in this video i'll be teaching you everything that you need to know about heart sounds and heart murmurs this is an incredibly high yield topic that for many years now i've been trying to come up with a good way to explain this it's very complex and actually getting this information in your brain will yield so many points on test day because on us emily and comlex a lot of the ways that test writers will go after heart sounds and heart murmurs is that they'll actually give you either a visual depiction of the amplitude of sound or they'll give you an audio file on your question or on your exam and you'll have to listen to that heart sound in order to get the question right so there's absolutely no way that you can get these correct on your test unless you thoroughly understand heart sounds and heart murmurs and this is both visually but also acoustically so in this video i'm going to give you all of the knowledge that you need in order to dominate these questions in this video this is what we're going to be talking about we'll start with just talking about what normal heart sounds sound like and the reason for that is because you can't detect abnormal unless you know what's normal so we'll talk about normal heart sounds and then we'll go into splitting of heart sounds specifically we'll talk we'll be talking about s1 and s2 and then we'll go through the actual high yield murmurs so we'll talk about aortic stenosis mitral and tricuspid regurgitation mitral valve prolapse ventricular septal defect aortic regurgitation mitral stenosis and a patent ductus arteriosus so let's begin by talking about normal heart sounds and i'll actually play for you what normal heart sounds truly sound like so you're going to hear real audio in a few moments but first let me just explain so when you're taking your exam what you might see is something that looks like this and this is just a visual depiction of the amplitude of sound so if you've ever gone online and listened to music on a website like soundcloud or something similar you've probably noticed that you see this sort of waveform of amplitudes and that just represents how loud is sound that you're hearing and just like that occurs on websites where you listen to music it's going to show up on your exams when you're taking us emily or comlex or in-class exams when they're trying to give you questions about heart sounds so when we talk about normal heart sounds and again the track of the audio file of what this actually sounds like is coming so just bear with me when we talk about normal heart sounds we're talking about an s1 and an s2 so close your eyes imagine any movie or tv show where you've heard a dramatic heartbeat in what you're watching you know that there are two distinct sounds of a heartbeat right there's two bombs and if we're being a little bit more scientifically accurate we would say there's a lub followed by a dub so instead of you know when we talk about normal heart sounds it would be more correct to say lub dub lub dub lub dub lub dub now the lub or the first heart sound in a normal heart sound is your s1 and the dub or the second heart sound in your normal heart sound is an s2 and if you look at the cardiac cycle graph and relax i know that you're getting overwhelmed here but we don't need to know this for the heart murmurs section but if you look at the cardiac cycle here what we see is that the s1 heart sound occurs just at the beginning of systole so that s1 heart sound occurs during the isovolumetric contraction right the mitral valve closes and the tricuspid valve also closes and then just after that s1 heart sound the aortic valve opens and you get that rapid ejection phase followed by the reduced ejection phase so what this tells you is that that s1 heart sound or the lub right lub dub lub dub lub dub that lub is the actual sound of the mitral valve and the tricuspid valve closing and if you think about how a heart is working when the mitral and tricuspid valve closes that tells you that you're starting systole because if the mitral and tricuspid valve close then you're not filling the ventricle but the ventricle is about to squeeze and eject the blood that's already been filled out through the circuit right think about it why would the mitral and dry cuspid valve be closed because we're about to start systole so the s1 or the lub is the sound that the mitral and tricuspid valves make when they close now the s2 sound or the dub let's go back to our cardiac cycle here the s2 sound or the dub happens just at the beginning of diastole so that's when the isovolumetric relaxation phase occurs and the s2 heart sound is the aortic and pulmonary valves closing okay so lub is mitral and tricuspid closing we're starting systole dub or s2 is the aortic and pulmonic valves closing and therefore we are starting diastole so if we look at this graphically we see lub followed by dub s1 followed by s2 and between the s1 and s2 heart sound we're in systole because think about it s1 means mitral and tricuspid valves close we go through that isovolumetric contraction followed by rapid ejection followed by reduced ejection and that whole stage or those three steps that i just named are during systole and then we have the s2 sound or the dub where the aortic and pulmonic valves close and therefore when that happens we enter the iso volumetric relaxation phase followed by the rapid ventricular filling followed by the reduced ventricular filling and all of the stuff that i just mentioned occurs during diastole so between s2 and between s1 or between the dub and the lub we are in diastole so it should make sense to you that depending on which heart sound you're hearing you can actually figure out where am i in the cardiac cycle so this is our summary so far the normal heart sound is s1 followed by s2 the lub followed by the dub the closing of the mitral tricuspid followed by systole followed by the closing of the aortic pulmonic followed by diastole and that entire cycle just runs on repeat so now for the actual audio file this is what normal heart sounds sound like now it's important to appreciate the sound you just heard because normal heart sounds are normal so if you know what normal sounds like then you'll know what's not normal and this is true of all of medicine whatever you're studying learn what's normal first this is why your first year of medical school they teach you physiology and your second year of medical school they teach you pathology because you don't know what's broken until you know what's normal so now that we understand normal heart sounds and we understand s1 and s2 and what's creating those sounds and what those sounds represent let's talk about splitting of heart sounds so when we talk about splitting what we're talking about is what happens to the s1 and s2 heart sound depending on how we're breathing and what different types of pathology we can have in the heart now because the s1 heart sound is two valves closing and the s2 heart sound is two valves closing technically the s2 could be rewritten as instead of s2 it could be rewritten as a2 and p2 because since both the aortic and the pulmonic valves are closing roughly simultaneously it's the two different valve closures collectively contributing to one sound so although in normal hearts without splitting you would hear them as one singular s2 or one singular dub what's actually happening in microseconds is that there are two distinct sounds and that dub is created from the closure of a and the closure of p so that's the closure of the aortic and the pulmonic singular purple line representing a2 and that singular red line representing p2 can actually have some shifting and depending on whether you're breathing in during inhalation or breathing out during exhalation those lines can slide now i'm going to explain all the physiology here and what's happening but let's start by talking about wide splitting of s2 so when you get splitting a2 and p2 will separate and then depending on again whether you're breathing in or out those individual lines will separate more so when you have your headphones on and you're listening to the audio file on your exam or you have your stethoscope on a patient's chest and the lub-dub doesn't sound like lub-dub lub-dub lub-dub but you hear lub-dub-dub dub-dub dub-dub lub-dub-dub now the dub is being separated or split so this is why splitting is important so when it comes to wide splitting of s2 let's talk about what's happening so the cause of wide splitting of s2 is anything that delays right ventricle emptying now the two highest yield exams are going to be pulmonic stenosis and a right bundle branch block so the rbb now let's talk about this so we can see here on the wide splitting graph that a2 and p2 separate and then during inhalation that p2 separates even more so it gets split out even more widely so let's just look at pulmonic stenosis as an example so imagine that you are breathing in so you got inspiration or inhalation and when you breathe in you take that deep breath in there's a decreased intrathoracic pressure now what does this what does this mean when there's decreased intrathoracic pressure you get an increase in right ventricle filling you also get an increase in right ventricle ejection time and right ventricle stroke volume so the net effect here is that we first drop our intrathoracic pressure and that means more blood is going to flow down down that gradient into the right ventricle so if more blood is flowing down into the right ventricle that means that the right ventricle will be squeezing out more flow through the pulmonic valve so this is going to increase the capacity of our pulmonary circulation and decrease the impedance of our pulmonary circulation now everything that i've just mentioned and everything that i've just summarized for you i'm highlighting that in green here because that's normal splitting we might call this physiologic splitting so under normal circumstances when somebody takes a breath in and they have increased right ventricular return which means increased right ventricular output that is going to have a slight shift during inhalation only to space out that p2 heart sound more because since more blood will be flowing over the pulmonic valve it will take longer for that pulmonic valve to close relative to the aortic valve so a2 will happen first because the aortic valve is closing since not as much blood is flowing over the aortic valve when we zoom in and look at these milliseconds but for that pulmonic heart sound during inhalation specifically because more blood is flowing over the valve it will have delayed closure of the p2 valve so when we look at this graphically we'll see the lub which is your s1 and then we'll see the dub and we're splitting the dub into the aortic and pulmonic valves closing separately again and i'm summarizing here to really drive this home when you take a breath in more blood goes to the right ventricle which means more blood flows over the pulmonic valve which means the pulmonic valve takes longer in milliseconds to close so that p2 heart sound will get spaced out and there'll be some normal splitting but during inhalation especially it'll get spaced out even more so this is normal splitting and i would summarize this by saying during inhalation the pulmonic valve closure or the p2 component of the dub or the p2 component of the s2 gets normally or physiologically split so it spaces out wide splitting occurs when you get this during inhalation in the presence of pulmonic pathology so basically anything that causes slower or longer blood flow over the pulmonic valve already causes normal splitting so introducing pathology such as pulmonic stenosis or a right bundle branch block will exaggerate an already exaggerated process spacing this out even more during inhalation so if we go back to our pulmonary stenosis example under normal circumstances when you take a deep breath in you get increased right ventricular filling stroke volume and ejection time increase flow over the pulmonic valve but in the presence of pulmonic stenosis or a right bundle branch block where in both of those conditions it will already cause slower or longer or exaggerated flow over the pulmonic valve the pulmonic valve will take even longer to close which means that when we look at a graph or a visual depiction of wide splitting the a2 sound and the p2 sound will get spaced out and during inhalation the p2 sound will get spaced out even more so i really hope that that makes sense this is wide splitting and this is how this works now that you understand why it's splitting let's look at our next example of splitting so now we'll talk about fixed splitting of s2 so in fixed splitting the a2 and p2 components of the s2 or those two separate components of the dub they get spaced out but during exhalation and inhalation it's fixed so you're not going to get that red line separating like we saw in wide splitting it's going to stay one line that during exhalation and inhalation it's going to be equal no matter what so let's talk about what causes fixed splitting so the classic example of fixed splitting is a left to right shot which you'll classically hear in an atrial septal defect or an asd and the reason that this is fixed is because it doesn't change with inhalation and let me just explain what's going on here so let's say we have an atrial septal defect again person takes a breath in you get a venous return that increases to the right ventricle now under normal circumstances that increase in right ventricular filling will attempt to overfill the right ventricle and it will attempt to put more blood through the pulmonary system like we just talked about in wide splitting but we've got an atrial septal defect so we've got a left to right shunt that's actually fixing the volume that the right ventricle can accept because think about it even if theoretically the right ventricle was going to accept more blood and pump more blood where would that blood be going it would be flowing through to the left side of the heart but because the atrial septal defect is present all of the blood in the left side of the heart would actually get shunted back to the right side of the heart so even if for a split second that right ventricle could put more blood through the pulmonic valve and cause a delayed pulmonic valve closure it wouldn't really matter what you did or what the patient did during inhalation or exhalation because eventually you're going to get equilibration between the left and right side of the heart because that atrial septal defect is there allowing that hole to pass blood and shunt blood from the left to the right side of the heart so in a split second you might get more flow through the pulmonic valve but over time and when you're listening to a patient with a stethoscope and when you're visually depicting splitting visually on your exams you're not going to see any difference because that asd is going to allow that blood to flow right back and you're going to get quick equilibration so again no change in pulmonic closure during inhalation or exhalation because that asd is open and it's basically shunting and equilibrating the left and right sides of the heart so it doesn't matter what happens during inhalation or exhalation those lines are going to be equal and again if we go back to this graph here this is what fixed splitting looks like when you breathe in when you breathe out that p2 doesn't move it's going to be separated from a2 but it's going to be equal it's not going to move during inhalation or exhalation so if you see this visual depiction we're talking about fixed splitting of s2 and you want to think about a left to right shunt because again physiologically you know under what circumstances would breathing in not cause more blood being pumped from the right ventricle through the pulmonary circuit there would have to be a shunt if you see this think asd so that is your atrial septal defect it's a little tricky but i think that if you understand what an atrial septal defect is it makes a lot of sense now let's talk about the most confusing splitting of s2 and that's paradoxical splitting and this really throws medical students for a loop so i'm probably going to over explain this so that you you really hammer this home so paradoxical splitting is caused by anything that causes delayed aortic valve closure the classic examples on your test will be either aortic stenosis or a left bundle branch block so let's look at our graph here what we see is we've got our s1 or our lub followed by what's normally our s2 or our dub now in all the other graphs you've seen the a2 or aortic component of the dub happen first and then you saw the pulmonic or p2 component of the dub happen second but in paradoxical splitting that actually gets reversed so let's talk about that so let's use aortic stenosis as our example so recall that normally we've got our a2 component right before our p2 component so i'm talking about the two different s2 sub components the dub usually it's a2 before p2 okay so normally it's a2 before p2 but in the presence of pathology of the aortic valve which causes a delayed closure of the aortic valve it means that the aortic valve will take longer to close than the pulmonic valve so that a2 and p2 sub component actually get flipped so now it's the pulmonic valve that closes first because you've got aortic stenosis so more blood flow or longer time of blood flow over the aortic valve delays the closure of the aortic valve so it delays the a2 subcomponent of the s2 dub so that's what would happen in aortic stenosis but let's say that a patient takes a deep breath in right they do inhalation slash inspiration what's happening now so now they take a breath in more blood flows to the right ventricle because we have that drop in intrathoracic pressure more blood flows over the p2 or the pulmonic valve which means that the p2 component takes longer to close because just like we saw in our original discussion of physiologic splitting and wide splitting when you take that breath in more blood to right ventricle more right ventricle ejection more right ventricle ejection time more blood flowing over pulmonic takes longer for the p2 sub component of the s2 dub so what does this mean or look like what does this look like on the graph well when you take that breath in the p2 sound should be happening earlier but when someone has aortic stenosis and when someone breathes in the p2 component actually slides closer back toward the a2 sound so the reason that this is called paradoxical is that you're supposed to hear pulmonic first and aortic second because aortic is actually stenotic but when you take a breath in you're re-normalizing them so you're sliding pulmonic back towards a2 and a2 is delayed right a2 is stenotic it's taking longer for the aortic valve to close that aortic heart sound or that a2 subcomponent should happen second but if you take a breath in then the pulmonic sound is delayed as well so taking the breath in makes what should be a reverse split paradoxically come back together and sound more normal so this is why medical students get confused it's paradoxical because you're supposed to hear a reversal but when you take a deep breath in it renormalizes what should be reverse order that's why it's called paradoxical so after i explained it i think it makes a lot more sense but let's do a summary slide so here is normal wide fixed and paradoxical splitting and what they're associated with so normal is just the physiological effects of taking a breath in wide splitting is associated with both pulmonic stenosis and a right bundle branch block thick splitting is associated with that left to right shunt so your atrial septal defect remember that if you see the p2 component of the s2 not changing with a breath in or a breath out that has to be due to a left to right shunt and then paradoxical is associated with any condition that delays the aortic valve closure that's paradoxical because then you're taking a breath in and re-normalizing what should be reversed to begin with so the way that i remember this is wide pulmonic right fixed atrial paradoxical aortic left so i i think wiper first aid pal wiper first aid pal and those are my stupid mnemonics wiper w for wide p for pulmonic r for right first aid f for fixed a for atrial and then pal p for paradoxical a for aortic and l for left so if you remember wiper first aid pal wiper first aid pal then if you get a question on splitting and you can't quite remember the associations knowing those silly very simple sounding mnemonics can actually pick you up a free point now this is my summary chart but the big takeaway from this section of the video is physiologically what's actually happening here because if you understand the in-depth explanation of where the blood is flowing through the heart which valves are taking longer to close and what happens when we take a breath in this should make perfect sense so i hope that you understand this i know that i really beat a dead horse here and probably over explained this but it's my experience that medical students don't get an explanation like this so they're stuck just kind of like memorizing what they see in first aid and what they hear in their in-class lectures but those explanations have historically been awful so hope this was useful this is splitting of s2 heart sounds so at this point in the video we've now talked about what normal heart sounds are what they look like and what they sound like and then i went into a very long-winded explanation of the different types of s1s2 splitting and if you're comfortable with this conversation so far let's transition now and talk about some of the main high-yield pathological murmurs we're going to run through these one at a time we'll start with aortic stenosis and as you can see on this slide how i want to approach this is to keep it stupid and simple so we'll do a description of what the murmur is reported to sound like we'll talk about clinical associations and then we'll list out that visual depiction of what the amplitude of sound looks like and i'll give you the audio file as well now this is important because when we talk about description and clinical associations this is the stuff that shows up in the exam questions so in usmle and comlex if they're going to give you buzz words or phrases or describe the murmur to you you want to know the description and the clinical associations so that when you see aortic stenosis you think oh i have to think about this association so if you see that association you can work backwards and get aortic stenosis basically the idea here is i want to give you guys a lot of different neural networks to connect in your brain so that you're getting these concept maps and you're generating ways to think about these questions in a high-yield way so let's start with aortic stenosis aortic stenosis is described as a systolic crescendo decrescendo ejection murmur so a couple important things here one it's systolic so it has to be occurring between s1 and s2 between the lub and the dub because remember between those two sounds is where systole occurs now it's described as being crescendo decrescendo and if you look down at the bottom of the slide at the visual depiction crescendo decrescendo means that the sound peaks and then it drops off so it gets louder and then it gets softer it gets louder and then it gets softer and that style of the sound being harsh and during systole cues you that you should be hearing and thinking about aortic stenosis now the associations of aortic stenosis there are a few the first one is called pulses parvus at tardis which is a fancy way of saying that there is a weak and delayed carotid upstroke now on clinical exam you can actually palpate somebody's carotid upstroke and if they have aortic stenosis because the aortic valve is sonatic and therefore blood will flow through that aortic valve more slowly and over a prolonged period of time the blood that would be flowing into the carotids is weak and delayed so if you're looking at the carotid upstroke it shouldn't surprise you that in the presence of aortic stenosis that upstroke will be weak and delayed and that is what pulses parvus at tardis refers to now as far as symptomatic wise patients might experience syncope angina and dyspnea and again think about it guys the aortic valve is stenotic so they're going to have trouble catching their breath because you're going to get some back flow this is usually associated with aortic regurgitation so you're going to get some back flow through the pulmonary circuit so you're going to get dysmea you're going to have syncope because the aortic valve is stenotic so it's difficult to have an ejection fraction that's going through that valve that's supplying blood to the brain in an adequate fashion and there's going to be angina because over time you're going to get left ventricular remodeling as the heart works harder and harder to pump through that stenotic valve now the other thing that's not listed on this slide that i just want to point out is a little bit about etiology so usually the most common cause of aortic stenosis is what we call aortic valve sclerosis and that's usually due to age related calcification so over time little calcium deposits will go around the valve and then that valve will become stiff and fibrotic and the aortic valve leaflets will not function like they used to so if you get a test question and this is more step two level two but if you get a test question that asks what is the most common cause of aortic stenosis the answer is age-related calcification and fibrosis better known collectively as aortic valve sclerosis now the other thing you want to think about with aortic stenosis is if it's an older patient it's usually safe to say that that's due to age-related calcification but if a younger patient has aortic stenosis you want to think about a bicuspid aortic valve and a bicuspid aortic valve simply refers to when two of the aortic valve leaflets fuse usually that happens in utero and if that happens the person is obviously going to have dystrophic aortic valves so they'll get a functional aortic stenosis because of that bicuspid aortic leaflet fusion on usmle and comlex if you have a young patient who has aortic stenosis i want you to think bicuspid aortic valve and usually but not always on us emily and comlex the association with bicuspid aortic valve that you should think about is going to be turner syndrome so if you see a young patient with aortic stenosis immediately think turner syndrome and then that will open up the door to all of the other clinical findings associated with turner syndrome so you can see that a test question could start with just giving you the audiophile of aortic stenosis tell you that it's a young patient and then they're going to ask you something like what other clinical sequelae could we see in this patient and you know they're telling you it's a it's um turner syndrome so you got to think about all that other stuff that you see with turner syndrome the last thing i want to say about aortic stenosis before we get into the audiophile is you also want to think about rheumatic fever so if you're in the us you probably don't associate aortic stenosis with rheumatic fever this is a higher income country and there has been consistent eradication and monitoring and treatment of strep pharyngitis but in lower income countries there is still a pretty significant association between aortic stenosis and rheumatic fever and where treatment is perhaps not as available not as widespread you can see the complications of rheumatic fever one of which would be aortic stenosis so that's aortic stenosis takeaway from this slide is crescendo decrescendo occurs during systole is very harsh sounding you see pulves pulsus parvus at tardis syncope angino dyspnia so people say that aortic stenosis makes them sad sad syncope angina dyspnea and remember that in an older person it's usually due to calcification in a younger person think bicuspid aortic valve think turner syndrome so now with that said what you want to listen to when you hear an audio file is look for that first initial loud sound and then that second drop off so in just a second i'll play for you what aortic stenosis sounds like and i want you to really appreciate that although it's faint it's very harsh sounding and the first part of the sound is louder the second part of the sound drops off so that first part is crescendo that second part is decrescendo and it occurs between the lub and the dub or between s1 and s2 so we know that it must be aortic stenosis so this is what aortic stenosis sounds like all right so i hope you were able to appreciate the crescendo part at first and then the decrescendo part following that but that's aortic stenosis all right so we've now talked about aortic stenosis and let's move on to mitral and tricuspid regurgitation so mitral and tricuspid regurgitation get grouped together when we talk about heart murmurs because they both sound identical so the only difference between how you pick up whether you're listening to mitral or tricuspid regurgitation is where the stethoscope is placed either on a real live patient's chest or on your exam where the stethoscope is in the like visual simulation of the patient so these are both described as holosystolic high-pitched blowing murmurs holosystolic hollow all systolic systole so this happens continuously throughout all of systole and if you look down at the bottom of the slide at the visual depiction the amplitude of sound doesn't change so the volume is going to be roughly the same throughout the entire murmur now the clinical associations it really depends on whether we're talking about mitral or tricuspid regurgitation so for mitral regurgitation you want to think about some type of degenerative heart process where you get direct rupture of the corta tympani so that could be like post myocardial infarction it could be due to chronic remodeling of the left ventricle resulting in left ventricle dilatation and then subsequent rupture it can be a whole host of different things but usually for mitral regurgitation you want to think of structural and ischemic heart disease you can also see it in infective endocarditis and like i said ischemic heart disease for tricuspid regurgitation you want to think about the causes of right-sided heart failure so classically you want to associate this with intravenous drug abuse because again as pathogens and i've said this in other videos but again as pathogens pass over the tricuspid valve they're going to preferentially damage the tricuspid valve before the body figures out a way to filter them out so you get preferential right-sided heart failure in the setting of intravenous drug abuse also think about marfan syndrome carcinoid syndrome and pulmonary hypertension as other high-yield things to associate with right-sided heart failure more specifically tricuspid regurgitation of note rheumatic fever can cause either mitral or tricuspid regurgitation and when you're listening to this sound on exams the only way you're going to know whether it's mitral or tricuspid either the clinical vignette will hint heavily at an association so if they say the chord of timpani was ruptured then you want to think mitral if they say the person has a 20 year history of shooting heroin then you want to think tricuspid but otherwise really the only way to get this is where's the stethoscope so if the stethoscope is at the apex and the sound is described to radiate toward the axilla that's mitral but if the stethoscope is at the tricuspid area then that's obviously tricuspid so other than that there's really no other way to delineate whether you're talking about mitral or tricuspid because both of them are hollow systolic high-pitched blowing murmurs that sound identical and last for all of systole between the s1 s2 heart sound so looking at our visual depiction when your headphones are on this is going to be hollow systolic high pitched blowing and continuous from s1 to s2 so put your headphones on and listen because this is what mitral and tricuspid regurgitation sound like all right so i hope you can appreciate that that murmur goes continuously and is high pitched and blowing between the s1 lub and the s2 dub so that's mitral and tricuspid regurgitation so here's what we've covered so far and we're making really good progress so just bear with me everybody as we keep the momentum going now let's talk about mitral valve prolapse so mitral valve prolapse is classically described as a late systolic crescendo murmur that has a mid systolic click and that description that buzzword the mid systolic click is so unique to mitral valve prolapse that if you get either the audio file of this murmur on your exam or you get the amplitude waves which you see visually at the bottom of this slide on your exam you really should get this free point because it's incredibly unique now usually mitral valve prolapse is asymptomatic in a lot of patients but of course you're taking us emily and comlex so chances are if the test writer wants you to think or pick mitral valve prolapse they're actually going to give you somebody who's symptomatic so for the associations you want to know that mitral valve prolapse is heavily associated with connective tissue disorders like ehlers-danlos syndrome and marfan syndrome it's also associated with less common presentations which would include osteogenesis imperfecta fragile x syndrome and autosomal dominant polycystic kidney disease but the huge or high yield genetic associations are definitely those connective tissue disorders you also want to associate mitral valve prolapse with rheumatic heart disease and infective endocarditis now what's happening here is actually really interesting and i'm just going to take a moment to explain the pathophysiology now in these connective tissue disorders you have the abnormal deposition of different substances you've heard me talk in other videos about what happens in these connective tissue disorders but the same thing that you see elsewhere in the body you also see in the heart so in the case of ehlers-danlos syndrome and marfan syndrome you get the deposition of different types of substances such as dermatitis sulfate etc onto the mitral valve directly and what happens here is that all of this excess and abnormal deposition of this material creates this elongated fat floppy dysfunctional mitral valve leaflet and when the mitral valve can't function the way that it's supposed to it kind of bulges through and hence the name mitral valve prolapse into the left atrium during systole so while mitral valve prolapse initially starts as its own unique valvular disorder eventually what happens over time is mitral valve prolapse actually leads to mitral regurgitation because as those leaflets just kind of bulge into the left atrium which over time leads to papillary muscle dysfunction ischemia and possible rupture of the cortitendine you actually get the onset of severe mitral regurgitation so if you're taking your exam they could give you mitral valve prolapse and then ask you which of the following other murmurs is this patient likely to experience in the future and the answer would be mitral regurgitation so that's the association with mitral valve prolapse that's a little snippet of the pathophysiology again if i were to summarize that complex picture i would say that there's deposition of substances such as dermatitis sulfate and other glycosaminoglycans which cause the mitral valve leaflets to be floppy and fat and not work bulge into the left atrium and then downstream create mild to severe mitral regurgitation because those leaflets just can't function like they're supposed to now look at the bottom of this slide and look at the visual depiction of what this murmur looks like you're going to hear the audio file in just a second but basically when you're listening with your headphones on you want to try to appreciate that mid systolic click and this is a late systolic crescendo murmur which means that for the first half of the heart sound between the lub between s1 and the onset of that mid-systolic click you really don't hear anything so it's like a brief millisecond or so of silence and then you hear the mid-systolic click and then from that mid-systolic click to the s2 dub then you hear a gradual increase in volume for the remainder of systole so hearing that click is so unique to mitral valve prolapse that if you hear that this is the answer now i have another video where i go through all of my different mnemonics for how you memorize the description of the murmurs so for example for mvp you would it's the mid-systolic click and and i'm going to reuse one of my mnemonics here because it's so helpful so when i think of mitral valve prolapse i think of mvp which classically to me means most valuable player and that i use that in the context of sports so if you want to be the mvp your team has to click and that reminds me that mitral valve prolapse is associated with this mid-systolic click so when your headphones are on if you hear that click up your team has to click you're the mvp mitral valve prolapse so when we listen to mitral valve prolapse we really need to pick up on that late systolic crescendo murmur with the mid systolic click so i'm going to play that for you now this is what mitral valve prolapse sounds like all right so i hope you were able to pick up on the fact that it's pretty silent between the s1 and the click and then once you hear the click you get a gradual increase in volume until the s2 if that's difficult for you to pick up i want you to close your eyes and see this visual wave amplitude while you listen to the sound and really follow that with your eyes and your ears connecting these two is huge but that's mitral valve prolapse all right so here's where we are i am super proud of everybody you are making incredible progress learning what is obviously the most difficult section of cardiology to learn let's keep this rolling by talking about actually an easier murmur to learn ventricular septal defects so vsds are described as hollow systolic harsh murmurs and if we just jump ahead and look at that visual depiction of the wave amplitude of this murmur you can see that this looks almost identical to tricuspid and mitral regurgitation and that's because just like those other murmurs that we've already talked about this is also hollow systolic the associations with ventricular septal defects are a lot of your genetic abnormalities so we're talking about down syndrome edward syndrome and patau syndrome you can also look for associations with your various torch infections so we're talking about toxoplasmosis the o stands for other which is varicella and parvo b19 rubella cmv herpes hiv and syphilis you also can see less commonly in association with cry ducat syndrome recall that that is the disease that is due to a problem on chromosome 5 and that's where your patients will present with intellectual disability some other congenital skeletal abnormalities and then that classic cat-like high-pitched cry scream but really the big thing about ventricular septal defects that you need to understand is that these are just hollow systolic harsh murmurs and on a test you might be thinking well how am i going to differentiate this from tricuspid or mitral regurgitation and i have two answers the first is that ventricular septal defects are harsher sounding as and not as high pitched as the other two that we already talked about which are also hollow systolic so if you're really stuck and there's no other clues in the vignette whichever one sounds harsher which is like more disorganized and ruffled that's what you want to pick for the vsd and if you think that it sounds high pitched and it's also hollow systolic then that pushes you more in the direction of tricuspid or mitral regurgitation but really where the clues will come in is in the vignette there'll be other buzzwords or diseases or you know genetic statements that will give you an association so you want to know what's associated with ventricular septal defects because if they describe a patient that might have down syndrome then obviously you hearing a hollow systolic murmur should make you think vsd so ventricular septal defects are really not that complex in terms of what you need to know i would just encourage you to know what happens in down syndrome edward syndrome and patel syndrome and if you see any of those clinical sequelae or clinical features and you hear a hollow systolic murmur guess ventricular septal defect so that you're not in a position where you're like is this harsh is this high pitched i wish that the testing center gave me better headphones than these four dollar sets of headphones that have been worn by thousands of people and i'm probably gonna get otitis because they're disgusting but anyway that's ventricular septal defect um not a whole lot to know like i said and when it comes to picking up what this sounds like it's going to be holosystolic and harsh so this is what a ventricular septal defect sounds like all right so as you can probably appreciate it's hollow systolic so it goes throughout all of systole between the s1 lub and the s2 dub the sound is from s1 to s2 with no breaks or interruptions in between it's kind of harsh sounding and if you rewind the video and you go back to the mrtr this is harsher sounding and not as high pitched and that's the really subtle difference but again just know the associations because the test rater has to give you some clue to differentiate this from the ones we've already talked about all right so now let's talk about aortic regurgitation and aortic regurgitation will actually be the first diastolic murmur that we'll talk about this is described as a high-pitched blowing early diastolic decrescendo murmur so if you jump down to the bottom of this slide and look at the amplitude waveform what you'll notice is one it's diastolic and two is that not only is it diastolic but it's decrescendo so right after that s2 dub this murmur will start off loud but then it will kind of gradually taper down and that's what the decrescendo part refers to so when you have your headphones on and we'll get to that sound in a few moments you'll hear it blowing and it'll be louder right after the s2 and then kind of taper off before you hear the s1 now when you associate aortic regurgitation you want to associate it with a few things and it really depends on if we're talking about an acute aortic regurgitation or a chronic one acutely you want to think infective endocarditis but more chronically you want to think about things that alter the structural integrity of the aortic valve this should make sense if it's just an acute problem it's something temporary like an infection like infective endocarditis and ideally we would like to think about infective endocarditis as being treatable so it only causes an acute or temporary aortic regurgitation but chronically this is going to be due to the integrity of the aortic valve being lost completely usually due to some type of congenital or structure or abnormality and that's why in chronic aortic regurgitation you associate it with things like bicuspid aortic valve and some connective tissue diseases now you see this picture of an orange hammer here on the slide and the reason that i put that there is because one of the biggest buzzwords or biggest descriptions or just high-yield snippets that the test writer will give you either on usmle comlex or your in-class exams is what's known as a water hammer pulse now a water hammer pulse refers to a widened pulse pressure in aortic regurgitation and you see this thing called the water hammer pulse as a physical exam finding so what this is is that because of aortic regurgitation there is an increased stroke volume every time the left ventricle does its systolic stroke and as you could imagine with aortic regurgitation that blood flowing retrograde back through the aortic valve causes an increased end diastolic volume in the left ventricle what this means is that every time the left ventricle squeezes it's squeezing out what was previously of an increased end diastolic volume so the systolic part and the volume of blood that the left ventricle squeezes is really increased because of the aortic regurgitation now what happens is when you look at that on physical exam you see this rapid rising of the pulse right you see this rapid rising whenever the heart is squeezing out that increased end diastolic volume but the second part that makes the water hammer pulse such a unique finding is that then in the diastolic phase there's a rapid collapse so just as big as there was that pulse going up and increasing with that extra large stroke volume that's also mirrored by the rapid collapse during diastole and what's happening there in diastole is that because blood is regurgitating back from the aorta back into the left ventricle there's a very rapid what we call aortic runoff so normally that blood that diastolic pressure would not collapse as quickly but again it's aortic regurgitation guys and girls which means that there's retrograde flow so that retrograde flow happens more rapidly backwards and then in addition to that the arterial system just generally speaking empties more rapidly and this is a change over time due to some remodeling of the arterial system in the setting of aortic regurgitation but if i were to summarize the water hammer pulse what i would say is that it's due to an increased stroke volume because of an increase in end diastolic volume due to retrograde blood flow back over the aortic valve so you see a rapid upstroke of the pulse followed by a rapid collapse due to again aortic runoff where that blood flows back over the aortic valve so what i just described is a little bit long-winded but if you can imagine that and you were with me on what was happening and why stroke volume was increased but then why the diastolic section or the diastolic part was just like rapidly collapsing then you're in good shape because this is bound to show up on exams if they're pointing you in the direction of aortic regurgitation they either have to describe that that finding that i just gave you or they have to give you the murmur either visually or acoustically and you've got to pick it up now before we get to the murmur sound the there is one other somewhat high yield association clinically that i want to point out and you might see in your test question what's called head bobbing head bobbing is also known as de mousset sign um i'm probably butchering the pronunciation of the person's name but it's d e space m-u-s-s-e-t de musit or de musee and what this is is that it's just head bobbing so the de music sign is basically the the patient will be bobbing their head um which will synchronize with the beating of their heart and this was observed way back in the day which is why this is not really high yield it's just sort of an incidental thing that some patients have but because the the pulse pressure is so widened due to the aortic regurgitation patients actually feel the systolic pulse so they feel that huge excess stroke volume that's trying to squeeze out all of that blood that gets retrograde retrograded if that's a word back into the left ventricle so with every stroke there's such a high volume of blood coming out due to the regurgitation the patients actually feel it and in synchrony with that that stroke they'll bob their head and this is called demusic sign so if you're taking an exam and you see either the water hammer pulse where that you know the rapid upstroke and that rapid collapse or head bobbing the test writer is telling you yo dude hey lady it's aortic regurgitation now let's go down to the wave amplitude and listen to the sound here so again this is an early diastolic decrescendo murmur that's described as high pitched and blowing so this is what aortic regurgitation sounds like alright so as you can hear you hear the s2 dub then you hear the onset of the high pitched blowing murmur and it gets softer over time until we get back to the s1 lub and then during systole there's silence because this is a diastolic murmur so that's aortic regurgitation so here's where we are you guys are doing amazing great progress there's really only one more murmur to learn and that's mitral stenosis because patent ductus arteriosus is pretty easy so i only need your attention for a little while longer mitral stenosis is referred to as a diastolic opening snap which is followed with a delayed diastolic rumbling so if you you know look at the bottom of this slide you see in the waveform that orange highlighted line that's the opening snap and then there's sort of this decrescendo style slightly diminishing diastolic rumbling that becomes a little bit louder in the later stage of diastole just before the s1 lub but the opening snap happens after the s2 dub and then there's a little bit of a delay between s2 the dub and where you hear the opening snap now as far as associations go you want to think when it comes to mitral stenosis about rheumatic fever that's going to be the big one alternatively and less commonly on usmle and comlex you want to be on the lookout for patients with some types of rheumatological diseases so lupus and rheumatoid arthritis can also give rise to mitral stenosis but for some reason test writers love to go after the things that functionally mimic mitral stenosis so you see on this slide i've written mimickers and those include both a left atrial mixoma so that's like tumor growth in the left atrium as well as bacterial endocarditis which is due directly due to the growth of those vegetations on the mitral valve and i just want to illustrate this because this does show up so often on usmle and comlex that imagine you're looking down through the mitral valve and this is the opening that you see under normal circumstances this is the nice patent open valve where again we're looking down through into the left ventricle but in the case of bacterial endocarditis now let's imagine we have growth of bacterial vegetations because these vegetations are just chilling on the valve functionally the amount of open space that the mitral area has is now reduced so although there's technically not a mitral stenosis functionally the effect on the heart is identical there's reduced volume or reduced space through which the blood can flow from the left atrium into the left ventricle so this is functionally a mimicker of mitral stenosis likewise if we do another example imagine the growth of a tumor in the left atrium you've got this big juicy left atrial mixoma and then once again we have a reduction in the functional space available for which blood can flow through the left atrium into the left ventricle again mimicking mitral stenosis but what you really want to think about with mitral stenosis is what does it sound like and what does the waveform look like and this is another really unique murmur because of that opening snap that opening snap is so unique to mitral stenosis that it's a test favorite to just give you the audio file and force you to work backwards either directly asking you which of the following murmurs does this sound correspond to or asking you for the associations but it all would start with the audiophile so in another video i have a very high-yield buzzword high-yield mnemonics that i lay out for associating mitral stenosis with opening snap but just to use that mnemonic again here because we're obviously talking about mitral stenosis my when i think mitral stenosis i think ms and when i think ms i think os for opening snap and the mnemonic here is that the operating system is microsoft so the os equals ms the operating system equals microsoft and the os being opening snap equals ms being mitral stenosis so you absolutely need to know if you see the buzzword opening snap they're talking about mitral stenosis now i'm going to play the audio file for you now so this is what mitral stenosis sounds like all right so i hope you're able to appreciate the dub a little bit of a like a micro delay and then you hear the opening snap followed by the decrescendo and then later a little bit of crescendo delayed diastolic rumbling now what i want to do just briefly before we wrap up mitral stenosis is just talk about pathophysiology here and why you hear an opening snap because i'm a big believer in that if you understand the pathophys this topic which would otherwise just be super vague and confusing makes a lot more sense because we're putting things in the context of physiology so the reason that you hear an opening snap in mitral stenosis is that snap is the sound of the opening of the mitral valve so i want you to close your eyes and sort of imagine this as i describe it to you so the mitral valve which in this case is stenotic will open when the pressure in the left atrium exceeds the pressure in the left ventricle and when that happens it we're in ventricular diastole so in ventricular diastole the pressure within the left ventricle drops and as you should know at this stage in your medical education blood or any liquid really wants to flow from high pressure to low pressure so it wants to flow from the left atrium which is higher pressure into the left ventricle which is in ventricular diastole which is lower pressure now because the mitral valve is stenotic it's not going to open up until the pressure in the left atrium greatly exceeds the pressure in the left ventricle and because the valve is stenotic to begin with there's going to be even more pressure in the left atrium because imagine trying to squirt blood from the left atrium into the left ventricle but the lumen or the area within the mitral valve which in this case is stenotic is decreased so the circle the lumen the space through which you could push that blood is thinner and thinner and thinner so there's sort of like a backlog of pressure going into the left atrium and this is really high yield to understand because as the severity of the stenotic mitral valve gets worse or as that lumen closes up even more the pressure in the left atrium is only going to increase so when that pressure increases and it shoots open the mitral valve to pop it open and send that blood from the left atrium into the left ventricle you hear that forceful opening snap and then the reason that it's a little bit decrescendo is because once it snaps open now blood can flow and it can sort of equalize pressure for a little bit so that opening snap corresponds to the opening of the mitral valve which again happens when the increased pressure in the left atrium snaps open the mitral valve but the truth is is that if you understand pathophysiology this makes just infinitely more sense so that's mitral stenosis all right and to wrap things up last but certainly not least we have patent ductus arteriosus so i'm not going to play the sound for this one because this sound bite rarely shows up on exams usually if test writers want to go after patent ductus arteriosus they're going to do it with buzzwords descriptions and associations so patent ductus arteriosus is described as a continuous machine like murmur so because this is obviously a structural defect in the heart you could expect that the murmur is continuous it doesn't matter if the heart is in systole or diastole and for that reason if you look down at the waveform you see that the murmur which is described to sound like a machine is going to be taking place during both systole and diastole the highest yield part of patent ductus arteriosus is knowing the associations so the big high yield associations number one you want to think congenital rubella but then after that you also want to think about any infant that's born prematurely now usually but not always this will be due to either fetal alcohol syndrome or fetal heightened tone syndrome and just recall that fetal heightened tone syndrome that term it's really an umbrella term that refers to a bunch of congenital defects that happen in response to something like phenytoin use which is an anti-seizure drug so anything that causes premature infancy can cause a pda but classically on exams it's either fetal height and tone syndrome or fetal alcohol syndrome rarely it could be due to the trisomy so you want to remember that down syndrome can and other associated trisomies can also cause a pda but again no congenital rubella and know your premature congenital diseases the last thing that i'll say just to touch on it you've probably seen it a thousand times already but the treatment of a pda so it depends on if you want to keep it open or not so if you want to keep it open you would give prostaglandins because prostaglandins will keep the patent ductus arteriosus open if the infant that has the patent ductus arteriosus needs surgical correction but it can't take place yet and that would happen in situations where you have something like a hypoplastic left heart or transposition of the vessels in those situations you do want to keep it open generally until you can get the infant the surgical correction it needs but you could also close the patent ductus arteriosus and if prostaglandins keep it open then to close it you would be giving something like indomethacin which just acts exactly the opposite so for patent ductus arteriosus i kind of hinted at this when we were talking about mitral stenosis but it's kind of easy continuous machine like murmur it's the only murmur that they'll give you in the audio file that will be in both systole and diastole so for that reason i'm not going to put the file here it's pretty easy to pick up if you hear it between the lubs and the dubs and then it just keeps cycling into patent ductus arteriosus keep your eye open for congenital rubella and other premature conditions like fetal alcohol syndrome and fetal height and tone syndrome that's it this is a very very long video but it's a tough topic and it was honestly hard to collapse this into digestible bits of information but you're now an expert on splitting and heart sounds good luck