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Valvulopatías 2025 Diagnóstico y Tratamiento | VILLAMEDIC — Transcript

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0:07Alright, we're entering a part that is
0:11quite, quite important because it talks
0:14about a very profitable topic, because
0:17if we learn it like robots, we'll ace
0:20it right away, huh? Which is valvular
0:23heart disease. Valvular diseases, we
0:26shouldn't complicate our lives, we
0:28shouldn't; we must master everything
0:30we're going to talk about in this class
0:32. I recommend you don't delve deeper
0:35than what we discuss in this class,
0:38okay? Eh, and when you go to study any
0:44valve question, anywhere, you stick to
0:47this class. It's as simple as that.
0:50Right? So, first we have to understand
0:54some concepts. Uh, the numbers first,
0:58the age group, generalities. When we
1:03talk about valves, we are going to
1:05understand that talking about valvular
1:07disease in almost every exam question
1:09we're asked, they are older people;
1:11there won't be any questions about kids
1:14. So, the majority are older people. So
1:18, the majority are people over 70 years
1:23old, that is very important. And
1:26because of that, when they talk about
1:29the age group, there is one valve that
1:31they ask us about the most, which is
1:34aortic stenosis, where just with the
1:36age one already has to more or less be
1:42able to say what the cause is, right?
1:44Calcification is the most asked-about
1:49valvular disease and it's the most
1:51frequent. Out of 10 patients who come
1:53to a hospital with a valve problem, out
1:55of 10, seven are aortic stenosis. So,
1:59practically this is the cause you will
2:01see most in all your exam questions.
2:05When they are younger, the causes are
2:11highly related to a pattern we call
2:13bicuspid aorta. And the bicuspid aorta
2:20is highly related to, what is it?
2:26Turner syndrome, and Turner syndrome is
2:32also highly related to coarctation of
2:34the aorta. This is an exam question.
2:36Whoever remembers these two already has
2:38two points. So, age in the matter of
2:42aortic valve, no-brainer. Yeah, that's
2:46a given. Another one, the clinical
2:49presentation. You will see that the
2:53patients will have a similar clinical
2:57presentation. There's, all valvular
3:02diseases, all, look, when they have an
3:04acute case, all of them start with
3:11dyspnea. It’s easy to understand,
3:19right? For example, it says patient who
3:22comes in with dyspnea, there's a murmur
3:23, damn, it could be anything, you
3:25understand? I mean, you can't just say
3:28aortic stenosis or aortic, you're crazy
3:30. It could be any of them. I mean,
3:32whatever they tell you with dyspnea and
3:34a murmur, it could be anything. I mean,
3:37you can't just say, "No, that's caused
3:38by mitral insufficiency, you're not
3:40crazy." So, in an acute state, they're
3:43all going to tell you dyspnea. So,
3:46you'd have to be crazy to check off a
3:48valve just for saying dyspnea. But this
3:52is the most common clinical
3:54presentation in decompensation
3:56scenarios. Okay? Right. When the guy is
4:05compensated, meaning he's in a chronic
4:08state, he's compensated, right? The
4:10typical patient where you say, "The
4:12gentleman over there, he has aortic
4:13insufficiency." Oh, yeah, yeah. He's a
4:16regular, he's come to his check-up.
4:18He's supposed to be chronic, but he's
4:19stable, he's coming to his appointments
4:21, right? In chronic cases, each valve
4:24does have its own characteristics, do
4:26you understand? So, for the chronic
4:30ones, you will have to learn the
4:33characteristics of each valve. They
4:39have their own traits. For example, let
4:41me put it here, let's put, let's divide
4:46this. Aortic stenosis, aortic
4:53insufficiency, mitral stenosis, mitral
4:59insufficiency. What does characteristic
5:03mean? Let's use another color. It means
5:05that if I hear that word, I don't even
5:08need to reason. Do you understand? I
5:13mean, I just mark it and move on to the
5:14next question. Look, aortic stenosis,
5:19if there's any question about a patient
5:22who comes in with a murmur, syncope is
5:32basically the hallmark of aortic
5:35stenosis. "No, doctor, I've seen my
5:38uncle has insufficiency and he had
5:40syncope, doctor." Yeah, but your uncle
5:41is taking an exam. No, doctor. Do you
5:45understand? I hope I'm making myself
5:47clear. Okay. You guys are machines, for
5:50the exam you have to be machines and
5:52for your patients you have to be human,
5:57not the other way around. That's what I
6:00tell my residents. For the patient,
6:05human; but for the exam, a machine, a
6:11machine, none of that "well, maybe it
6:13could be this." No, no, no. For the
6:16exam, there's no "to err is human." You
6:18are a machine, you cannot fail. Oh, how
6:22demanding. You're destroying my mind,
6:24my mental health. No, for the exam,
6:26there is no mental health. For the
6:29patient, there is mental health, do you
6:31understand? I mean, stop the nonsense.
6:34Ah, for the exam, there is no mental
6:38health, there isn't. Become machines,
6:44no feelings for the patient. Become
6:48superhuman. Cry, hug each other, throw
6:51yourselves on the floor. That’s what
6:55you studied medicine for. I mean, you
6:58aren't just machines and you aren't
6:59just purely human. You are a mix of two
7:02perfect things. Do you understand? That
7:06is why you are going to get into that
7:07dilemma, right? Saying, "I feel a bit
7:09strange." Of course, because you live
7:12in a brutal ambivalence of being a
7:13machine and being a human. Do you want
7:16to cry sometimes? Sure, but you are
7:18with humans, yet sometimes you feel
7:20like a machine because you are in
7:21active mental activity, right? So, stay
7:25calm, but right now we are in class, we
7:27are preparing for an exam and here you
7:30do have to be a machine. When you take
7:33your exam, the day before your
7:35boyfriend or girlfriend breaks up with
7:37you, you take the exam like a machine,
7:40you get in, and then you cry. It's
7:43because the machine took it, do you
7:45understand? Machine, nothing affects
7:49you. Nothing affects the machine. Get
7:53that into your heads. Doctor, I can't
7:55take it anymore. Or get out of here.
8:00Nothing affects the machine. But it
8:02does affect the human. When you are
8:04with your patient, you won't tell them,
8:06"No, ma'am, your husband has already
8:08died." But doctor, why do you say that
8:09to me? That is how it is. And there you
8:12forgot that with them you have to be
8:13human, do you understand? Separate
8:17those two and you will be successful,
8:19but do it well. But it is an art, it is
8:22a line that some don't know how to
8:24separate. Some move on from the exam,
8:27enter residency, and continue to be
8:29machines. Yes. So, don't lose sight of
8:32that. And some have been very human at
8:35home and entered medicine and saw that
8:37they encountered machines, they said
8:38how inhumane. It's just that it is that
8:42problem. So here I am going to teach
8:45you a little bit to balance those
8:47patterns. Yes. Mitral stenosis. I see
8:51the word and I mark it quickly. What
8:54thing? A word that appears and I mark
8:58it quickly. Otherwise it's
8:59instantaneous. The word is clear. it
9:04says like this, opening snap, rumble.
9:15Look, they are words that appear in the
9:22construction of a question and you have
9:24to mark, don't waste time. I see a
9:31patient comes in with a murmur and a
9:34very strong pulse, water-hammer pulse,
9:42a bounding pulse, a pulse, everything
9:44that has to do with the pulse, giant
9:47pulses, large pulse, giant bounding
9:55pulse, aortic insufficiency. There are
10:00only two questions on an exam that can
10:03scare you when they ask about a murmur
10:06and a wide pulse. Aortic insufficiency
10:11and the ductus. When you see wide
10:15pulses it is typical of the ductus, it
10:19is classic. But doctor, did you have
10:22doubts if it was ductus or aortic
10:24insufficiency? And and I failed, doctor
10:29, I marked ductus. What a shame. But
10:32why didn't you see at the beginning
10:33that it said an 85-year-old man? Ah, do
10:38you see? So, age is useful to
10:40differentiate between ductus and aortic
10:41insufficiency. So, you have to see the
10:43difference between one and...but
10:45remember, those two are the ones that
10:46make everyone fall for it. Murmurs with
10:48wide pulses, those two are classic for
10:50tripping people up. Okay. Mitral
10:53regurgitation. Same murmur as the VSD,
10:59you can also fall for systolic murmurs,
11:00but that's not what you're going to
11:01mark, that's not what's going to guide
11:03you—the radiation. No one radiates so
11:06strongly to the axillary area. Axillary
11:09radiation. Just like aortic stenosis
11:16radiates to the carotid. This is the
11:19radiation. The the word axillary
11:20radiation marks mitral regurgitation
11:21immediately. Don't waste time. I mean,
11:23these are the four things I'm telling
11:26you, characteristic words that you have
11:28to mark right away. You can't waste
11:31time here. This is either you know it
11:34or you don't, and you move on to the
11:35next one. Yes. Good. The diagnosis for
11:38all valvular heart diseases is an
11:40echocardiogram. The best is the
11:44transesophageal. The transesophageal is
11:48always better because it sees finer
11:50structures. If it's endocarditis, for
11:54example, it sees vegetations smaller
11:57than 5 mm. So that's why the
12:01transesophageal is better. A
12:04transthoracic echo measures vegetations
12:06larger than 5 mm and a transesophageal
12:09measures those smaller than 5 mm.
12:12That's why the esophageal is better.
12:14Are we good? So that's from now on,
12:18look, we are currently on the
12:19generalities. Ah, you have to become a
12:21pro at this. Now, regarding the
12:23therapeutic part, for all patients when
12:27they are going to be treated for a
12:29valve, step one, they will always
12:32determine the severity, and the
12:34severity is done by the ultrasound.
12:38Correct? Ultrasound. Okay. So, the
12:44ultrasound will study, the
12:46cardiologists will stratify the
12:48patient's risk, and that doesn't matter
12:51to me. You might say, "I'm not
12:54interested because, in the end, I treat
12:56it...if I treat it, you want to know
12:58how I treat that." But it depends on
13:00that. Why? Look, are all severe cases
13:04operated on? No, no, no. There is a
13:12rule that says that when valves are
13:15severe, it doesn't necessarily imply
13:17operating on them or changing them. If
13:21it is severe and has symptoms, yes,
13:26surgery must be performed. So, severity
13:33alone, echocardiographically, is not a
13:36criterion for surgery; there must be
13:38symptoms. There are men walking down
13:43the street with their severe aortic
13:45stenosis for 10 years and they have
13:50nothing, no discomfort, do you
13:53understand? But what would happen if
13:55they had been operated on? Many of them
13:57would already be dead. Why? Because the
13:59risk of dying in the OR exists. So, ah,
14:04geez, doctor. And what would happen? If
14:10the patient is not severe, they would
14:14be in a moderate state. Could someone
14:18who isn't severe be operated on? They
14:21could. Mm. In what situations, if it's
14:25not severe, could they be operated on?
14:30For example, when it's in conjunction
14:33with another surgical indication. For
14:37instance, here, concomitance.
14:41Concomitance with another indication,
14:46with another indication. For example, I
14:53have a patient with severe aortic
14:55stenosis or a moderate aortic stenosis,
14:58let's say. and they need two bypasses,
15:02so you aren't going to open their chest
15:05just to do two bypasses, do you
15:09understand? A medical board is held,
15:12the valve is replaced, and they also
15:14get their two bypasses. So, those go to
15:16a medical board; they're going to ask
15:18you that on an exam, right? Because
15:20they go to a medical board. So, which
15:22are the ones you'll only be asked about
15:24where no one has doubts, where there is
15:26evidence? Ah, a recommendation, one,
15:29this one here, severe with symptoms,
15:32and that applies to all valves, and
15:35with that, you’ve got it locked, nice
15:38lesson. All valves go through that
15:41stage. All, all the valves, all of them
15:47. Is a coronary angiogram indicated?
15:50Not all. Only those over 40 years old
15:56to rule out coronary lesions. Maybe a
15:59valve replacement plus a couple of
16:00bypasses is needed. Step three, medical
16:05treatment. You are going to provide
16:08medical treatment if heart failure
16:09requires it. And the treatment, let's
16:13analyze it; all valves are treated via
16:16open surgery. We have the aortic valve
16:20and the mitral valve. Well,
16:23percutaneous treatment has developed
16:26very well in the aortic valve, very
16:31well developed in the aortic valve,
16:37especially in patients at high risk.
16:43You will find this as TAVI. Yes, it is
16:49the transcatheter aortic valve
16:51implantation in patients who have a
16:57higher surgical risk, and if the
17:02patient doesn't have such high surgical
17:05risk, an open treatment can be done by
17:10opening the chest. And by opening the
17:14chest, we have two options. We have a
17:18valve called biological and a valve
17:20called mechanical. What is the
17:24difference? That the biological one
17:28doesn't need anticoagulation, and the
17:33mechanical one does. And this means the
17:39biological one needs replacement in 15
17:43years. Replacement in 15 years. On the
17:49other hand, the mechanical one is
17:51permanent. A question, when
17:56anticoagulation is performed, what is
17:59it like? It is done only with warfarin.
18:05Only with warfarin. And then a student
18:13asks me, "Doctor, can I use waran?" But
18:17what did I write there? I want you to
18:20read it again. Did I write warfarin or
18:22what did I write there? Read the whole
18:24thing. Just warfarin, but you, ah, only
18:30you. You're the one who's surprised
18:32there. Yes. No one else. So, how is
18:37anticoagulation with warfarin monitored
18:40? With INR. Question, the INR should be
18:48between what values? Very good. Between
19:002.5 and 3.5. I say it like that, don't
19:04I? 2.5 to 3.5, half of that for aortic
19:08valves and the other half for mitral
19:13valves. Right? So here for aortic, here
19:20for mitral. So you can remember. Yes.
19:25Right. Now comes a question from
19:28someone. Doctor, I have a patient with
19:31an INR of 4, is that okay? But what
19:34number did I put up to? Do you see? If
19:38those are the questions, I anticipate
19:40the questions. Oh, doctor, that was the
19:42question I was going to ask you. But
19:44that question says three point
19:45something there. Why do I tell you that
19:47? Because they are going to put that
19:48there. They are going to ask, how much
19:50anticoagulation can a human being
19:52receive? Up to 3.5. A human being with
19:56more than 3.5 is at risk of a brain
19:58hemorrhage. Spontaneous. So, be careful
20:02. And there are people, I think the
20:04case I saw, I tell you, I saw it
20:06because I later started checking the
20:08literature and I found higher cases,
20:10right? But I saw a patient with nine. I
20:14, I saw it as a resident, I remember in
20:16the ER a patient with an INR of nine
20:18who had been bleeding from the nose,
20:20epistaxis. So, we had to give him. What
20:24would you, how would you treat a guy
20:26who comes in with a valve and an INR of
20:27nine? What would you do? What is the
20:30first measure? Plasma. Exactly. Correct
20:34. No, the first measure is plasma. You
20:37stop the warfarin, you give him plasma.
20:40Yes. And why do I say stop it, doctor?
20:42It's evident, it's logical. No, it's
20:44not. It's not logical, because in the
20:47ER they kept giving him his warfarin,
20:49as it is indicated, and they were
20:51giving him his plasma too. And he's
20:55been hospitalized in the ER for 7 days
20:57and his INR was still at five. But
21:01they've been giving him plasma every
21:02day, but they are also giving him his
21:04warfarin every day. I'm telling you
21:06that happens. Yes. Look how important.
21:11I, no, I'm always going to say that
21:13doesn't happen, but that's obvious,
21:16there is no "obvious" in Peru. Always
21:20write it down, write it down. Just put
21:24it there, write it down. It is very
21:27important. Very well. Understanding
21:30this, I will now highlight the most
21:32important aspects of each one for you,
21:34and you must take each of those aspects
21:36with you. Right. A question: the age
21:48ranges for biological and mechanical.
21:50Have you noticed that I haven't given
21:52you the age ranges? Why do you think
21:54that is? Because it's changing. If you
21:59had listened to one of my lectures 3 or
22:014 years ago, or a year or two ago, I
22:03would have set a 70-year cutoff. Today,
22:09I no longer set ranges because there
22:11are 70-year-olds today using biological
22:14valves because you see them, they're 70
22:17. Tom Cruise, how old is he? He doesn't
22:23look 65, do you understand? So those
22:27people say, "Why are you going to put
22:29me on warfarin, why would I expose
22:30myself to that if I make my Mission
22:32Impossible movies?" I won't be able to
22:36jump, won't be able to climb down
22:37towers, won't be able to do my whole
22:38show—you're crazy. So, what is
22:42happening? Current valve guidelines are
22:45no longer as strict because in the past
22:48, it was said that anyone over 70
22:50should get a biological one, since
22:53they're older and won't live long, and
22:55anyone under 70 should get a mechanical
22:58one so it doesn't have to be replaced.
23:02Today, the guidelines are no longer
23:04that strict. I'm telling you this
23:07because now, you are mandatorily
23:08required to ask the patient before
23:10surgery and inform them of this
23:12currently. You go and say, "Sir, we are
23:15going to place a biological valve.""Do
23:17you agree?""It doesn't require
23:19anticoagulation.""Oh, that's cool.""But
23:22we also have the mechanical one, which
23:23we probably won't have to operate on
23:25again, but we do need to anticoagulate.
23:26""But I like the other one because I
23:30won't take pills, I'll do my exercises
23:31and live a normal life, even if there's
23:33a chance of reoperation in 15 years.""
23:35But in 15 years, that's fine, operate
23:36on me again, no problem, I'll just sign
23:38." And why? Because the TAVI, the TAVI
23:41valve is also made with a biological
23:43valve. So, there are currently changes
23:48in surgery regarding valves. Yes? So,
23:51well, what you are receiving right now
23:54is a very, very current lecture. Yes,
23:57the one who bought the bootleg version
23:59doesn't know that. Good, so in aortic
24:02stenosis, this is very important. Look,
24:05the most frequent valvulopathy of all,
24:07that is, the one they will ask me about
24:10the most on exams. Got it? Now, what is
24:13the etiology? The etiology is
24:16calcification. So they are going to ask
24:18me, I’m going to change the color of
24:20the text. Look, over 70, calcification;
24:25under 70, bicuspid. Right,
24:30pathophysiology, the outflow tract
24:33closes. Look, as the outflow tract
24:36closes, what we are going to observe is
24:39that the patient will have a higher
24:42pressure gradient. There is a lot of
24:45pressure here with respect to the aorta
24:47. There is a large pressure difference.
24:49That is called a pressure gradient. So,
24:52there is a large gradient difference.
24:55The gradient difference is what one
24:58measures for severity on the echo.
25:03Right. That is very important. Okay?
25:05Now, watch how I am going to explain
25:08the entire clinical picture to my
25:11patient based on this process. Number
25:15one, since the valve is closed, the
25:18patient develops hypertrophy, right?
25:22Significant ventricular hypertrophy.
25:25Since the valve is closed, the blood
25:27flow to various organs will suffer,
25:29especially the brain. So, the patient
25:32will generate the famous DAS.
25:35Clinically speaking. Here we will put
25:37DAS. Dyspnea, Angina, and Syncope. This
25:43is very important because I am going to
25:45put it here for you. Observe this, exam
25:47question. This is the survival once
25:51they appear. For example, the patient
25:55usually when they are diagnosed goes to
25:57the doctor and the doctor says, "Sir,
26:00you have aortic stenosis on the
26:02echocardiogram.""Oh no, doctor, I have
26:05stenosis," and they have aortic
26:07stenosis. Oh, and how was it diagnosed?
26:11Because the gentleman had gone either
26:14for Dyspnea, or for Angina, or for
26:16Syncope, with any of these three.
26:19It’s not known. I mean, no one goes
26:22to a place to get diagnosed without
26:24having those three, unless they get an
26:26EKG and on the EKG they find what? EKG
26:30hypertrophy. Left ventricular
26:33hypertrophy. Is it well understood? So,
26:38what have we seen? That when a patient
26:40develops severe aortic stenosis, Look,
26:46here the patient is severe, but the
26:48patient can be severe for many years,
26:51but once they develop symptoms, look
26:54how many years they have to live. Look,
27:00If the patient develops heart failure,
27:02dyspnea, survival 2 years. If the
27:08patient develops syncope, survival 3
27:10years. If the patient develops angina,
27:125 years. Exam question. So, which
27:15symptom has the worst prognosis?
27:21Dyspnea? Because its survival rate is 2
27:26years. Okay? So, when a patient with
27:33aortic stenosis comes in, in exam
27:35questions they will always present with
27:38either angina or syncope. In exam
27:42questions, they never present it with
27:44dyspnea. Did you notice? A patient who
27:47comes to the office because they have
27:49anginal pain or a patient who comes to
27:51the office for syncope. Why? Because
27:53these two are at the onset. They never
27:57put that they come in for dyspnea,
27:58because dyspnea is the one with the
28:00worst prognosis, it has a shorter
28:01survival. Correct? Right. When studying
28:07the patient's clinical presentation,
28:08what do you find? Look, sound, first
28:11heart sound, second heart sound.
28:15Between the first and second heart
28:17sound, observe the pattern. It is a
28:21diamond-shaped murmur, a diamond-shaped
28:24systolic murmur. Okay. So, we are
28:29talking about a systolic,
28:31diamond-shaped murmur, okay? Systolic
28:35murmur. All of this, always remember
28:38that between the first and second heart
28:40sound is systole, and again between the
28:41second heart sound and the next first
28:43heart sound is diastole. So, it is a
28:46systolic murmur, guys. It is a systolic
28:49murmur, don't forget this. The
28:53treatment, you already know, if it is
28:55low risk it will be TAVI. Low risk TAVI
29:02. Okay. Sorry, high risk. I'm talking
29:05nonsense. If it is high risk, it will
29:08be TAVI. High risk precisely so they
29:13can handle it. If it is low risk, open
29:17surgery. I'll erase it with this. Very
29:26well. So, this is what you have to take
29:29away. You already know that TAVI uses a
29:32biological valve, okay? Open surgery
29:34can be biological or mechanical,
29:36depending on what is proposed to our
29:38patient. This is very important. When
29:42studying these little patients, this
29:44systolic murmur has a characteristic.
29:48The radiation, radiation to the neck.
29:54There will only be two radiation
29:55questions that will come your way.
29:59Aortic stenosis with radiation to the
30:00neck and mitral insufficiency with
30:02axillary radiation. No others will come
30:04, so with that, you will get them right
30:07away. Okay? Aortic insufficiency, the
30:13other side of the coin. Aortic
30:16insufficiency. We have two situations,
30:19an insufficiency that appears suddenly,
30:22an acute case, or a chronic case. If
30:26the insufficiency is an acute case, it
30:28may have happened due to two situations
30:31. A first situation is that the
30:34ascending aorta dilated significantly,
30:37and this happens a lot in aortic
30:39dissections. Another situation could be
30:44that the aortic valve itself has become
30:48infected, as in infectious endocarditis
30:51. So, these are two situations that
30:53happen a lot. There are patients who
30:54will present with acute aortic
30:55insufficiency. You should think: aortic
30:57dissection or infectious endocarditis,
30:59right? It's a classic. And in cases of
31:02chronic aortic insufficiency, meaning
31:04you've had it for a good while, there
31:07are also two very frequent situations.
31:10We have ascending aortic aneurysms that
31:13end up causing this, and patients where
31:17the valves are affected, like in
31:19rheumatic fever. Okay? Rheumatic fever.
31:27So, this right here is very frequent;
31:29it's very important for us to take it
31:31into consideration. Very frequent. So,
31:35realize that in the case of aortic
31:37insufficiency, there are four ways it
31:40presents. Aortic dissections are very
31:43closely associated with Marfan syndrome
31:46. On any exam questions that mention
31:49MARFAN, please mark aortic dissection.
31:52It's always like that, okay? And
31:54especially, this is the pattern that
31:56comes into emergency rooms a lot.
31:58Classic, always when they call, right?
32:00Hello, Dr. Briseño, a patient with
32:02Marfan, and you immediately think aorta
32:04; I'm in aorta, you never lose. Aorta
32:07is classic, it's always like that. So,
32:09you have to keep this in consideration.
32:11Remember: one cause of the aorta and
32:13one cause of the valve in acute cases.
32:15One cause of the aorta and one cause of
32:17the valve in chronic cases. Now, in
32:20pathophysiology, what happens? Since
32:24the aortic valve is failing, when the
32:26aortic valve fails, what happens? The
32:29blood is falling back, it's falling.
32:34All the blood is leaking back down. So,
32:37as the blood falls, the blood leaves
32:39and falls right back in. So, that is
32:43where a problem is occurring. So, let's
32:45look at the ventricle here. The blood
32:48is falling back in again. Who is
32:50opening at that moment? The blood
32:53should be outside, right? And it's
32:56affecting whom? The anterior mitral
33:01valve. The anterior mitral valve cannot
33:06open well. Why? Because the blood is
33:09leaking back from the aorta. So, it
33:12doesn't allow the diastolic filling to
33:14descend properly. So, the type of
33:18murmur we are going to see is a
33:20diastolic murmur, okay? So, it is a
33:25predominantly diastolic murmur, unlike
33:27in stenosis. While we see a systolic
33:32predominance in stenosis, in aortic
33:34insufficiency, the predominance will be
33:37more of a diastolic type. Yes, that's
33:41very interesting regarding the
33:43predominance, okay? The predominance is
33:46going to be of that type, very, very
33:48regurgitant in this state. This moment,
33:52this murmur of interference that is
33:55leaking blood from the aorta and
33:57doesn't let the anterior mitral valve
34:01open well for blood to pass. That
34:04murmur has a name, it's called an
34:06Austin Flint murmur. And it's happening
34:09here. It is precisely an aspirative
34:12murmur. This is very important, the
34:17Austin Flint murmur. So, the Austin
34:20Flint murmur happens because of that.
34:24Austin murmur Flint. So, what is
34:31happening here? The heart keeps filling
34:35up, right? It pumps blood and fills
34:37with more blood again. The left
34:40ventricle fills with blood coming from
34:42the atrium and blood leaking from the
34:44aorta. So it is dilating the heart. So
34:47these patients, what? They are going to
34:49have dilation of the left ventricle and
34:52since they develop dilated heart
34:55disease, these patients tend to have
34:58large hearts. Patients with aortic
35:00insufficiency have large hearts, they
35:03develop big hearts. So these patients
35:07develop larger hearts and the clinical
35:10onset for these patients is more of a
35:13dyspnea type. They present quickly with
35:17dyspnea. Why? Because they present with
35:20heart failure, because they have
35:22dilated heart disease. Did you notice?
35:25So, the most important accompaniment.
35:29What are they going to ask you? This,
35:32the Austin Flint murmur. Why? Because
35:35this happens clinically. What else will
35:38they ask you? The clinical signs that
35:40occur in aortic insufficiency. The
35:44blood leaves, look. The flow leaves,
35:46look, the flow leaves and then it's
35:53lost, right? The aorta pumps flow, but
35:57right away the valve, instead of
35:58staying closed, it steals it from you.
36:00So it does this, did you notice, it
36:03does this. Right. When the
36:05insufficiency is mild you don't feel it
36:07, but when it's moderate you feel it
36:09more. When it's severe you feel it more
36:11. And those sudden changes begin to
36:15cause a whole series of clinical
36:17symptoms and they have names. That's
36:20what's striking. They have names. For
36:23example, the most frequently asked in
36:25history, the pulse water-hammer or also
36:35called Corrigan's pulse. Corrigan's
36:40pulse. Another, for example, we have,
36:47you see the nails and you see the nail
36:50turning pale red, pale red, like it's
36:53pulsating. That is called Quincke's
37:01sign. Positive Quincke typical in nail
37:06pulsation. I will never forget aortic
37:13insufficiency. Aortic insufficiency
37:16really left a mark on me in
37:18cardiovascular semiology. Why? Well,
37:22exactly, uh, when I was rotating in
37:29ophthalmology, I remember I was
37:31rotating in ophtho, but I remember, I
37:34don't know, I wasn't studying anything
37:36in ophtho, I mean, I was doing
37:39something else, I wasn't doing any
37:41ophtho and the ophtho professor noticed
37:44during practice, he saw me distracted.
37:49"Let's see, design, come here." I
37:53didn't even get close. "Ah, examine the
37:56gentleman from...""You're in love, for
37:59sure.""No, he's distracted.""No,
38:02professor.""Go over there and give me
38:05his,""what's this called?""The
38:10flashlight." He gave me his little
38:13flashlight, right? When I started to
38:15put the flashlight on, no, I'll never
38:17forget it. So the gentleman is sitting
38:19like this and I put the flashlight on
38:23him, right? And the pupil did this. I
38:31look and I turn around, right? And I, "
38:36Doctor, excuse me.""Keep examining." I
38:41look, I keep looking at the pupil and
38:43the pupil did this. The pupil was
38:45pulsing. I was so amazed, right? And I
38:51started to look at him, to touch him,
38:52and then I kept looking at the
38:53gentleman. The gentleman kept looking
38:55at me, right? No. And he did this,
39:00right? Like he was confirming for me,
39:04right? I was saying, "Man, the
39:06gentleman realized I wasn't studying,
39:08right?" Because he was doing this to me
39:10. So I thought, I was waiting for the
39:17doctor to stop talking to my classmates
39:19, since it was like a punishment
39:21sending me to examine the patient,
39:23right? So I started to keep examining
39:26him, right? And I clearly saw the whole
39:30aortic arch area pulsating, it was
39:33popping out. "Well, it's this." I said,
39:35I was discovering the patient myself. "
39:38It's this." And then for the first time
39:41I saw Quincke's sign, I saw his fingers
39:43. His fingernails were pulsating. I had
39:48him lie down on the gurney. "Sir, can
39:50you lie down on the gurney?" The
39:52gentleman lay down and the professor
39:54told me, "Okay, did you realize it yet?
39:57" So then I realized that the professor
40:00had sent me so that I would notice it.
40:06So I say, "Yes, now.""Who can tell me
40:09what he had in his pupil?" He asks the
40:14question. "Whoever tells me what he has
40:17in his pupil gets a 20 on the exam and
40:19goes home right now." Oh, I don't know.
40:25Once again, everyone started looking at
40:26the pupil; the pupil is like this. The
40:30gentleman was also cooperating. This is
40:31this is the topic. This is the topic.
40:33It is everyone was watching. It was the
40:38Landolfi sign. That is a sign, for
40:42example, that is also seen in aortic
40:44insufficiency. The Landolfi sign or the
40:51pulsating pupil. Why am I telling you
40:55this? Because the only valvulopathy
40:58that uses many eponyms and that keeps
40:59appearing on all exams, including the
41:01latest ones, is this aortic
41:03insufficiency. It has too many eponyms,
41:07so they put them there, right? The
41:08Landolfi sign. And the gentleman, why
41:10was he doing this to me? Well, doctor,
41:13the Musset sign, which is that they are
41:16doing this all day because the head
41:18movement is just like nodding. So, when
41:21you see your girlfriend doing this,
41:22check that she doesn't have aortic
41:24insufficiency. So, the Musset sign,
41:27let's see here, right? Or the sign of
41:33affirmation, right? So those little
41:39things appear in these conditions,
41:41right? It is very characteristic of
41:44these patients with aortic
41:45insufficiency. Okay? Now, the treatment
41:48, well you already know, if you
41:51demonstrate severity plus symptoms,
41:56surgery. Correct? Very important. In
42:15mitral stenosis, what can we take away?
42:17In mitral stenosis, we must remember
42:21that the etiology in Peru is rheumatic
42:24fever. Yes, generally a history of
42:27rheumatic fever, more or less 20 years
42:30having had rheumatic fever, and what is
42:32striking here is that since the mitral
42:35valve is tightly closed, the left
42:37atrium grows too much. Look, it looks
42:39like an extraterrestrial, right? An
42:42alien. Look, a huge left atrium. So,
42:45and all of this goes towards the lungs,
42:51right? So, the lung is swollen,
42:55practically full of water. That is why,
43:01since the lung is full of water, the
43:03patient can cough and generate
43:04hemoptysis. So, a lot, the only
43:09valvulopathy, the only one clinically
43:12that will have hemoptysis is this one.
43:15If you see an exam question, hemoptysis
43:17mark mitral, don't waste time. Do you
43:20understand? It says, "But, which one
43:21could it be?" It said diastolic murmur.
43:23But it says hemoptysis, "Hey, why are
43:24you wasting time?" Oh, you were right.
43:27Do you understand? Good. So, by having
43:30such a large and dilated atrium, a
43:33dilated left atrium, what it does is
43:35promote the formation of atrial
43:37fibrillation, which will generate
43:39thrombi. It generates thrombi. By
43:46generating thrombi, it is the main
43:48cause of embolism, the most frequent
43:50cause, the most frequent cause of
43:52embolism, correct? Where do embolisms
43:55like to go the most? To the leg. Good.
44:00To the leg. Which section? Good.
44:04Hunter's canal. Where is Hunter's canal
44:07? Very good. Between the femoral and
44:13the popliteal. That's where it forms,
44:14right? When the femoral transforms into
44:16the popliteal, that's called the
44:17Hunter's canal. So, what is the
44:21catheter that removes clots called?
44:24Fogarty. Very good. So, this right here
44:28is characteristic, as everything
44:30continues to get congested, the facial
44:32veins here also form the famous malar
44:34flushes, right? The face becomes all
44:36congested, right? The flushes, if you
44:48see the word flushes, malar, mark it
44:53right away. You're wasting time. Ah,
44:57and is this pressure high or not? And
45:00how is the ventricular pressure? Low.
45:07That is a test question. That is a test
45:16question. High pressure in the left
45:19atrium and low pressure in the left
45:21ventricle. Okay. Good. So, regarding
45:25the clinical signs we have seen:
45:26hemoptysis, thrombosis, the malar
45:31flushes. Well, here comes the topic of
45:37the murmur. This murmur is the easiest
45:40one to identify on an exam. The famous
45:43opening snap because everything is
45:46tightly closed. After the snap, look,
45:50this is a question. Comes the blum blum
45:54blum blum blum blum blum blum blum blum
45:56blum blum. Second question. Rumble.
46:02Diastolic rumble. Second question.
46:06Diastolic rumble. Third question.
46:14Presystolic accentuation. Why do they
46:18say presystolic? Because it is before
46:20the next systole that occurs here. Who
46:23creates the presystolic accentuation?
46:25The contraction of the atrium. Do you
46:27remember that in diastole there were
46:29three phases? Do you remember that in
46:34this phase this is isovolumetric
46:39relaxation? Here 80%was filled with
46:42rapid filling and here 20%is filled
46:45with atrial contraction. Okay. This
46:47phase is the presystolic accentuation.
46:50Exam question. At what stage is the
46:53presystolic accentuation lost? When the
46:58patient with mitral stenosis enters
47:00what? Atrial fibrillation. When the
47:03patient develops atrial fibrillation,
47:04they lose the presystolic accentuation.
47:13Did you notice? That is a well-crafted
47:15exam question, right? A patient with
47:18mitral stenosis in whom the loss of
47:20presystolic accentuation is observed.
47:22The patient would be entering what type
47:24of arrhythmia: flutter, atrial
47:25fibrillation, multifocal atrial
47:27tachycardia, ventricular tachycardia.
47:29That is how they will present it to you
47:30. And why? Because it loses atrial
47:34contraction. Which is that part, the
47:36third stage of diastole. Very important
47:39, you see? Of course. Treatment. We
47:44have two things. We have the famous
47:49valvuloplasty. Look, valvuloplasty. And
47:58we have mitral valve replacement. What
48:04is a valvuloplasty? We insert a balloon
48:07through the femoral vein, pass a little
48:09needle, puncture the interatrial septum
48:12, and insert a balloon. The balloon
48:16goes in and performs an angioplasty.
48:18Wow, doctor, and why is that done?
48:20Those patients who are already, shall
48:22we say, in a bad way, you know, playing
48:26in stoppage time, they won't tolerate
48:30surgery. So, for valvuloplasties, what
48:33kind of patient would that be? This is
48:35percutaneous. This is percutaneous,
48:38remember. Right. Patients who are in a
48:42terrible, really terrible state. So,
48:46which patients are in a really terrible
48:47state? Basically patients who won't
48:51tolerate surgery. Just get that into
48:54your head: patients who won't tolerate
48:57surgery. Keep in mind a mitral stenosis
49:01that definitely won't tolerate surgery.
49:05Already a patient in cardiogenic shock,
49:08for example, but one who won't tolerate
49:12the surgery. Cardiogenic shock, but
49:15they can't tolerate the surgery. It is
49:19a possibility, that's very important.
49:22Another could be a patient, for example
49:25, who has signs of severe pulmonary
49:28hypertension, meaning where surgery is
49:32contraindicated. Do you see? No, or the
49:36patient here, we're going to do a
49:37mitral valve replacement, maybe, but if
49:39they have severe pulmonary hypertension
49:40, that patient is not, surgery is
49:42contraindicated. It's a lot, but look
49:44at their condition. We have to do it,
49:48let's get them in. So it could be, okay
49:52? So those are two situations that
49:55could easily be improved. Mitral valve
49:59replacement is done in our country for
50:02all patients with mitral stenosis,
50:04everyone, everyone. Mitral valve
50:07replacement, mitral regurgitation. What
50:12do we do in mitral regurgitation?
50:14Causes. Now look, a question.
50:23Presystolic reinforcement is a
50:24physiological phenomenon.
50:26Presystolic reinforcement is a
50:27physiological phenomenon. Presystolic
50:29reinforcement. Right. Presystolic
50:32reinforcement is the third stage of
50:34diastole and it is a physiological
50:37thing.
50:37It is in all of us.
50:38It is in all of us. Yes, of course.
50:41Exactly. Yes. It's just that they are
50:44going to ask you, in what case, in a
50:46patient with mitral stenosis, in what
50:47cases would they lose the presystolic
50:49reinforcement? Fibrillation. Why would
50:52they ask us that? Because we know those
50:54with stenosis develop fibrillation
50:55because the atrium is very dilated.
50:57That is why they would ask you that
50:58question. In mitral insufficiency, you
51:02know that in mitral insufficiency we
51:05can have...Why can a mitral valve fail?
51:08Due to two situations. The first is
51:12because the valve is damaged, I mean,
51:16it's that simple. And the valve is
51:19directly ruined by infectious
51:20endocarditis or rheumatic fever. Okay?
51:25This is very important. The other
51:27reason is due to a situation that
51:29affects the heart itself, the
51:31myocardium. And the most frequent
51:35situation is ischemia. Ischemia can be
51:39acute ischemia or chronic ischemia.
51:43Acute ischemia affects the papillary
51:45muscle, we have seen this. And by
51:48affecting the papillary muscle, it
51:49causes, right, a papillary muscle
51:51dysfunction. And you remember, heart
51:53attack with a murmur, right? Sure. And
51:56when it is chronic ischemia, what
51:58happens? It dilates. The heart dilates.
52:01Every patient who has heart failure has
52:05a dilated heart, okay? Dilatation. So,
52:10if the heart dilates, everything
52:12dilates. Ventricular dilatation. As the
52:17ventricle dilates, it dilates the ring
52:19and that causes mitral insufficiency.
52:23So, normally, what is seen? No. Uh,
52:28this is what I'm telling you, it's very
52:31important. Why? Because surgical
52:35treatment, I'm going to skip ahead here
52:36so it's understood quickly. Look,
52:38regarding treatment, I'm going to tell
52:40you what they do in Peru, okay? Peru
52:44and in the world, to take advantage of
52:47the etiology, because this is very
52:49important. In Peru, whether the valve
52:51fails or the myocardium fails, everyone
52:53gets a replacement. Replacement. Okay?
53:00On the other hand, in the world, when
53:03the origins are valvular, it is
53:05replaced. However, when the origins are
53:10myocardial, a repair is performed. Did
53:14you understand? A repair means, for
53:18example, if it's a papillary muscle,
53:20you put in an ePTFE, which are like
53:22some attachments, uh, and you stitch up
53:24that part that has failed; you don't
53:26have to remove the whole valve because
53:28it is too much, too much sacrifice, do
53:30you understand me? If, for example, the
53:33entire ventricle is dilated, the ring
53:35is repaired. So, but when it is the
53:37valve you do replace it, when it is the
53:39muscle, you do a repair. In contrast,
53:42in Peru, they replace everything. And
53:44why, doctor? Because of the costs of
53:47the devices to perform repairs, nothing
53:49more. Okay. So, if a question comes up
53:52here, you will surely see to mark
53:54replacement regardless of the cause.
53:56Regarding the pathophysiology of mitral
54:00insufficiency, you will see that the
54:03patient has the valve leaking
54:06everything upward, right? No,
54:10everything leaks upward. So, this is
54:13very important. Why? Because you are
54:16seeing here exactly the famous
54:18radiation to the axillary area, which
54:21is an exam question, right? It radiates
54:24to the axillary area. And precisely in
54:27clinical practice, the heart of these
54:28patients is a dilated heart, which is
54:30why many of them debut saying, "What is
54:35the murmur like so you can identify it
54:37quickly? Is it a murmur or holosystolic
54:41? Like a VSD holosystolic, right? So,
54:48many will confuse them there, they can
54:51confuse them, right? It is very
54:53important to remember that when one
54:57talks about mitral insufficiency, one
54:59must talk about a condition that is
55:02mitral valve prolapse. For example,
55:05here I have mitral valve prolapse. Uh,
55:11in the case of mitral valve prolapse,
55:13the mitral valve has an anterior
55:15leaflet and a posterior leaflet. The
55:18one that suffers the most effects is
55:20the posterior leaflet. The posterior
55:23leaflet. So, the posterior leaflet is
55:26normally held like this by the chordae
55:29tendineae. But what happens? These
55:31chordae tendineae can have uh an
55:35abnormal deposit. That is what happens.
55:38Abnormal deposits of dermatan sulfate.
55:42Exam question. Dermatan sulfate. They
55:47put this here in pathology, in
55:49anatomical pathology questions at
55:51universities. They put it as a
55:54specialty question, they ask you during
55:56your rotations, they will say," No,
55:58what is the histopathological
56:00definition of mitral valve prolapse? "
56:03Myxomatous degeneration. Myxomatous
56:08degeneration. This is very important.
56:15Okay. Now, why does mitral valve
56:18prolapse occur? How do I identify to
56:22mark a mitral valve prolapse in an exam
56:24question? I mean, what is the typical
56:28patient? Right? That is very important,
56:30right? I mean, you say, how do you
56:36identify it? There is something one has
56:40to do that makes you think about valve
56:43prolapse. The behavior of the murmur.
56:47What happens? Murmurs have a general
56:53behavior. For example, what happens
56:57when I do this? I inhale, I increase
57:01venous return, right? No. Okay. It is
57:06assumed that when I increase venous
57:07return, uh, I can hear right-sided
57:09murmurs, the murmurs get louder. That
57:12is called the Rivero-Carvallo maneuver,
57:14for when murmurs are of right-sided
57:16origin. Theoretically, it is said that
57:20when one inspires, more blood reaches
57:22the heart and, well, the murmur will be
57:24heard more, right? What happens when I
57:29bear down, for example, it's called
57:31Valsalva, right? If I bear down with my
57:34whole belly, it presses on the vein, it
57:36pushes it, and decreases venous return.
57:38And what happens to the murmurs? They
57:40decrease. So, theoretically, when I do
57:43Valsalva, the murmurs decrease, right?
57:50And when I inhale, which is what they
57:52don't say in exam questions—they say"
57:55squatting, "because when you squat, you
57:58squeeze the veins in your legs. When
58:02you squat, venous return increases,
58:06therefore the murmurs increase. This
58:08happens with all murmurs, it is the
58:13rule of murmurs, but there are two
58:15murmurs that do not follow the rule.
58:19Which are mitral valve prolapse and
58:22hypertrophic obstructive cardiomyopathy
58:28, which occur in reverse; when you do
58:31Valsalva, they increase their murmur,
58:37and when you squat, their murmur
58:40decreases. So that is why I place it
58:43here. The exam question that makes one
58:47suspect they are asking me about
58:48prolapse is because of this. It says,"
58:52No, a patient who presents with an
58:55increase during Valsalva, look, with
58:58Valsalva, they notice an increase in
59:01the murmurs. "Right away, this could be
59:03prolapse or hypertrophic cardiomyopathy
59:06. The patient notices a mid-systolic
59:10murmur. That is where it starts, that
59:12is where the questions come from.
59:13Murmur. What is the murmur I am going
59:16to find here? How am I going to find
59:19that murmur? So, the degeneration,
59:22since it is a mitral insufficiency,
59:24what is the murmur like? Mid-systolic
59:29is a mid-systolic murmur. And that is
59:40how exam questions appear. Now you are
59:43going to ask me immediately, because
59:44you always categorize the disease,
59:45taking the four pillars of a disease,
59:46right? Etiology, clinical presentation,
59:48diagnosis, and treatment. It has to
59:49appear in your mind like that. So, we
59:54don't know. Idiopathic. The clinical
59:59presentation, we don't know,
1:00:01asymptomatic. Man. So, what do we do?
1:00:05They are just going to tell you
1:00:06mid-systolic murmur and they will tell
1:00:07you nothing more than this maneuver,
1:00:08and with that, you have to do it on the
1:00:10exam. How annoying. And the diagnosis
1:00:13is echo. The echocardiogram will tell
1:00:18you if the patient is mild, moderate,
1:00:21or severe. It’s not Monday, Tuesday,
1:00:24and Saturday. It's mild, moderate, or
1:00:26severe. Another one wrote to me. It's
1:00:29Monday, Tuesday, or Saturday, mild,
1:00:31moderate, severe. Got it. So, remember
1:00:34this. Very important. Question.
1:00:40Treatment. Do I provide treatment, yes
1:00:45or no? If it's asymptomatic, right? If
1:00:53it's symptomatic, I give a beta-blocker
1:00:56. Correct? If it's severe, severe,
1:01:06which actually happens in few cases,
1:01:08less than 5%. and has symptoms, they go
1:01:16to surgery. They go to surgery. So,
1:01:25just because a question came up, we
1:01:27have to cover the whole topic. Yes,
1:01:32it's very important for you to keep
1:01:34this in mind, right? Well, from here,
1:01:40just to cover the right side. Tricuspid
1:01:45valve in tricuspid valvulopathy, just
1:01:47remember this, tricuspid stenosis, the
1:01:50only cause they'll ask for is rheumatic
1:01:53. In tricuspid regurgitation. Remember
1:01:58this, we see this a lot. We have
1:02:01primary tricuspid regurgitation and
1:02:04secondary tricuspid regurgitation,
1:02:07which is the most frequent. What does
1:02:11secondary tricuspid regurgitation mean?
1:02:14That the origin was the left side and
1:02:16it complicates the right side. Primary
1:02:21is of congenital origin, Ebstein's
1:02:24anomaly. Okay, that is very, very
1:02:31important. That is primary, which
1:02:33originates because something happened
1:02:35right there in the valve itself. It can
1:02:39be congenital from Ebstein's anomaly,
1:02:42it can be because the valve was damaged
1:02:45by endocarditis, but, I mean, due to a
1:02:48specific valve issue; secondary has
1:02:50nothing to do with the valve, but
1:02:53rather with the dilation of the ring.
1:02:56So, here we will talk about a dilated
1:02:58heart. We see that a lot in ischemic
1:03:02conditions. Ischemic, in pulmonary.
1:03:08Pulmonary stenosis, most frequent cause
1:03:10is congenital. That's it. And in
1:03:16pulmonary regurgitation, the most
1:03:19frequent is pulmonary hypertension.
1:03:22Pulmonary hypertension causes it.
1:03:25Pulmonary hypertension can generally
1:03:27lead to pulmonary regurgitation. Now,
1:03:31how is pulmonary hypertension generated
1:03:33? One of the most frequent causes is
1:03:36cor pulmonale. What is cor pulmonale?
1:03:40Heart-lung. It's when a patient, for
1:03:44example with COPD, where normally COPD
1:03:47has low oxygen, the low oxygen causes
1:03:50vasoconstriction. Unlike other organs,
1:03:54for example, any artery in the body,
1:03:56when you give it little oxygen, the
1:03:57arteries actually dilate so more blood
1:03:59enters. On the other hand, in a lung,
1:04:02when you give it little oxygen, they
1:04:03close. They are resentful. You give it
1:04:07little, oh, I don't want it. Whereas in
1:04:09other parts of the body you give it
1:04:10little, oh, give it to me. So it
1:04:12dilates. So with COPD, you give it
1:04:15little oxygen, it constricts, and what
1:04:17does that do? Pulmonary hypertension.
1:04:20And by developing pulmonary
1:04:21hypertension, it leads to right-sided
1:04:23heart failure. That is the famous cor
1:04:27pulmonale. Okay. And here, just as
1:04:31Austin Flint is in aortic insufficiency
1:04:33, in pulmonary insufficiency you will
1:04:35see the famous Graham Steell, the
1:04:41famous Graham Steell murmur, right?
1:04:44Just so you keep it in mind. Okay, very
1:04:49good. Within the world of valvulopathy,
1:04:53although I am not covering the
1:04:56infectious chapter, I would like to
1:04:58give you a couple of small pearls on
1:05:01endocarditis regarding valves, so you
1:05:04leave with a very clear concept of
1:05:06valves. How do I recognize endocarditis
1:05:11? In an exam question, I have to know
1:05:13my robot. First, there has to be a
1:05:20fever. 90%of the questions have to have
1:05:25a fever. There is no endocarditis
1:05:28question without a fever. If you say,"
1:05:31Doctor, but what if they didn't have a
1:05:33fever this time, maybe they were
1:05:34immunosuppressed, they didn't have one.
1:05:36"" That exists in the real world. In an
1:05:38exam, no. The exam is a robot. Do you
1:05:40understand? Remember, exams are robots,
1:05:44they are machines. You turn into
1:05:46machines. Now I'm not talking about the
1:05:48robot patient anymore, now I'm talking
1:05:50about the robot student. Sure, we
1:05:54always innovate because students tell
1:05:58me, "Doctor, excuse me, what is the
1:05:59robot patient?""Listen to me, now you
1:06:01have to be the robot student, not just
1:06:04the robot patient." And I have to be
1:06:07the robot doctor. We all become robots,
1:06:10do you understand? So, fever 90%. What
1:06:15else? A murmur. But a new murmur. Now,
1:06:25the murmur is the next one that follows
1:06:27, right? 75%. Another fact. This one,
1:06:36never forget damage with a D. This is a
1:06:38classic. I tell you with D. Why? Look,
1:06:44D is important. First, the D for dental
1:06:52. When they ask you questions about
1:07:00teeth, remember Streptococcus viridans,
1:07:07okay? Dental. When they tell you drugs,
1:07:16you will remember whom, Staphylococcus
1:07:18aureus. Okay. D for drugs. so you more
1:07:25or less have an idea. Another one, when
1:07:30they tell you, for example, damage, and
1:07:33here I am talking about serious damage,
1:07:35that is, damage to the heart, damage to
1:07:43the heart. Remember rheumatic fever,
1:07:46for example, they could put rheumatic
1:07:48fever or perhaps congenital holes. Look
1:07:54, cyanotic congenital defects, damage
1:08:01to the heart so that you keep seeing
1:08:03the D. Another D, devices. This is very
1:08:12important because for devices we have
1:08:15prosthetics, we have pacemakers, we
1:08:19have defibrillators, right?
1:08:21Self-implantables, the realize, they
1:08:26can give you any of these things plus a
1:08:28murmur, plus fever, endocarditis. Do
1:08:30you understand? All the situations that
1:08:32may arise there. You can't miss it,
1:08:34guys. With that, you will easily handle
1:08:36the definition of your robot
1:08:38endocarditis patient. Okay? Important.
1:08:43Now, to move from definition to
1:08:45diagnosis, you will talk to me about
1:08:48criteria. To talk about criteria, I
1:08:51have to know the clinical presentation.
1:08:53So, we are going to talk here. I'll use
1:08:55another color for you. Wait. Here about
1:08:59clinical presentation, because if we
1:09:04don't know the clinical side, how do we
1:09:06enter the diagnosis? Clinically, mitral
1:09:09endocarditis is more frequent than
1:09:12aortic. This is m, look, M for world.
1:09:22Here, aortic more than mitral. Peru.
1:09:32You will see many, many studies, many
1:09:34studies say there is more mitral,
1:09:35mitral, mitral, mitral, mitral, mitral,
1:09:37mitral, and you will see that in your
1:09:39specialty questions they put aortic,
1:09:40aortic, aortic, aortic, and you say, "
1:09:42Doctor, what is it?" How is it? How is
1:09:44it? "And that is what you will find.
1:09:47And in reality, I think it's more
1:09:49mitral than aortic, it's just that
1:09:51there are fewer publications here.
1:09:53Anyway, but I'll leave this with you,
1:09:55right? Another one so you have an idea
1:09:59of what the clinical presentation is
1:10:01like. 10%have embolisms, renal
1:10:08embolisms, splenic embolisms. And the
1:10:15other thing, this is the most important
1:10:18, they present with immune complex
1:10:21clinical signs, for example, on the
1:10:24nail, splinter hemorrhages, right? The
1:10:32nails on the little fingers, on the
1:10:34fingers, do you remember well? Janeway
1:10:44lesions, Janeway lesions, do they hurt
1:10:48or not? They don't hurt. And Osler's
1:10:55nodes? Very good. Osler's nodes. They
1:11:04hurt. Okay. Osler's nodes hurt and in
1:11:13the retina Roth spots on the retina,
1:11:19right? Roth spots, R for retina. This
1:11:30clinical picture of immune complexes
1:11:32and embolic processes. So, with these
1:11:35little things you will see that the
1:11:36questions appear, right? They appear,
1:11:38your robot patient plus their clinical
1:11:40picture, and then they tell you to
1:11:42diagnose, right? That's how it comes.
1:11:45So, regarding the criteria, we will go
1:11:48straight to the major ones. For that,
1:11:54we will remember blood cultures. Blood
1:11:56cultures. And imaging are the two most
1:12:00important criteria, echocardiogram and
1:12:03blood culture. And the gold standard is
1:12:07culture. If someone asks you, they ask
1:12:12what the confirmatory one is, the
1:12:14culture. And how do you get, how can
1:12:16you know the culture, how do you
1:12:18extract the culture, the culture from
1:12:19whom? Gold standard, from the valve.
1:12:22And how do you extract the valve
1:12:24culture? When you open the chest, you
1:12:27have to have operated on them, you have
1:12:29to have removed the valve, and you have
1:12:31to have replaced the valve. Only then
1:12:33do you get the gold standard, do you
1:12:35understand? I mean, when you diagnose a
1:12:38patient, you can only diagnose them
1:12:40with blood cultures and echo, and you
1:12:41treat them with that, but when you say,
1:12:43man, they aren't responding to medical
1:12:45treatment and you open them up, how do
1:12:47you say it? And then, when you're
1:12:51opening the chest, drying it, opening
1:12:52the heart, you take out the valve. Hey,
1:12:54here's the valve, send it for culture.
1:12:56That valve culture, that is the gold
1:12:58standard, do you understand? And so you
1:13:02don't think the gold standard is just
1:13:03any culture, because many have gone
1:13:05with the idea that it's a blood culture
1:13:07, right? And it's not, it's the valve
1:13:10culture. That is the gold standard
1:13:13maximus. Okay. Valve culture. Right.
1:13:19And the minor ones: fever is minor,
1:13:22immunological phenomena are minor. I
1:13:25highlight this because sometimes we
1:13:26miss it, sometimes we get overconfident
1:13:28. Guys, don't forget these little
1:13:30things then. Okay. Two minor, two major
1:13:33, or five minor. Yes. Well, medical
1:13:37treatment, antibiotics for 6 weeks, 40%
1:13:44respond. Yes. Surgical treatment, 60%
1:13:52end up in this. 60%end up needing
1:13:58surgical treatment. Yes. The germ that
1:14:01medical treatments target is
1:14:03Staphylococcus aureus. It's that simple
1:14:08, because it is the most frequent in
1:14:11general. It is very important. You will
1:14:15see that you also have to keep two
1:14:17others in mind. In many subacute
1:14:21endocarditis cases, on exam questions,
1:14:23viridans comes up a lot, and for
1:14:25prosthetic endocarditis, it's
1:14:27epidermidis, right? For prosthetics,
1:14:31it's epidermidis, but aureus is the one
1:14:37that is currently taking everyone down.
1:14:40Okay? When do I operate urgently or as
1:14:43an emergency? Urgency means any patient
1:14:46who does not respond to medical
1:14:47treatment, right? If they don't respond
1:14:50, they don't respond to medical
1:14:52treatment, right? You have to schedule
1:14:54them, the patient, doctor, that is the
1:14:56most frequent scheduling, right? They
1:14:59don't respond to medical treatment. And
1:15:01here in an emergency program, today,
1:15:04remember, we schedule emergency surgery
1:15:06for patients who are developing heart
1:15:09failure, for example, cardiogenic shock
1:15:11associated with endocarditis, so, you
1:15:14know, nobody is going to tell you not
1:15:16to do it. Or those who have evidence of
1:15:21vegetation on an echo greater than 10
1:15:24mm, because it is highly likely they
1:15:26will have an embolism anywhere, and the
1:15:29most dangerous is the brain, which we
1:15:32are very afraid of, so it must be done.
1:15:35Right. If someone comes and tells you,"
1:15:37Doctor, they aren't responding to
1:15:38antibiotics. "Everything would be
1:15:40urgent, but emergency, that is, for you
1:15:43to take them to the OR right now on
1:15:46shift, these would be the two criteria.
1:15:49Why am I teaching you this? So that now
1:15:52, if you are on a medical ward, you
1:15:54know how to justify it. This helped me
1:15:58a lot because I remember I was, I
1:16:00remember I was in Mexico, I think, and
1:16:03a doctor calls me whose husband is—
1:16:06she was a Villamedic student, she got
1:16:09in, and her husband was a Villamedic
1:16:12student who was preparing. I was in
1:16:16Mexico, I remember now, this year I was
1:16:18at a congress. She says," Doctor, I
1:16:21have my husband with infectious
1:16:23endocarditis. He has been in treatment
1:16:28for 3 weeks already and has had a fever
1:16:31for those 3 weeks. On the echo, the
1:16:35vegetation is at 8 mm. Right. Uh, the
1:16:41blood culture shows nothing. Look, 8 mm
1:16:46of vegetation. Blood culture shows
1:16:49nothing. He has a fever every day. Um,
1:16:53they don't want to operate on him, they
1:16:56say he should finish the 6 weeks. You
1:16:59doctors, what would you decide? Would
1:17:08you think about it or not? Knowing the
1:17:12class, the probabilities of success,
1:17:15the cutoff, the probability that this
1:17:21person—look, 3 weeks; I just told you
1:17:246 weeks of antibiotics, 3 weeks, I tell
1:17:26you 60%end up in surgery. He has 8 mm
1:17:29and I tell you that vegetation of more
1:17:30than 10 goes to emergency surgery.
1:17:33Between us, between doctors, being
1:17:36blunt. Your husband, negative blood
1:17:44cultures.
1:17:49And so she says to me, "Doctor, what
1:17:52would you do?" I tell her, "Operate on
1:17:54him, doctor. I should—they should
1:17:58operate on him, right?""Yes, of course,
1:18:00a while ago, but they don't want to
1:18:02operate.""No, operate on him." But he
1:18:06didn't meet the emergency criteria. No,
1:18:09look, more than 10 and cardiogenic
1:18:11shock, for example. These don't exist,
1:18:14but maybe he is in an urgency criterion
1:18:15, he is within the range. He should
1:18:18respond. A week passed, I was already
1:18:22on my way, didn't make it, and they
1:18:24write to me, "No, doctor, my husband
1:18:26has had endocarditis for 4 weeks now."
1:18:29They did a new echocardiogram, the
1:18:30vegetation is at eight. Yes, there's a
1:18:34fever, but they did a pro-BNP. His
1:18:38pro-BNP was at 900 a week ago. What?
1:18:44900, later he didn't even have more
1:18:46than 40. I have heart failure. That
1:18:49heart is suffering, but since he's
1:18:52young he's holding on, it's suffering,
1:18:54yes, clearly. That's, that's, with that
1:18:58data you can justify heart failure. So
1:19:02I tell her, "Tell your husband, well,
1:19:04he has all the clinical signs of heart
1:19:07failure and he needs to be operated on
1:19:09immediately." And here it comes. Then
1:19:14the husband says to her, "Tell the
1:19:15doctor if I'm presenting retrograde or
1:19:17anterograde clinical signs."
1:19:23Hey, what stage is your husband in then
1:19:25? So, doctor, the patient collaborates,
1:19:32the doctor doesn't do it, he does his
1:19:35own drama regarding heart failure,
1:19:38right? And the echo guy does the echo
1:19:43again, and there's some support there
1:19:46that makes a mistake, 1 millimeter more
1:19:48, 10 up, no. So they operate, they send
1:19:52it for culture, it comes out. What do
1:19:56you think the diagnosis was?
1:19:58Brucellosis. Question, is brucellosis
1:20:03treated with antibiotics? The diagnosis
1:20:08of Brucella is 100%surgery. What would
1:20:10have happened one more week with that
1:20:12patient, that colleague, a stroke and
1:20:14left with sequelae? Right now the guy
1:20:17is fine with his valve. At peace. I
1:20:21mean, there comes a moment where your
1:20:23medical judgment, the knowledge you
1:20:25already have, you have to make
1:20:26decisions, understand? You have that
1:20:30power. Guidelines aren't made to be
1:20:33rigid, they're made so you can make
1:20:36better decisions. Yes. Very good.

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