's not the circumstances of the world that would determine how I respond. I would determine the where I respond to circumstances.

And that gentle persona, it just makes you go through tough situations and just go through, like just float right through and do well, right? And again, God rewards people that are gentle, right? Blessed are the meek. The person that is meek is a gentle person. Blessed are the meek, they will inherit the earth. And if you read the New Testament some more, gentleness is actually one of the fruits of the spirit. So again, just encourage you, just be gentle, have that gentle mindset, have that gentle persona. Later, reflect in the way you relate with people, in the way you talk, in the way you even go about your life. You don't have to do things with such intensity, right? That is unfortunately something you see a lot in medicine, right? Even being guilty of this, I'm not saying this as some more perfect and everyone business. No, I have definitely been intense, I've definitely been impatient, right? In the past, right? But the thing I will just encourage you, and it's something I'm still working on. So again, we're all learners here, right? And it's almost like this life lesson, I'm teaching myself something, right? So like not being intense, just being calm and gentle, right? That is just always very helpful. It actually is a good way to be, if you want to be a patient person in life, you need to be gentle. The person that is impatient cannot be gentle, right? So think that gentle persona, it will really take you along with life.

So thank you for listening to me, speak for, this is about 36 minutes now. And I will see you in the next podcast. God bless you and I will show the best with your application cycle on your exams. Thank you.

Chronic elevation of cardiac output that ultimately tires out the heart muscle, leading to systolic heart failure.

Anemia (iron deficiency), AV fistula formation, Paget's disease, hyperthyroidism, nephrotic syndrome, etc.

The low oxygen-carrying capacity of the blood causes tissue hypoxia, stimulating the heart to increase cardiac output (CO) to compensate.

It bypasses the capillary bed, preventing gas exchange and causing chronic systemic hypoxia.

Thiamine (Vitamin B1) deficiency (Beriberri).

Increased vascularity and blood volume demands within the bone marrow.

Low O2 carrying capacity $\rightarrow$ Tissue hypoxia $\rightarrow$ Compensatory increase in Cardiac Output (CO) $\rightarrow$ Heart failure.

Paget's disease (or Osteosarcoma risk).

Bypassing capillaries $\rightarrow$ Loss of gas exchange $\rightarrow$ Hypoxia $\rightarrow$ Increased CO.

Pulmonary Arteriovenous Malformations (AV Ms) creating a shunt, bypassing oxygenation in the pulmonary capillaries.

Protein loss $\rightarrow$ Decreased oncotic pressure $\rightarrow$ Reduced effective circulating volume/BP $\rightarrow$ Increased CO attempt to maintain perfusion.

Hyperthyroidism (increases beta-1 adrenergic receptors).

Thiamine (Vitamin B1) deficiency.

Low O2 carrying capacity $\rightarrow$ Tissue hypoxia $\rightarrow$ Compensatory increase in Cardiac Output (CO) $\rightarrow$ Heart failure.

Paget's disease (or Osteosarcoma risk).

Bypassing capillaries $\rightarrow$ Loss of gas exchange $\rightarrow$ Hypoxia $\rightarrow$ Increased CO.

Pulmonary Arteriovenous Malformations (AV Ms) creating a shunt, bypassing oxygenation in the pulmonary capillaries.

Protein loss $\rightarrow$ Decreased oncotic pressure $\rightarrow$ Reduced effective circulating volume/BP $\rightarrow$ Increased CO attempt to maintain perfusion.

Hyperthyroidism (increases beta-1 adrenergic receptors).

Thiamine (Vitamin B1) deficiency.