Heart Sounds & Murmurs | Clinical Medicine

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0:06what's up Ninja nerds in this video

0:08today we're going to be talking about

0:09heart sounds and heart murmurs again

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0:39without further Ado let's start talking

0:41about heart sounds and heart murmurs

0:43when we talk about these I think it's

0:45really important for your exams and also

0:47for the clinical world to be able to

0:48understand normal heart sounds

0:51when there's some extra heart sounds

0:53like S3 and S4 and if you really want to

0:55go to the advanced level if you're

0:57planning to go into Cardiology then I

0:58could say let's talk about the splitting

1:00of the S2

1:01all right so first things first real

1:03basic stuff here S1 S2 heart sounds

1:06these are the normal heart sounds

1:08so S1 which you're going to represent on

1:10this graph with the time on the x-axis

1:12is going to be this guy here this is our

1:14S1

1:15S1 is going to represent two things one

1:18is it's going to represent the closure

1:21of one of the valves which is going to

1:23be the mitral valve so the mitral valve

1:26should close because what happens is as

1:28the pressure inside the ventricles rise

1:30and it tries to push blood out of the

1:32left ventricle into the aorta it should

1:34close the mitral valve

1:36same concept as blood is going from the

1:38right ventricle

1:39into the pulmonary artery it should open

1:42the pulmonary valves but close the

1:44tricuspid valves so for S1

1:47it should be the closure of the mitral

1:51valve and the tricuspid valve should

1:54close

1:55and then subsequently the aortic valve

1:58and the pulmonary valve should open

2:00that's the basic concept behind that but

2:01the sound is the closure of these valves

2:04S2 is the opposite so blood is already

2:08exited the left ventricle in the right

2:10ventricle it fills the pulmonary artery

2:12and fills the aorta what happens is

2:14during diastole some of the blood will

2:15try to recoil we don't want it to go

2:17back into the left ventricle so we

2:19should close the aortic valve

2:22same concept blood from the pulmonary

2:24artery will want to kind of fall back

2:26into the right ventricle but it

2:28shouldn't be able to go back into the

2:29right ventricle because of the pulmonary

2:31valve should snap shut

2:32so whenever these two valves snap shut

2:35that is the S2 heart sound so it'd be

2:38the aortic we're going to put a little o

2:40there aortic valve closing

2:43and the pulmonary valve will also close

2:46one important thing to remember though

2:49is that the aortic side it's the

2:51pressure is really kind of high and so

2:54naturally the the actual aortic valve

2:56should close quicker than the actual

2:58pulmonary valve should so sometimes we

3:00represent this S2 as two parts we

3:04represent an A2 which is the second

3:07heart sound which is the closure of the

3:09aortic valve and pulmonary valve but

3:10particularly the aortic component and

3:13then the other component here is the P2

3:16which is the pulmonary valve closing

3:19which is a component of the S2 but both

3:21of these make up the

3:23S2 okay

3:25all right that's the basics what we're

3:27going to do is we're going to add in

3:29some sounds and talk about the splitting

3:31of the aortic and the pulmonary vowel

3:33sounds for the S2

3:34let's come to the S3 and S4

3:37so S3 and S4 are interesting sounds

3:39they're extra heart sounds so now we

3:41should know that you'll have an S1 and

3:44then you'll have this A2 and P2 so we're

3:47going to put S1 and we're going to put

3:48A2 and P2 that's the S2 hearts on though

3:52you add another heart sound in this

3:55which we're going to talk about is S3 S3

3:57the concept behind this is there's left

4:00ventricular dilation that's the words I

4:01want you to remember

4:02there's left ventricular dilation so

4:04these ventricles are gargantuous and so

4:06what happens is the actual left

4:07ventricle can easily fill they actually

4:10rapidly fill with blood and as they

4:12rapidly fill the blood bounces off the

4:16walls of the ventricles as it starts to

4:17distend and it creates this turbulence

4:20of blood flow which triggers a murmur

4:23that is that turbulence of blood flow

4:25within the super dilated rapidly filled

4:28ventricles is the S3 heart sound

4:32so again just to recap it it's going to

4:34be rapid

4:38ventricular we're going to put in this

4:39case left ventricular filling

4:42which creates a massive turbulence

4:46of blood flow within the left ventricle

4:49and you could say the right ventricle

4:51and that is what precipitates the actual

4:53extra heart sound all right so that is

4:56going to be the S3 so this will

4:58precipitate what sound the S3 so then we

5:02have to ask ourselves the question

5:03what's the reason for the rapid left

5:04ventricular filling super dilated

5:06ventricles what are some causes of

5:08dilated ventricles CHF which one

5:11systolic heart failure so one cause

5:14would be systolic

5:17heart failure the other one would be

5:19dilated cardiomyopathy would be another

5:21really really big one

5:24this can happen not just pathologically

5:26but physiologically sometimes in

5:29patients who are super young and healthy

5:31athletes they can have dilated

5:32ventricles so they can trigger super

5:34large stroke volumes so you can't see

5:36this as well in young athletes

5:39so these are the concepts that I want

5:40you guys to understand is the causes

5:42whether it be pathological or

5:44physiological of the S3 so we know that

5:48it's during the filling process so that

5:51means that these valves are open the

5:53mitral valve and the tricuspid valve are

5:55open so if those are open it can't be

5:57after the S1 it's got to be after the S2

6:00because they're closed from S1 all the

6:03way to S2 during S2 after that they open

6:05up a little bit again so the sound would

6:07have to be right here and have to be

6:08very early so what we're going to do is

6:11we're going to add in this extra sound

6:12here we'll do it here

6:14where there's going to be a sound that

6:15comes right after this

6:17and this is going to be the S3 so you'd

6:20have S1 the S2 which is the combination

6:22of these

6:24and then right afterwards the S3 if you

6:26have systolic heart failure

6:28cardiomyopathy are very young healthy

6:30athletes

6:31let's go into this next one so S4 heart

6:34sound what do you notice the difference

6:35between the ventricles here thin super

6:37dilated ventricles thick ventricles so

6:40whenever you have a very rigid

6:43left ventricle it actually will do what

6:45it will decrease ventricular

6:49filling

6:51and if you decrease the ventricular

6:53filling process what this does is this

6:55causes the Atria to have to generate a

6:57very high pressure and so the Atria will

6:59contract super late so you develop a

7:01late

7:03atrial contraction because the Atria are

7:06going to have to really really work very

7:08hard to push blood from the Atria and

7:10the ventricles because of the super high

7:12pressure of the ventricles and how poor

7:14their filling process is so again rigid

7:16left ventricle will decrease the

7:19ventricular filling that'll make it

7:21really hard to get blood into The

7:22ventricle so then the Atria has to

7:24contract and very powerfully and when it

7:26does it generates the S4 heart sound so

7:30the S4 heart sound is usually the result

7:32of the atreus super working hard to

7:34contract and squeeze blood down so it

7:36goes hard to get blood in

7:39whenever that happens and it makes it

7:41difficult to get blood in the Atria will

7:43then pound on the remaining blood in the

7:45Atria to squeeze it down into the left

7:48ventricle

7:49that is referred to as the S4 heart

7:51sound

7:52but it comes later so it has to go S1

7:58A2

7:59P2 which is your S2 and then in

8:03comparison to S3 S3 will come right

8:05afterwards if you have a dilator rapidly

8:07filled ventricle for S4 it has to come a

8:10lot later because now the H we have to

8:12contract to push the remaining amount

8:13down so this would be your S4 and S3

8:16will be somewhere in here as comparing

8:18the two so now we've compared S3 and S4

8:22the question comes is what's causing

8:24this rigid left ventricle to not fill

8:26diastolic heart failure that would be a

8:29big one where they're super super kind

8:31of hypertrophic and very poor at being

8:33able to fill

8:34another one is anything that causes left

8:38ventricular hypertrophy what are two

8:39things that cause left ventricular

8:40diversity

8:41aortic stenosis

8:45this will definitely precipitate left

8:47ventricular hypertrophy and if you

8:49hypertrophy this Can you feel it no it's

8:51a very small space

8:53and the last one is chronic hypertension

8:55this will also precipitate left

8:57ventricular hypertrophy so these are the

8:59things that I want you guys to remember

9:00for the causes of an S4 heart sound okay

9:04beautiful at this point we covered

9:06normal s1s2 we've covered what happens

9:09when you have a dilated rapidly filling

9:11turbulent left ventricle and what

9:13happens when you have a rigid left

9:14ventricle with poor ventricular filling

9:16and the atrium to contract to push the

9:17remaining blood down S3 S4 accordingly

9:21now if you're a cardiologist level you

9:25got like that insane uh stethoscope in

9:27the ears of an eagle I guess and you can

9:29really really pick up on some of these

9:31things sure we can talk about the

9:33splitting of the S2

9:34the concept behind this is

9:37when you have a patient who's let's say

9:39we're in two phases so one is we're

9:42going to say that the patient is

9:44particularly having an inspiration

9:47and actually let's do it like this let's

9:49say expiration first and inspiration

9:52later so expiration first

9:55inspiration later what happens is

9:58you have that S1 and then you have again

10:01the S2 which is the A2 and the P2

10:03naturally in normal people it should go

10:06A2 and it should go P2 and they should

10:09be really hard to be able to

10:10differentiate one another on the

10:12expiration

10:14but let's say that the person decides to

10:16take a deep breath in when they take a

10:18deep breath in what happens is you

10:20massively fill the right ventricle

10:22because your intrathoracic pressure

10:24drops and if you feel the right

10:25ventricle this thing is going to get

10:27over filled

10:29more than usual during expiration if

10:31it's overfilled it now has to push a

10:34larger volume of blood that it usually

10:36does out of the right ventricle

10:40into the pulmonary artery during systole

10:42and then during diastole come back and

10:43snap it shut

10:45if it has to deal with more blood than

10:46it usually has to what do you think is

10:48going to happen to that sound is it

10:49going to come a little bit earlier later

10:50stay the same it's got to push it a lot

10:53more it's going to come later so what

10:55happens is is you have something called

10:57the S1

10:59the A2 will stay there but the P2 will

11:02just extend out a little bit more and

11:05that'll only happen during inspiration

11:07why because of increased

11:11filling so because of increased

11:14right side venous return

11:18the heart is on the right is going to

11:19have to deal with more blood during

11:21inspiration

11:22than it usually does during expiration

11:24and that's the concept behind this okay

11:27so physiological split S2 is a

11:30physiological thing so the cause is

11:33usually it's due to resperophasic

11:36changes

11:37is that special way of explaining that

11:40the S2 can split during inspiration as

11:44compared to expiration that's all it is

11:47okay cool now we move on to the next

11:49concept of a split S2

11:52a wide split S2

11:54so this one's weird and what happens

11:56with this one is the patient usually has

12:00again their S1 is the same no change

12:03there

12:04but what you'll notice is is that their

12:08actual again aortic sound and Pulmonary

12:11sound appear again farther away during

12:13expiration

12:15but during inspiration they appear even

12:18farther

12:19so here that's really hard to

12:21differentiate in physiologically Split

12:23S2

12:24but in a wide split S2 you can actually

12:26differentiate the A2 and P2 and both

12:29expiration and inspiration so now we

12:33have to ask ourselves the question

12:35why am I able to hear

12:37the splitting of the S2 in both

12:39expiration inspiration and compared to

12:41the physiological one

12:42and that's because

12:44the right ventricle is being overloaded

12:47constantly or it's having a hard time

12:50getting blood out of the right heart in

12:52general

12:53so let me explain something let's say

12:55that a patient has something called

12:57let's say a right bundle branch block

13:00let's say that they have a pulmonary

13:03hypertension

13:06where their pulmonary artery pressures

13:09are super high and it's really hard in

13:11both of these scenarios if I have a

13:13right bundle branch block this right

13:15ventricle is not going to contract on

13:18time it's going to delay the time of

13:19contraction the other thing is if I have

13:22pulmonary artery hypertension it's going

13:24to be harder for the right ventricle to

13:26generate enough pressure to push blood

13:28out into the pulmonary artery that's

13:30going to delay the time to get blood out

13:32if either delay the blood getting out of

13:35the right ventricle that'll cause the

13:36pulmonary sound to come later in general

13:39expiration but then make it worse

13:42take a deep breath in

13:44you take a deep breath in and now your

13:46right heart venous return is going to

13:47increase now you give the right heart

13:49that's already struggling to get blood

13:50out even more blood and it's going to

13:53make it even longer so that's the

13:56concept here is that you're actually

13:58extending this during inspiration but

14:01it's still present

14:02during expiration

14:04what's the reason why behind this the

14:07reason why is

14:08is again you're increasing

14:12the right Venus return

14:14in a strained right heart

14:17and if you overload that right heart

14:19it's going to make it even harder to

14:20take a longer time to get blood out of

14:22the right ventricle that's the concept

14:24here so for a wide split S2 think about

14:27right heart diseases right bundle branch

14:30block pulmonary hypertension anything

14:31that is delaying the transit of blood

14:33out of the right ventricle

14:35all right

14:37fixed split has two this one's actually

14:38super super cool and I only want you to

14:40remember one of these but what happens

14:42in this one is again you're going to

14:43notice S1 S1 is not changing

14:47but what you're going to notice here is

14:49watch this this is actually kind of cool

14:51there is a splitting of the S2 the A2

14:54and P2 component during expiration but

14:57it is if I can do this perfect

15:02exactly the same

15:04length apart so now this one it went

15:08from there's a split to holy crap

15:10there's a split from here there's a

15:11split and the split's the same all right

15:13no split to a split split to holy crap

15:16there's a big split and split split same

15:20what in the heck is causing the split to

15:23be the exact same during both

15:26expiration and both inspiration

15:31okay good question the primary cause is

15:34something called an atrial septal defect

15:37that is it there is other ones but this

15:40is going to be the one that you'll most

15:41likely see on your exam what happens is

15:44during expiration the pressure in the

15:47left heart is higher than the pressure

15:48in the right heart so what will it do

15:51it'll shunt blood

15:53into the right heart filling it with a

15:56good amount of blood so you're going to

15:57fill this right heart with blood and if

15:59it's going to fill it's going to take a

16:00little bit of a longer time to be able

16:02to squeeze that blood out of the right

16:04heart into the pulmonary artery and

16:06eventually close the pulmonary valve

16:08in comparison to the aortic valve

16:10during inspiration what happens to the

16:13Venus return to the right heart it

16:15increases because you're pulling blood

16:17from the Supreme vena cava and the

16:19inferior vena cava filling the right

16:21heart with blood giving it more blood to

16:23have to deal with a longer Transit time

16:25between the right ventricle to the

16:26pulmonary artery and eventually shutting

16:27the valve so what you'll notice is is

16:30that the right heart venous return is

16:32fixed

16:33that's the cool thing about this is that

16:35there is a right Venus

16:37return

16:40that is fixed

16:42during both inspiration and expiration

16:46and what I mean by that is

16:49is that in this patient they're having

16:51blood coming from the left atrium to the

16:53right atrium during expiration because

16:56left atrial pressures are higher and

16:58that the blood coming from the superior

17:00vena cava inferior vena cava going into

17:01the right atrium is occurring because of

17:04inspiration dropping the interthoracic

17:06pressure but the Venus return to the

17:08right heart is constant during

17:10inspiration and expiration that's the

17:12cool concept here and it's because

17:14there's a hole allowing for the

17:15equalization of blood flow because of

17:17the ASD that's the cool concept let's

17:20come to the last one here which is a

17:21paradoxical split S2 so this one's

17:23really kind of a wonky one what happens

17:25here is again you have that S1 that's

17:27going to be the constant thing that

17:28you'll notice out of all of these this

17:30is the same

17:31but here's what's really cool

17:33you have the P2 that comes first

17:38and then the A2

17:41comes after and you're like wait a

17:43second I thought that it always was a2p2

17:45yeah this is why it's weird it's wonky

17:47right and the same thing during

17:49inspiration you'll notice that the P2 is

17:51still coming before the A2 it's just

17:53it's just a little bit closer so what

17:55you'll notice is you'll notice a reverse

17:59kind of of the reversal of the roles of

18:01these two

18:02right and you notice that it's wider

18:05during expiration and less wide during

18:09inspiration let's dive into this okay so

18:12the only reason that the P2 would come

18:13before is because the left ventricle was

18:15taking probably a super long time to get

18:18blood out of it that's what was the

18:20common theme out of all of these before

18:21the reason why the P2 is becoming later

18:24or whatever it may be is because it was

18:26taking a longer time for the right heart

18:28to get blood out so if the A2 is coming

18:30later it's because it's taking a long

18:31time to get blood out that's the whole

18:33concept so there has to be a delay

18:37and left ventricular expulsion

18:42of blood and therefore if there's a

18:44delay in the left ventricular expulsion

18:46there'll be a delay in the closure of

18:48the aortic valve and pulmonary valve

18:50of blood

18:53so we have to ask ourselves the question

18:55okay what's causing this well one is

18:57we're having a hard time getting blood

18:59out of the left ventricle into the aorta

19:01this part is not occurring very well

19:03what was the problem in this one it was

19:05because the left the right bundle branch

19:07was actually blocked but what if the

19:10left bundle branch is blocked wouldn't

19:11that cause a delay in the left

19:12ventricular depolarization and

19:13contraction yeah so a left bundle branch

19:16block would be one particular reason

19:19the other one was that if a patient had

19:20like chronic hypertension right so if

19:22they have pulmonary hypertension same

19:24thing anything that causes the afterload

19:27to be super super high so usually this

19:30would be things like aortic stenosis

19:32would be a really really big one so

19:34aortic stenosis is a really one

19:35important one to remember

19:37oh um hypertrophic obstructive

19:40cardiomyopathy where the septum is so

19:42thick and chunky that it blocks the

19:43blood flow out of the left ventricle

19:45that would be another one that delays

19:46the blood flow

19:48and again you could definitely add in

19:50systemic hypertension as well so we

19:51could add in systemic hypertension

19:54that's also going to be this one as well

19:57so all of these could definitely lead to

19:59the left ventricle having a harder time

20:02to get blood out of it delaying the

20:05blood flow getting out and then

20:07subsequently delaying the closure of the

20:09aortic valve and that's why it comes

20:11later

20:11question is is in all of these we notice

20:14that during inspiration it increased

20:17that space between the two why is it

20:20increased in expiration and decrease in

20:22Inspiration well let's kind of use logic

20:25here during the

20:28process of expiration

20:30more blood flow is coming to which side

20:33of the heart

20:34to the left heart

20:36so it'll get filled with more blood it's

20:37going to make it harder to be able to

20:38get blood out already now add more blood

20:41it's going to delay the actual process

20:42even more

20:44inspiration you're doing what to the

20:46heart you're increasing right side

20:48venous return if you increase right side

20:50venous return now the right heart is

20:52going to have a little bit more of a

20:53struggle to get blood out of it because

20:55it's going to have to deal with more

20:56blood so that should cause the P2 to

20:59come a little bit closer to the A2

21:02because now it has to deal with a larger

21:03volume of blood expiration left

21:05ventricles to do with more blood

21:06inspiration right ventricles to deal

21:08with more blood that's why it just gets

21:10a little bit shorter during inspiration

21:12super cool right all right that covers

21:15the heart sounds now let's talk about

21:17heart murmurs all right my friends so

21:19now we have to talk about murmurs when a

21:20patient has a heart murmur right so

21:22you've gone through you've said okay let

21:23me do the auscultate I hear S1 I hear S2

21:26I don't hear any S3 S4 no real weird

21:28splitting of the S2 but here's something

21:30super odd in a particular area one of

21:33the first things that you have to do is

21:35know where you're supposed to be

21:36auscultating first thing where's the

21:38murmur that we actually auscultate so we

21:39go there we grab our stethoscope and we

21:41say oh right secondary call space aortic

21:43area that could be associated with

21:45aortic stenosis so start thinking about

21:46that right away

21:48second intercost is based on the left

21:49side pulmonic area think about pulmonic

21:51valve diseases

21:52left third intercostal space think about

21:54aortic regurgitation and HCM

21:57left fourth intercal space tricuspidary

21:59think about a vsd left fifth intercostal

22:02space usually on the midclavicular line

22:03think about any mitral valve disease

22:05stenosis regurgitation and prolapse so

22:07right away if you hear those locations

22:09think about the possible types of

22:12diseases that you will actually have

22:13occurring there so once you've gone

22:15through each particular location and you

22:17hear a murmur let's say that you hear a

22:19murmur in a particular location then you

22:21have to ask yourself the question okay

22:22is it a systolic diastolic or continuous

22:25murmur that's important so we're going

22:27to go through that now

22:28four systolic murmurs you are hearing it

22:30between S1 and S2

22:32so when you listen to these you want to

22:35be able to use the particular

22:36terminologies of how they describe like

22:38the quality of the murmur or the

22:40characteristics of the murmur when you

22:42hear a murmur

22:43that's referred to as a crescendo de

22:46Crescendo systolic murmur this is two

22:51typical typically two particular types

22:53of pathologies that are usually classic

22:56of what we call a crescendo de Crescendo

22:59murmur so it sounds really loud

23:00initially and then it decreases in

23:03intensity as you go on two particular

23:04murmurs one is there's a pathology with

23:08the aortic valve so we refer to this one

23:10as aortic stenosis

23:13so in aortic stenosis what happens is is

23:17it's really hard for blood to be able to

23:18get from the left ventricle out into the

23:21aorta and what happens is his blood is

23:23trying to move through this area it kind

23:24of like bends these valves a little bit

23:26and it kind of bows them and when it

23:28bows them it produces this

23:31click

23:32and that's usually one differentiating

23:34factor between these two types of

23:36murmurs as you'll hear like this what's

23:38called an ejection click and then a

23:41crescendo decrescendo murmur that's

23:43classic for aortic stenosis

23:45the other thing is that this murmur is

23:48usually right upper sternal border so

23:51that right second intercostal space and

23:53it radiates usually to the carotids

23:57and that's another particular thing that

23:59you can help to differentiate between

24:01this next one that I'm going to talk

24:02about

24:03this other one is Crescendo de Crescendo

24:05but it doesn't have an ejection click

24:07this one is usually due to the left

24:10ventricular outflow tract being super

24:11super narrow and obstructed this is

24:14called hypertrophic and sometimes they

24:16insert in the O obstructive but I'm

24:18going to put hypertrophic cardiomyopathy

24:21but it's a type of left ventricular

24:22outflow tract obstruction

24:24and what happens is it is really hard

24:27for blood to squeeze through this tiny

24:29little area from the left ventricle and

24:32into the aorta but there's nothing

24:33that's actually causing a valve to bow

24:35or bend or anything like that that

24:37precipitates this click

24:39so there's no click but it is louder in

24:41the beginning and decreases as you go

24:43throughout systole

24:44this one though again usually her

24:47particularly around for the most part

24:51usually kind of like Herb's point is the

24:53common area for this one so you usually

24:55hear this around herbs

24:58point and this one doesn't usually have

25:00any radiation to the carotids so that's

25:03one real big thing so that's how you're

25:05going to differentiate these two types

25:07of murmurs location timing and maybe

25:10some extra heart sounds and radiation

25:12okay cool

25:14the next one here is it's not a

25:17crescendo so let's actually mod like

25:19denote that it's a crescendo de

25:21Crescendo Crescendo de Crescendo murmur

25:25another big thing here is we have

25:27another one and this murmur is super

25:28interesting what happens is is you hear

25:32a murmur sometimes and it's usually

25:34pretty like

25:36it doesn't change an intensity

25:38throughout the systolic process

25:41but usually what happens is

25:44blood and this disease well normally

25:47during Sicily you're supposed to pump

25:49blood out this way but there's a defect

25:51within this valve and this valve is

25:53supposed to block the mitral valve is

25:55supposed to block blood from going back

25:56into left Atria what happens is the

25:58valve buckles and it bends and when it

26:01bends it opens up this opportunity for

26:03blood to kind of Squirt back here into

26:05the left atrium which produces this

26:07regurgitation

26:09but you'll hear this click sound that

26:11actually comes about right before the

26:13actual murmur takes place

26:15and so this is called a ejection click

26:19and then this one right here this is

26:21called we're going to put Holo a hollow

26:24systolic murmur usually what that refers

26:27to is it means that you hear it

26:29throughout the entire process of

26:32assistively but it's not technically the

26:34case because it depends upon where the

26:36ejection click occurs so sometimes this

26:39ejection clip can move so it can occur

26:42earlier and usually scenarios where the

26:44patient is super let's say having a very

26:46low venous return or it can come a lot

26:50later if you increase the advancement so

26:52we'll talk about Maneuvers that affect

26:53that later

26:54all right but that's the concept here

26:56now if you look at these other two if we

26:57come down here

26:58same concept here so again we're going

27:00to have a patient here who has what's

27:02called a mitral valve prolapse so we'll

27:05say this one is a mitral valve prolapse

27:08they may have a regurgitating murmur

27:09associated with it

27:10another patient may have the same thing

27:13but this may again occur throughout the

27:15entire so this is truly what we refer to

27:17as more of a hollow systolic murmur so

27:20we're going to put here again this is

27:22definitely more classic of what we would

27:24use that term of holocystolic you're

27:26hearing it throughout the entire process

27:27sometimes they say pan systolic

27:29holocystolic same thing

27:31but it's occurring between S1 and S2

27:33continuously this is because during

27:35systole blood is supposed to go from the

27:39left ventricle into the aorta but all

27:41this blood during the immediate part of

27:43Sicily floods right back into the left

27:44Atria this is true mitral

27:48regurgitation

27:50so if a patient has mitral regurgitation

27:52there will be no click unless they have

27:55a prolapse of the actual valve and then

27:57regurgitation

27:59all right

28:00big thing to remember is both of these

28:02can be heard at the Apex

28:04this one has a click this one does not

28:06have a click but it also can be heard of

28:09the Apex the other thing is that this

28:10usually radiates it radiates and if you

28:12listen at the fifth intercostal space

28:14you go over here you might be able to

28:15hear it in the axilla so sometimes this

28:18may also radiate

28:20to the axilla so that's one way that you

28:22can help to differentiate between these

28:24two but then there's one more

28:26another one

28:27is where you again can hear this murmur

28:30and it appears to sound

28:32holosystolic or pan systolic so you hear

28:35it throughout the entire systolic

28:37process

28:39this one is again

28:42when we say holosystolic

28:45it's because of a vsd

28:47so we had mitroval prolapse mitral

28:49regurgitation and what's called a vsd

28:51now the vsd is usually particularly

28:55heard more likely around that fourth

28:58intercostal space so if you really

29:00wanted to you could add it you'll hear

29:01this on the left fourth

29:04intercostal space

29:05but what happens is the moment Sicily

29:08occurs blood is supposed to go from the

29:09left ventricle into the aorta the blood

29:12will jet over here into the right

29:14ventricle so the smaller the hole is the

29:17louder the murmur is generally the

29:19larger the hole the softer the murmur is

29:21that's just because of like the actual

29:22turbulence of blood flow but in that

29:25concept here whenever this happens is

29:26going to be out throughout the entire

29:27systolic process one of the big things

29:30is location all right that's going to be

29:33one of the key things here and we'll

29:34also talk about Maneuvers so this is the

29:37ways that I want you guys to think about

29:38a systolic murmur is occurring between

29:41S1 occurring between S2 think about

29:44location think about this extra heart

29:46sounds added on and think about

29:48radiation

29:50and then again use your terminologies to

29:53differentiate the quality or

29:54characteristic of the murmur

29:56all right cool deal

29:59one quick thing before we move on I

30:01mentioned pretty much all leftover heart

30:03murmurs right it doesn't seem like I

30:04mentioned many right heart murmurs the

30:06reason why is left is the ones that

30:08we're more concerned with right or less

30:10common plus guess what aortic stenosis

30:13and pulmonic stenosis will have the same

30:15type of quality of murmur it'll just be

30:17a different location

30:18mitral regurgitation and tricuspid

30:21regurgitation will have the same type of

30:23murmur it'll just be a different

30:24location and so that's the big things to

30:27be able to understand the difference

30:28about

30:29cool diastolic murmurs what does that

30:31mean that means that these murmurs are

30:33occurring between

30:35S2 and S1 it's occurring after diastole

30:39or during diastole I should say so in

30:41this particular scenario

30:43we don't have any murmur between S1 and

30:45S2 is coming after S2

30:47this one's interesting

30:49what happens in this one is you'll hear

30:51this murmur and it'll be the same

30:52between these two they'll look exactly

30:54the same in configuration and it looks

30:57like it's decreasing in intensity as you

30:59go throughout diastole right

31:01this is called a decrescendo type of

31:05murmur all right what's the difference

31:08between these two all right in this one

31:12the patient has what's called aortic

31:14regurgitation and again it'd be the same

31:17concept if they have pulmonary

31:18regurgitation they would have a

31:19decrescendo murmur

31:21in this particular scenario blood will

31:24be jetting

31:26backwards during diastole blood supposed

31:28to come back but it gets blocked by the

31:30aortic valve if the aortic valve is

31:32damaged it'll jet back in and

31:34precipitate turbulence of blood flow

31:35precipitate a murmur

31:37in this scenario for aortic

31:39regurgitation where would you generally

31:41hear this it's usually around that left

31:44uh third intercostal space we refer to

31:46this as herbs point so you should be

31:48able to hear this around herbs

31:50point

31:52right if it was pulmonic regurgitation

31:54it'd be a little bit different right so

31:55that's usually around like again usually

31:57more of like that left

31:59secondary causal space rather than the

32:00left third intercostal space

32:02so now that's one particular point

32:05the next thing here is that in this

32:07other disease

32:08this is mitral stenosis

32:11so this is called mitral stenosis what

32:14happens in mitral stenosis is this valve

32:16is so thinotic and it's really difficult

32:18to get blood from the left atrium into

32:21the left ventricle super difficult

32:23and what happens is is as you're trying

32:26to push blood through here these valves

32:28will start to kind of like Buckle if you

32:31will

32:32and they kind of buckle at a certain

32:34point which kind of gives them this

32:36weird sound as you're trying to squeeze

32:38blood through this small area here they

32:40precipitate a kind of a clicking sound

32:42or a snapping sound and that happens

32:44right here

32:46before the bakrescendo murmur you know

32:48what they call this an opening snap

32:50we're going to put o s

32:53so you'll hear this opening snap at the

32:55apex of the heart then a day Crescendo

32:59murmur that comes after that one that's

33:02classic of mitral stenosis so if I say

33:05opening snap Dickerson a murmur Apex

33:07mitral stenosis if I said herbs point a

33:11decrescendo murmur that was auscultated

33:13you would say this is a Aortic

33:15regurgitation type of murmur all right

33:17so we got these down

33:20same concept would exist if I were to

33:22say different location for pulmonic

33:24regurgitation different location for

33:26tricuspid stenosis but same type of

33:28quality characteristics of the murmur

33:30and same timing of the murmur

33:32we come down to the last one

33:34the last type of murmur here is going to

33:36be a continuous murmur this is usually

33:38seen in the Pediatric population

33:40what happens with this one is that they

33:42have this murmur that usually is

33:44occurring between S1 and S2 and

33:47continues after S2

33:50and the characteristic terminology

33:52behind this one is continuous but they

33:56add in something

33:57it's machine like so it sounds like it's

34:01a machine like murmur

34:04and whenever you hear that terminology

34:06you want to think about a particular

34:08disorder called a PDA a patent ductus

34:11arteriosus

34:12what's happening in this particular

34:14murmur is blood is supposed to move left

34:16ventricle into the aorta and flow

34:19through the aorta but the left side

34:21heart pressures are generally higher

34:23than the right heart pressures and

34:24babies that are already born

34:27so naturally where will this blood flow

34:29it'll flow this way during systole

34:32then the heart will go into diastole so

34:34blood is supposed to kind of flow back

34:36shut that aortic valve closed

34:38but what do you think about the aortic

34:39pressures during diastole in comparison

34:41to the pulmonary pressures during

34:42diastole it's still higher so regardless

34:45blood will keep shunting from the aorta

34:47into the pulmonary artery during both

34:49systole and diastole that's why it's

34:52continuous

34:53well one of the weird things is that

34:55this one is usually located around

34:56What's called the left

34:58infra

35:00clavicular

35:02area

35:04so this one is not a part of that

35:05classic locations that we uh kind of

35:08annotated prior

35:09so this is the way that we would Define

35:11murmurs in a very simple concept

35:14also take the locations remember ape TM

35:17right from there oh you hear a murmur

35:20what is the timing is it systolic if

35:23it's systolic is it Crescendo de

35:24Crescendo or is it Holo does it have a

35:27click before or does it not have a click

35:30where is it again location and does it

35:32radiate that should help you oh it's not

35:34so solid it's diastolic okay does it

35:36have a decrescendo pattern oh it does

35:38does it have a CL opening snap that

35:40comes before or not and what's the

35:41location that's the key ways of

35:43differentiating and lastly is it a

35:45continuous one usually continuous one is

35:47the easiest one to be able to pick out

35:48because it's the only one we have here

35:49and that's usually associated with PDA

35:51from there if you're still stuck with

35:54saying I don't really know the type of

35:56actual murmur it is then we can come to

35:58the Big Daddy we say okay

36:01I'm struggling between determining what

36:03kind of murmur this is I'm going to do

36:05specific Maneuvers to see if I can

36:07increase the intensity or decrease the

36:09intensity of the murmur and that may add

36:11to my confidence that this is the type

36:14of murmur and if after all of that

36:16you're still not sure the classic thing

36:18that we usually go to is an

36:20echocardiogram to really Define the type

36:21of murmur all right let's start talking

36:23about the Maneuvers now to determine the

36:25type of mirror we get to the point where

36:27we say Okay location it's systolic

36:29versus diastolic

36:31then we can say what is actually

36:34happening if I do this particular

36:36position change this is really important

36:38to memorize

36:39one inspiration

36:41any right side murmur we didn't talk

36:44about the right side murmurs here

36:45because they're not commonly tested but

36:46it's the same exact concept

36:48any right side murmur will be increased

36:51in intensity during inspiration because

36:53you're increasing the right side venous

36:54return

36:56any left-sided murmur would be decreased

36:58because you're not improving the venous

37:00return on that side that would be a one

37:02helpful sign

37:04expiration you're increasing the left

37:06side venous return and decreasing the

37:09right side of minutes return so the

37:10right side of murmurs will be decreased

37:11with expiration and left side murmurs

37:13increase with expiration straightforward

37:16if I lean forward it brings the aortic

37:18valve closer to the chest wall so it'll

37:20increase the intensity of all aortic

37:22murmurs

37:24if I have them in the lateral decubitus

37:26position so I lay them on their left

37:27side and I listen there it'll bring the

37:29mitral valve closer to the chest wall so

37:31it'll increase the intensity of all

37:33mitral valve murmurs

37:35here's the big stuff if I increase

37:37venous return I have them squat I have I

37:40lift their legs up I'm increasing the

37:43venous return to the heart

37:45increasing venous return will increase

37:47the intensity of all murmurs except two

37:51it'll increase the intensity of all

37:52murmurs except two which are

37:54hypertrophic cardiomyopathy and mitral

37:56valve prolapse

37:58it'll bring the the actual mitral valve

38:00prolapse remember there's a click and

38:01then a murmur it'll bring the click

38:04later and make the murmur shorter and

38:07it'll also decrease the intensity of the

38:10hypertrophic cardiomyopathy murmur

38:13if you do the opposite here which is

38:15decrease the venous or new balzava which

38:17increases the intrathoracic pressure and

38:19reduces venous return or you stand which

38:21reduces venous return that'll decrease

38:23the intensity of all murmurs except

38:26what mitrobot prolapse and hypertrophic

38:29cardiomyopathy in this it'll actually

38:31increase the intensity of HCM

38:33and then what it'll do is

38:35in this scenario here from mitral valve

38:38prolapse you have to think about it it's

38:40actually going to cause the click to

38:41come earlier and then the actual murmur

38:44after that to be much longer and that's

38:46the big thing to remember

38:48okay next one is afterload when you

38:50increase afterload you're squeezing

38:52these hand grips and what this will do

38:54is

38:55this will increase the intensity of an

38:57aortic regurgitation murmur and mitral

38:59regurgitation murmur and it'll decrease

39:02the intensity of an aortic stenosis

39:04mitral valve prolapse and HCM murmur

39:07for decreasing afterload this is going

39:09to be using things like ammo nitrate and

39:11super short acting it'll dilate the

39:13vessels

39:14if it dilates them it's going to do the

39:16opposite it's going to decrease the

39:17aortic regurgitation of micro

39:18regurgitation remember and increase the

39:20aortic stenosis and mitral valve

39:22prolapse and HCM armor the whole concept

39:25behind this is if you increase afterload

39:27the pressure inside of the order it's

39:28going to shoot blood back into the

39:30actual ventricle and also make it easier

39:33for blood to fly back into the left

39:35atrium that's why it'll increase these

39:37murmurs if you decrease the afterload

39:39the blood won't be shooting back into

39:40the ventricle and shooting back into the

39:42Atria that's why it decreases in this

39:44types of murmurs

39:46for aortic stenosis mitrobot prolapse

39:49and HCM

39:50again if you increase the afterload here

39:52what you're doing is you're making it

39:54harder for blood to leave the left

39:56ventricle and move out into the aorta

39:58that's going to decrease the flow across

40:00the aortic semilunar valve decreasing

40:02aortic stenosis that'll decrease the

40:04buckling of the mitral valve decreasing

40:06that click and then murmur and also

40:09it'll actually help because what it'll

40:10do is when you increase after that we'll

40:12talk about this a little bit later but

40:14it keeps more blood in the left

40:15ventricle and stretches out the left

40:17ventricle and flattens out that septum

40:19and reduces the obstruction there in HCM

40:21but that's the concepts I need you guys

40:23to remember

40:28[Music]

43:32all right my friends we covered aortic

43:35diseases I hope that made sense I hope

43:36that you guys enjoyed it and as always

43:37until next time

43:40foreign

43:42[Music]