Full transcript
0:00So let's get started with the
0:01oscultation. So there are four very
0:04distinct locations where stethoscopes
0:07get placed. And what might happen on
0:09your exam is that you'll be given the
0:11location of where they're oscultating
0:13these murmurss. So the pneumonic for
0:15remembering these positions is apartment
0:18M. We filled that in here. A ptm
0:23apartment M. The right second
0:26intercostal space is known as the aortic
0:28area. The left second intercostal space
0:30is known as known as the pulmonic area.
0:33The left fourth is the tricuspid area.
0:36And then you have the apex which is the
0:39mitral area. So get this down and commit
0:42this to memory first. This is good not
0:43only for exams but also for when you
0:45enter your clinical rotations and start
0:47to have to you know know where to place
0:49your stethoscope when you're actually
0:50listening to somebody's heart. Now,
0:53let's I I want to transition now and and
0:55kind of use an example to show you how
0:57to figure out what the murmur is simply
1:00based on a few clues in the description.
1:03So, here's an example. A 78-year-old
1:06male presents complaining of dysnia on
1:08exertion and exertional anga for the
1:10past 3 months. On exam, you note a two
1:13out of six systolic murmur when your
1:15stethoscope is placed in the apical
1:17area. Which of the following is the
1:19correct murmur? So this is much simpler
1:23than it needs to be. People get really
1:24overwhelmed when they get murmur
1:26questions, but let's simplify this.
1:28Basically, you need to look for a few
1:31things. One, is the murmur systolic or
1:33diastolic? And where is it occurring? If
1:36you know those two pieces of
1:38information, you can solve the murmur
1:40without any other clues. You don't even
1:42have to listen to the audio file to see
1:44what the murmur sounds like. In this
1:46question, they told us that it's a
1:47systolic murmur and it's in the apical
1:50area. So you can see in the top left
1:52here, I included our diagram with our
1:54four different oscultation spots. So we
1:56know that we're in the apical area. So
1:58we know this has to be a mitral sound.
2:00Now the question is, is it mitro
2:02stenosis or mitro regurgitation?
2:05So starting from the ground up here, if
2:08you knew of the apartment M pneumonic,
2:10you would already know this has to be
2:12mitral. So you've got part one of this
2:14question solved. Part two is is it mitro
2:16stenosis or mitro regurgitation and
2:19that's where the systolic versus
2:20diastolic part comes into play. So now
2:23you have to ask yourself what happens at
2:25the valve during cy versus diastily.
2:30So we're talking about the mitro valve
2:32and we know that during diastily blood
2:34is going to flow from the left atrium
2:37into the left ventricle and fill during
2:39diastily. But in cy blood is going to be
2:42ejected out of the left ventricle
2:46and it has the potential of going back
2:48across the mitro valve if it's going to
2:51regurgitate back into the left atrium.
2:53So I've kind of already given it away
2:55here but basically we know that we're
2:57talking about a systolic murmur. And the
2:59only time that a murmur occurs on the
3:02mitro valve during cy is during mitro
3:05regurgitation.
3:07Again, if it was if it was mitro
3:09stenosis, it would have to be a
3:11diastolic murmur because the only time
3:13that you hear mitro stenosis is when
3:16blood flows across the mitro valve when
3:18the left atrium is trying to throw blood
3:21into the ventricle as it fills that
3:23ventricle. So, I want to take a step
3:25back here and make sure that you're up
3:27to speed. First, you have to know the
3:29APM, apartment M, pneumonic. That tells
3:32you where the murmur is located or what
3:35area we're listening to. Then you have
3:38to ask yourself what happens at that
3:41valve during cy versus diastily. And if
3:44you know all of that information, you
3:46can solve what the murmur is based on
3:48just those two pieces. You don't have to
3:51even listen to the audio file. So it's a
3:53really nice trick if you can get that
3:54down and understand the basic physiology
3:57about what happens at the valve in cy
4:00versus diastily. Now with that in mind
4:03this is the basics the absolute basics
4:05that you need to know the systolic
4:07versus diastolic murmurss. What I
4:09recommend is that you pause the video
4:11right now and ask yourself what happens
4:14at the aortic valve, what happens at the
4:16pulmonic valve, what happens at the
4:18tricuspid and what happens at the mitral
4:20during cy versus diastily. If you can
4:23understand whether blood is going to be
4:26ejected or going to be filling a
4:28ventricle, then you will be able to
4:31solve almost every question. If you're
4:34ready to move on, we're going to now
4:36talk about what makes murmurss louder or
4:38softer. And this is usually what people
4:41get tripped up on. So, it's very
4:43important that we get a few things down.
4:46First is that during inspiration,
4:48right-sided murmurss get louder. And
4:50during expiration, left-sided murmurss
4:52get louder. This is just a general rule,
4:54and I need you to memorize it because
4:56it's going to go a long way for you. So,
4:57what I always remembered was
4:59reinspiration and lexiration. Leftsided
5:02gets louder during expiration and
5:04right-sided gets louder during
5:05inspiration. This is something that you
5:08absolutely need to memorize. I wouldn't
5:10even think about why. Just memorize it.
5:14The more confusing topic is what happens
5:15with preload versus afterload. So, we're
5:18going to spend quite a bit of time on
5:19this slide. So, I really want to make
5:21sure that you understand this. When you
5:24increase preload, basically what you're
5:27doing is pushing more blood back to the
5:30heart. Therefore, as more blood flows
5:34over valves, the murmurss become louder
5:37because more blood is going to flow over
5:39them. So, as an example, if you usually
5:42have a mitro stenosis, the more blood
5:45that flows across that mitro valve means
5:48that that murmur is going to be louder
5:51because more blood is going to flow
5:53through an already stenotic valve. So,
5:55if you're oscultating it, it will be
5:57louder, aka worse. The exception to this
6:01rule is hypertrophic obstructive
6:04cardiomyopathy and mitro valve prolapse.
6:08This is a very high yield concept. So
6:10I'm going to explain this. When you have
6:12hypertrophic obstructive cardiomyopathy
6:15or hokum for short, the the heart
6:18becomes hypertrophied and the septum
6:21kind of bulges and blocks the outflow
6:24tract. So normally more blood flowing
6:28across a valve or into the heart makes
6:30murmurss louder. But in the case of
6:33hokum and mitro valve prolapse which is
6:36you know lower yield but still we
6:38include it in this discussion more blood
6:41in the heart actually pushes that septum
6:43back into its normal physiologic
6:46position. So in hokum if you can
6:48envision this diagram in your head the
6:51more blood or the more pressure on that
6:53septum pushes it back into its normal
6:56position and reopens that outflow tract.
6:59So generally speaking anytime you
7:01increase preload which you do via
7:04squatting or leg raising more blood is
7:07going to flow through the heart and
7:08anytime more blood flows over a valve
7:11whether it's stenotic or regurgitant
7:13you're going to get louder murmurss. The
7:16only exception to this rule is hokum and
7:18mitro valve prolapse. In hokum, it's
7:20because more blood pushes the septum
7:23back into its normal position, which is
7:24the picture all the way on the left. And
7:27in mitro valve prolapse, it's because
7:29the mitro valve is literally prolapsing
7:32and it's blocking normal blood flow. So,
7:34I want to simplify this to the most
7:36basic level. You don't need to
7:37understand what's happening with the
7:38mitro valve. You'll never be asked that.
7:40But just think of it as more blood going
7:42through the heart and returning the
7:43mitro valve leaflets back into their
7:45normal position. That's all you need to
7:48know. So again, I'm going to summarize.
7:51More blood, more preload, every murmur
7:54gets louder. The only exceptions are
7:57hokum and mitro valve prolapse. Hokum
7:59because you reopen up the outflow tract
8:01obstruction
8:03and mitro valve prolapse because you
8:05return the valves back into a relatively
8:08normal position where you don't hear the
8:10midstolic click that goes along with
8:12mitro valve prolapse. That's increased
8:15preload. Now let's jump to the other
8:16side of the slide here. If you decrease
8:19your preload, your murmurss will get
8:20softer. And it's the same exact
8:22reasoning, right? Less blood going back
8:24to the heart means less blood is going
8:26to flow across a stenotonic or
8:27regurgitant valve. Therefore, the
8:30murmurss will be softer, aka better,
8:32right? They're not going to sound as
8:33loud. They're not going to sound as bad
8:35because less blood is flowing over the
8:37abnormal valve. Again, the exception is
8:40hokum and mitro valve prolapse. Again,
8:43for the same reason. So in hokum if you
8:45look at our picture on the left here
8:47you've got you see the normal position
8:49of the heart but then the the image just
8:51to the right shows the heart with
8:52hypertrophic cardiomyopathy.
8:54If you have less blood flowing through
8:56the heart then less blood is there to
8:58push that septum back to its normal
9:01position. So hokum sounds worse in mital
9:04valve prolapse. You have less blood to
9:07return the mitro valves back to their
9:09normal position.
9:11When you decrease preload, you do that
9:14via valalva. So you bear down. If you,
9:16it's like telling a patient, I want you
9:17to bear down and pretend like you're
9:19having a bowel movement. This prevents
9:22blood from returning to the heart, aka
9:25it decreases your preload. So that's
9:27everything you need to know about
9:28preload, right? Think about preload as
9:30the amount of blood that gets loaded
9:32into the right atrium. Aka the amount of
9:34blood that is returning to the heart
9:36through the Venus system. Now I want to
9:39talk about afterload. Afterload is
9:41basically the pressure against which the
9:43heart pumps. So increased afterload
9:46means more pressure is being exerted
9:48upon the left ventricle as it tries to
9:52eject blood out of the heart. You can
9:55increase your afterload by doing
9:57something called hand grip. So when
9:58you're examining a patient, if you ever
10:00want to have them do hand grip, you're
10:01going to tell them to squeeze their left
10:03hand. And that hand grip is going to
10:06increase afterload, right? It's going to
10:08increase the pressure against which the
10:10heart has to pump. Now, usually when you
10:13increase the afterload, you get louder
10:15regurgitant murmurss. Now, why is that?
10:19Well, if the heart has to pump against a
10:21greater pressure, that means there is
10:24more pressure forcing blood backwards,
10:26right? Normally, blood is going to pump
10:27out of the heart. But if it's pumping
10:29against a greater pressure, then you can
10:31think of it as more pressure being
10:33exerted upon the heart, which is going
10:35to try to force blood backwards. And
10:38that's exactly what a regurgitant murmur
10:40is, right? Blood is going to
10:41accidentally flow backwards in the wrong
10:44direction back over the valve. So when
10:47you increase afterload, the regurgitant
10:49murmurs become louder.
10:52Likewise, when you increase afterload,
10:54you're going to get a softer hokum and a
10:58softer mitro valve prolapse. And this is
11:00the same reasoning as before. If we
11:02increase afterload, then hokum has more
11:06pressure propping that septum back into
11:09its normal position. The mitro valves
11:11have more pressure propping them back
11:13into their normal position, those valve
11:15leaflets. So again, a softer hookum or a
11:19softer MVP is really saying that the
11:22murmur is getting better, right? It's
11:24getting softer. You don't hear it as
11:26much because there's less of a
11:27mechanical issue since there's more
11:29pressure returning the heart to its
11:32physiologic position. And that's really
11:35important to understand.
11:37The last thing I want to talk about is
11:38decreasing afterload. You can decrease
11:41afterload by using a drug called AML
11:43nitrite. And this is probably the lowest
11:45yield of anything on this slide, but I
11:47include it for completeness sake here.
11:49If you decrease your afterload, hokum
11:52gets louder, right? Less pressure is
11:55forcing that septum back into its normal
11:57position. So the outflow tract gets
12:00obstructed and the hokum murmur gets
12:02worse, aka louder. If you decrease your
12:06afterload, you get a louder MVP. Again,
12:09same reason. less pressure is being
12:11forced upon those mitro valve leaflets,
12:13which means that the mitro valve is
12:15going to prolapse more and get worse or
12:18get louder. So again, this slide is
12:20talking about preload versus afterload.
12:22How we change preload, how we change
12:24afterload, how we make it increase
12:26versus decrease, how you do that with
12:28valva, squatting, leg raise, all this
12:30stuff. It's very high yield. The reason
12:33that this is important on your exam is
12:35that they'll give you a murmur and
12:37they'll tell you what, you know, they'll
12:39say that the patient bears down. What do
12:40you expect to happen? Something like
12:42that. They want to make sure that you
12:43can understand the physiology of what's
12:45going on in the chambers of the heart
12:47and how that changes the the strength of
12:50the murmur that you're hearing. The
12:53other thing that I want to point out is
12:54that hokum because it's such a high
12:56yield exception and again it's way more
12:58high yield than mitro valve prolapse.
13:00Hokum can sound like other murmurss, but
13:02the way that you differentiate them is
13:04based on what it's doing with these
13:06maneuvers. So if you want to distinguish
13:07hokum from something like a vententral a
13:10ventricular septile defect, they'll tell
13:12you what's happening with the murmurss.
13:14So keep this in mind. It's very high
13:16yield. Now what I want to get into is
13:18the last section of this video. This is
13:21going to be a rapid review of high yield
13:23associations and buzzwords that can help
13:25you get the murmur right. I've included
13:28a lot of my pneumonics here that helped
13:30me on my exam pretty extensively and I
13:33would say that I usually was getting
13:35between 90 and 100% of the murmur
13:37questions correct just because I had
13:39these in my back pocket. So up to this
13:42point you you should understand normal
13:44physiology.
13:45You should understand the APM locations
13:48and systolic versus diastolic. You know
13:50what's happening across that valve. You
13:53should understand how maneuvers change
13:54those murmurss. But if all else fails,
13:57if all of that normal physiology that I
13:59just explained is not enough to get you
14:01the answer right, well, fear not guys.
14:03I've got some pretty sick pneumonics for
14:05you. So, let's get into them. The first
14:07is aortic stenosis. And I would consider
14:09aortic stenosis to be probably the
14:11highest yield murmur that shows up on
14:13exams. This is known as a crescendo
14:16decrescendo murmur, which means that the
14:17murmur gets louder towards the middle
14:19and then softer. So, it kind of
14:21increases and then comes back down.
14:23There are two presentations for aortic
14:25stenosis. One is going to just be an old
14:27patient. If you have to take an absolute
14:29guess on your exam and you have a
14:30patient who's, let's say, 70 years or
14:33older, it's most likely aortic stenosis
14:35because over time with all of the
14:37changes that happen as you age, that
14:40valve just breaks down. You know,
14:41hypertensive hearts and remodeling of
14:44the heart really leads to a lot of
14:45pressure going through that valve and it
14:47causes an aortic stenosis. And what they
14:49say is that patients are sad. they get
14:51syncopy, anga and dysmia, right? So
14:55dysmia, anggina, syncopy. Remember that
14:57old patients are sad. Aortic stenosis is
15:00sad. The other thing that you should
15:02keep in mind is that it's possible to
15:04have a basically a functional aortic
15:07stenosis through a calcified valve. So
15:09if any patient has really high calcium
15:11levels, you can actually deposit little
15:14calcium crystals around the aortic
15:16valve. And because crystals accumulate
15:18around the valve, it's decreasing the
15:20space that blood has to pump through the
15:23aortic valve, which creates a functional
15:25aortic stenosis. So again, aortic
15:27stenosis, two presentations, anyone
15:29who's old and sad and the other person
15:31who has little calcification of their
15:33valve. The other thing that I want you
15:35to remember about aortic stenosis is
15:36that it radiates to the corateeds. And
15:38the way that you can remember this is
15:40that I take the letter A for aortic
15:42stenosis and I draw the up arrow and the
15:44down arrow which reminds me that it's
15:46crescendo decrescendo. The up arrow also
15:49reminds me that it radiates up to the
15:51corateed. So if you remember where the
15:53aortic area is on our kind of rib cage
15:56diagram that up arrow points right at
15:58the kurateeds. So aortic stenosis old
16:01and sad crescendo decrescendo radiates
16:03to the kurateeds. If you do have to
16:06listen to it on your exam and it sounds
16:08like it gets louder and then comes back
16:10down, that that's aortic stenosis.
16:12That's crescendo drescendo. And what you
16:15see at the top here is just the kind of
16:17diagram of the murmur based on what it
16:19sounds like. So again, aortic stenosis,
16:22crescendo drescendo.
16:24Mitro regurgitation is a holo systolic
16:27murmur. So it's usually about the same
16:29volume throughout, but it doesn't it
16:31doesn't stop. It's holo systolic. It's
16:33present for all of cy. So between S1 and
16:36that should say S2, you hear continuous
16:40murmur. The mitro valve is usually
16:42implicated if the patient has a history
16:44of rheumatic fever. So the pneumonic is
16:46rumit. Anytime they have a history of
16:48rheumatic fever, think about the mitro
16:50valve. That is the number one valve that
16:52gets involved. Mitro regurgitation
16:55radiates to the axilla. That's important
16:57and it's high yield because sometimes
16:59they'll tell you about the murmur and
17:00say that it's radiating and they'll give
17:01you the direction of the axilla. So
17:03again rumitral very important that's
17:06mitro regurgitation. Tricuspid
17:08regurgitation is very similar. It's also
17:10holo holo systolic between S1 and again
17:13that should say S2. It's there the
17:15entire time. The tricuspid valve is
17:18always damaged when you have patients
17:20who have a history of intravenous drug
17:21abuse. So my pneumonic is do you want to
17:24try some drugs? I want you to think
17:26about the tricuspid murmurss whether
17:28it's regurgitation or stenosis whenever
17:31you have a patient who has any risk
17:33factors or history for IVDA. So you know
17:36patients with HIV, hepatitis, obvious
17:39introvenous drug abuse, anything that
17:41points to them being a former drug
17:44abuser immediately think tricuspid
17:46valve. The reason that this is is
17:48because the first valve that blood flows
17:50across when it reaches the heart is the
17:52tricuspid valve. So if you have blood
17:54that's littered with pathogens as a
17:56result of intravenous drug abuse, the
17:58damage is going to be primarily
18:00concentrated at the tricuspid valve. So
18:03want to try some drugs? That's tricuspid
18:06regurgitation. Mitro stenosis is a very
18:09high yield murmur because of the
18:10description. It has what's called an
18:12opening snap. That's super high yield.
18:15And we'll come back to that in one
18:16second. But again, we're talking about
18:18the mitro valve here. So anytime a
18:20patient has a history of rheumatic
18:22fever, think rumit, it's always going to
18:25be the mitro valve. More often than not,
18:28this opening snap is really high yield.
18:30And my pneumonic for remembering this is
18:31that the operating system is Microsoft.
18:33That is to say that the OS is MS. The
18:36opening snap is Mitro stenosis. So
18:38anytime they describe an opening snap,
18:40it's going to be Mitro stenosis. And the
18:42reality of this is that it's really hard
18:44to hear an opening snap when you're
18:46actually listening to an audio file. So
18:48if they want you to pick mitro stenosis,
18:49they're usually going to include the
18:51buzzword opening snap. That could
18:53change, but that's what I would
18:55remember. So again, the operating system
18:56is Microsoft, aka the OS is MS, aka the
19:01opening snap is mitro stenosis.
19:04The next murmur we're going to talk
19:05about is Hokum, hypertrophic obstructive
19:07cardiomyopathy. And we already went
19:09through this pretty extensively on the
19:11slide about maneuvers and how they
19:12change murmurss. But anytime a patient
19:15has a family history of sudden cardiac
19:17death, I want you to think about hokum.
19:19So patients that are dying in their 20s
19:21or 30s while they're exercising, the
19:23reason that that happens is that again
19:25in hokum the uh the outlet is obstructed
19:28and you get functional heart failure
19:30because the heart is unable to pump
19:32blood to the rest of the body and one
19:34thing leads to another and patients die
19:36during exercise. when um increased
19:39demand is placed on their heart. So just
19:41to go through this one more time, hookum
19:43is going to be similar to other murmurss
19:44by the way that it sounds and the
19:45location in which you hear it, but how
19:47it changes during maneuvers gives it
19:49away. So it gets louder or worse with
19:52decreased preload. So less blood going
19:54to the heart means that the septum can
19:55push over more and obstruct more which
19:58makes the murmur louder or worse. Um it
20:01gets louder or worse with decreased
20:03afterload. So decreased afterload means
20:05less pressure forcing that septum over
20:08which means the septum is going to block
20:10the outlet. So the murmur gets louder or
20:13worse. Hook gets softer aka better with
20:16increased preload. So you want to
20:18increase your preload. Have the patient
20:20do some leg raising or some squatting.
20:22Get more blood going back to the heart.
20:24More blood in the heart is going to
20:25force that septum, push it to the side
20:27and make the murmur better or softer.
20:30And lastly, the murmur will get softer
20:32or better with increased afterload. So
20:34have the patient use some hand grip.
20:35Squeeze their left hand. You're going to
20:37make the heart have to pump against a
20:39greater pressure, which means more
20:41pressure is going to force that septum
20:42back into its normal position, which
20:44makes Hokum sound softer or better. The
20:48last murmur we're going to talk about is
20:50mitro valve prolapse, MVP. So mitro
20:53valve prolapse is high yield for a few
20:55reasons. One is that it has something
20:57called a midsystolic click. Anytime you
21:00have a young woman with a psychiatric
21:02history, I want you to think about MVP.
21:04We're still trying to understand the
21:06relationship between psychiatry and
21:08cardiology. And it's very, very
21:10extensive. However, usually patients
21:13with MVP are young women who are anxious
21:15or depressed. Don't ask me why. I cannot
21:18tell you why, but that is the
21:19association. So, um, keep that in the
21:21back of your mind. MVP can be caused by
21:24mixomatus valve disease. I'm throwing
21:26that in here because anytime they talk
21:28about this, I want you to think about
21:30the mitro valve. Think about MVP for
21:32mixommitus valve disease. And my
21:34beautiful pneumonic to remember MVP is
21:36that to win MVP, your team has to click.
21:39So that midstolic click is found in MVP
21:43or mital valve prolapse. That's it for
21:46this video. There are a few murmurss
21:48that I did not include because there's
21:50not much that you need to know about
21:51them. Those would include a PDA, um, a
21:55VSSD, and an ASD. If you're confused
21:58about those murmurss, I recommend
21:59googling them and learning the few
22:01basics that you need to know. But for
22:03the purpose of this discussion, I left
22:04them out because there's not much that
22:07you need to know about them, and there
22:08is one buzzword that can summarize most
22:10of them. So, I don't want to waste your
22:12precious brain space. This has been
22:14Heart Murmurs. Good luck.