Heart Murmurs | Retired (YouTube Video Transcript)

(00:00:00) Your YouTube transcript will appear here (00:00:07) all right ninja nerds in this video (00:00:08) today we are going to be talking about (00:00:10) heart murmurs lots to talk about and if (00:00:12) you guys actually enjoy this video it (00:00:13) makes sense we have a good time together (00:00:14) please support us hit that like button (00:00:16) comment on the comment section and most (00:00:18) importantly subscribe also if you want (00:00:20) some amazing notes illustrations to (00:00:21) follow along with to enhance your (00:00:22) learning during this process go down the (00:00:24) description box below i would link to (00:00:25) our website you guys can check that (00:00:26) stuff out all right let's dig into heart (00:00:28) members (00:00:29) we talk about heart murmurs we should (00:00:30) actually but first before we start (00:00:31) actually talking about the different (00:00:32) types of heart murmurs and dive right (00:00:34) into it we got to actually start off a (00:00:35) little slow and talk about how do action (00:00:37) murmurs develop what's the physiology (00:00:39) behind murmurs right that's a simple (00:00:40) thing and it's actually relatively (00:00:42) straightforward there's a guy he was (00:00:44) involved in the physics behind things he (00:00:45) talked about something called reynolds (00:00:47) number reynolds number reynolds number (00:00:48) basically in the simplest way of (00:00:50) thinking about it reynolds number (00:00:52) which you can represent as r lowercase e (00:00:55) the higher the reynolds number (00:00:58) the more turbulent the blood flow (00:01:01) and the more turbulent the blood flow is (00:01:03) through a particular (00:01:04) channel of like an actual vessel or (00:01:06) through a particular small valve orifice (00:01:08) the more turbulent blood flow is through (00:01:09) that particular area (00:01:11) the more murmur that you'll have right (00:01:13) so the more there'll be a murmur an (00:01:15) increase in the actual (00:01:16) murmur (00:01:19) so that's really where we get these (00:01:20) actual heart murmurs is really from the (00:01:22) turbulence of blood flow so we have to (00:01:23) think about what are the things that can (00:01:24) actually increase the rental number (00:01:26) because if we increase the rental number (00:01:27) we increase the turbulence of blood flow (00:01:28) through a vessel through a valve orifice (00:01:31) to a particular area (00:01:33) and if we increase the turbulence (00:01:34) through the area you bring about a (00:01:35) murmur that we can hear what are the (00:01:37) things that increase reynolds number so (00:01:38) the things that we can increase real (00:01:40) numbers actually is going to be one (00:01:41) thing velocity (00:01:43) so whenever you have a higher velocity (00:01:45) of blood flow (00:01:46) so higher velocity of blood flow this (00:01:48) can increase reynolds number and what (00:01:51) could be reasons by which we increase (00:01:53) velocity of blood flow (00:01:55) one is that you're having the heart in (00:01:56) this case really contract hard so it can (00:01:59) be situations where you have very high (00:02:01) contractile (00:02:04) strength (00:02:06) and we'll talk about scenarios some (00:02:07) scenarios by which there's a really (00:02:08) intense high contractile strength and (00:02:10) hyperdynamic activity of the heart the (00:02:13) other thing is whenever there's small (00:02:14) diameters so decreased diameters (00:02:18) of small valve areas or small vessels (00:02:21) where you have to squeeze a ton of (00:02:23) little blood through the smaller the (00:02:25) diameter the higher the velocity of (00:02:26) blood flow through that particular area (00:02:28) so these would be particular things that (00:02:30) will increase the (00:02:32) velocity and increase the reynolds (00:02:34) number and if you increase the rental (00:02:35) number you increase the turbulent blood (00:02:37) flow and cause murmurs all right that's (00:02:38) one thing (00:02:39) the second thing (00:02:41) that we actually have to talk about is (00:02:42) viscosity so viscosity (00:02:45) so viscosity is actually interesting (00:02:47) because it's inversely proportional to (00:02:48) reynolds number so in other words if we (00:02:50) want to increase reynolds number we (00:02:52) would need a lower viscosity so lower (00:02:54) viscosity of blood meaning there's less (00:02:57) particular formed elements like red (00:02:58) blood cells and platelets and things (00:02:59) like that if there's less red blood (00:03:01) cells which are the main component of (00:03:02) our blood one of the main components (00:03:04) there's less red blood cells there's (00:03:05) more of the plasma to run around there's (00:03:07) more of an opportunity for turbulence of (00:03:09) blood flow there's more space for blood (00:03:10) to actually flow (00:03:12) and so decreasing the viscosity (00:03:14) definitely will increase the reynolds (00:03:16) number increase the turbulence and (00:03:17) precipitate murmurs what are situations (00:03:20) by which the blood viscosity is low (00:03:22) anemia and we'll talk about that (00:03:24) the next thing that i want you guys to (00:03:25) remember is that there's actually (00:03:26) something that's not dependent upon (00:03:28) reynolds number has nothing to do with (00:03:29) it and it's actually when there is blood (00:03:32) flow so there's one as an increased (00:03:33) velocity decreased viscosity for (00:03:35) reynolds number this last situation has (00:03:37) nothing to do with reynolds number it's (00:03:39) actually blood flow (00:03:43) across (00:03:46) an incompetent valve (00:03:50) whenever blood flows across an (00:03:52) incompetent valve it creates a (00:03:54) significant turbulence of blood flow (00:03:56) enough to be able to precipitate a (00:03:58) murmur and that's the big things i want (00:04:00) you to remember so there's an increase (00:04:01) in velocity a decrease in viscosity or (00:04:04) there is something that has nothing to (00:04:06) do with reynolds number which is blood (00:04:07) flow across an incompetent valve let's (00:04:09) talk about the things that can actually (00:04:10) cause this because then we can (00:04:11) understand the physiology (00:04:12) so let's actually talk about the first (00:04:14) category which is velocity but (00:04:16) particularly those things that increase (00:04:18) velocity with respect to diameter so (00:04:20) small diameter (00:04:23) you know channels small diameter valves (00:04:26) all of these situations (00:04:28) one particular situation is (00:04:31) you know there's a condition called a (00:04:32) ventricular septal defect ventricular (00:04:34) septal defects are really interesting so (00:04:36) ventricular septal defects whenever your (00:04:37) left ventricle it's a higher pressure (00:04:39) system when it contracts it's going to (00:04:41) want to push blood from areas of high (00:04:42) pressure to low pressure so normally it (00:04:44) would want to go into the aorta (00:04:46) but there's also this channel here the (00:04:48) septal defect by which blood can jet (00:04:50) across into the right ventricle right (00:04:53) that's one particular thing (00:04:55) this is called a ventricular septal (00:04:56) defect now here's why i want to mention (00:04:59) this because it has something to do with (00:05:00) the intensity of the murmur (00:05:02) the smaller the diameter so the smaller (00:05:06) the vsd (00:05:08) that would mean that the smaller the (00:05:09) diameter of the ventricular septal (00:05:11) defect the smaller the diameter the (00:05:14) higher the (00:05:15) velocity so this would cause a higher (00:05:18) velocity (00:05:19) and the higher the velocity the more (00:05:21) turbulent the blood flow the more (00:05:22) turbulent the blood flow the higher (00:05:24) intensity the murmur (00:05:27) that is one of the big things to (00:05:28) remember and it's very interesting (00:05:30) because oftentimes when we think about (00:05:31) ventricular septal defects we would (00:05:32) think oh the bigger the septal defect (00:05:34) the worse the murmur it's actually (00:05:36) opposite the smaller the defect the (00:05:39) smaller diameter the higher the actual (00:05:42) pressure gradient across these (00:05:44) and the higher the velocity across that (00:05:46) area it's going to intensify the (00:05:47) turbulence of blood flow and increase (00:05:48) the intensity of the murmur so don't (00:05:50) forget that (00:05:51) okay so vsds particularly smaller vsds (00:05:54) that's one particular reason that can (00:05:55) cause turbulence and blood flow here's (00:05:57) another one (00:05:58) another one it's called a coartation of (00:06:00) the order so we're going to put (00:06:01) coarctation of the aorta you know (00:06:04) causation of the order is when there's (00:06:05) kind of this narrowing of the aorta (00:06:07) usually there's different parts it could (00:06:08) be before the left subclavian vein after (00:06:10) i'm sorry before the left subclavian (00:06:12) artery or after the left subclavian (00:06:14) artery we're not going to get too much (00:06:15) into that there's just a narrowing of (00:06:16) the aorta (00:06:18) if there's a narrowing of the order (00:06:19) whenever blood flows from the left (00:06:20) ventricle into the aorta now it has to (00:06:22) squeeze through that tiny little (00:06:24) diameter portion of the aorta that's a (00:06:26) small diameter that small diameter is (00:06:29) going to increase the velocity so (00:06:31) there's going to be a high velocity due (00:06:33) to the small diameter and that's going (00:06:35) to cause an increase in the turbulence (00:06:37) of blood flow and increase the murmur (00:06:39) that's another big thing all right what (00:06:40) about another one what if i have (00:06:42) somebody who has (00:06:44) aortic stenosis or they have another (00:06:46) situation here um (00:06:47) you know particularly if i have aortic (00:06:49) stenosis or if i have this big old thing (00:06:52) here that's kind of intruding off the (00:06:54) septum (00:06:55) you know if somebody has aortic stenosis (00:06:57) one of the things that you have a small (00:06:59) diameter opening here that i got to (00:07:00) squeeze all that blood through that (00:07:02) small diameter is going to cause you're (00:07:04) going to have to work really hard and (00:07:05) push a lot of blood across that area and (00:07:07) whenever there's such a small diameter (00:07:09) there's a high velocity right so high (00:07:10) velocity (00:07:11) and that's going to increase the murmur (00:07:16) the other situation is what if i have (00:07:18) this big old septum so you have an (00:07:20) asymmetric hypertrophy of the (00:07:22) interventricular septum and now i gotta (00:07:24) squeeze blood flow from the left (00:07:25) ventricle through this tiny little area (00:07:27) here up into the aorta (00:07:29) that's a small diameter so in conditions (00:07:31) such as hypertrophic obstructive (00:07:33) cardiomyopathy (00:07:34) there is a (00:07:35) very small diameter and that can (00:07:38) increase the velocity wherever that (00:07:39) small diameter is and increase the (00:07:42) turbulence of blood flow precipitating a (00:07:43) murmur so these are the particular (00:07:45) mechanisms behind which these murmurs (00:07:47) actually occur (00:07:48) so we have an increase in velocity due (00:07:51) to a (00:07:52) decrease in the diameter of the vessel (00:07:54) the valve (00:07:56) the particular orifice by which blood is (00:07:58) flowing through now when we talk about (00:07:59) viscosity right which is the thickness (00:08:01) of blood flow think about pushing (00:08:03) molasses versus pushing water right (00:08:06) molasses is going to flow really slow (00:08:08) right so if it's really slow that's not (00:08:10) going to give you a lot of turbulence of (00:08:11) blood flow but if you have kind of a (00:08:13) thinner type of substance that you're (00:08:14) moving through a vessel or through a (00:08:15) channel or through an orifice it's (00:08:17) definitely going to give you more flow (00:08:18) more rapidity of the flow more (00:08:20) turbulence of the blood flow it's a (00:08:21) simple concept right so what we want to (00:08:22) think about is when there is a reduction (00:08:24) in the viscosity so something that's (00:08:26) going to make the blood a little bit (00:08:27) more watery not have as much components (00:08:29) or solutes to it that are going to make (00:08:31) it more thick and sticky in that (00:08:33) situation the things that would actually (00:08:34) decrease the viscosity you'd want to (00:08:36) remember as anemia (00:08:38) okay and again it's a pretty (00:08:39) straightforward concept that as we (00:08:41) think about from what we've established (00:08:43) from the relationship below a decrease (00:08:44) in viscosity is going to increase the (00:08:46) turbulence of blood flow so decreased (00:08:48) viscosity (00:08:49) will do what to the actual turbulence (00:08:51) it'll increase the turbulence and i just (00:08:53) think about that example of pushing like (00:08:54) something like water versus like (00:08:56) molasses through a small channel which (00:08:57) one's gonna move faster the watery (00:08:59) substance that's one thing the next (00:09:01) thing is let's go back to the velocity (00:09:03) really quick so velocity now we said it (00:09:06) could be due to a small diameter which (00:09:07) i'm not going to push a ton of things (00:09:09) through (00:09:10) or it could be something that's really (00:09:11) kind of like i'm generating a lot of (00:09:12) force (00:09:13) so if the the actual (00:09:15) the the origin of where all the blood is (00:09:17) coming from if the strength by which (00:09:19) that origin is contracting and pushing (00:09:21) the blood through that higher force is (00:09:23) going to have higher velocity through (00:09:24) those channels and orifices and small (00:09:26) areas (00:09:27) so i have to think about things that (00:09:28) will increase the contractility of the (00:09:31) heart (00:09:33) anything that increase the contractility (00:09:34) of the heart is going to increase the (00:09:37) force by which we're going to push blood (00:09:39) and that will definitely increase the (00:09:40) velocity (00:09:42) of blood through these different types (00:09:44) of channels that'll increase the (00:09:46) turbulence and as you increase the (00:09:47) turbulence of blood flow through these (00:09:49) channels or through these orifices or (00:09:50) through these particular areas that will (00:09:52) definitely give you (00:09:54) these murmurs (00:09:56) so the question that we have to ask is (00:09:57) what are the things that can increase (00:09:58) the contractility of the heart let's (00:09:59) come down and think about this things (00:10:01) that would increase the contractility of (00:10:03) the heart what would that be due to well (00:10:06) we got to think about this what would (00:10:07) cause the heart to just clang in a (00:10:08) banging and every you know going crazy (00:10:10) and pushing hard hard hard amounts of (00:10:12) blood out of the left ventricle so left (00:10:14) ventricular is just slanging it's (00:10:15) banging and it's pushing this blood out (00:10:18) of (00:10:19) the heart into the aorta okay when this (00:10:22) happens we need situations where there (00:10:24) is a hyperdynamic heart (00:10:26) what are the situations by which we can (00:10:28) have a hyperdynamic heart where it is (00:10:29) just really pumping hard (00:10:31) these would be things that are driving (00:10:33) the sympathetic nervous system of the (00:10:34) heart so things that are increasing the (00:10:36) sympathetic nervous system of the heart (00:10:38) this could be due to (00:10:40) exercise (00:10:42) this could be due to fever (00:10:45) this could be due to sepsis (00:10:48) you know what else it could be due to (00:10:50) certain situations where there's an (00:10:51) increase in the amount of thyroid (00:10:53) hormone increased levels of t3 and t4 (00:10:55) such as in thyrotoxicosis (00:10:58) you know what else it could be due to it (00:10:59) could also be in situations where (00:11:01) there's higher volume states (00:11:04) where you're having more volume more (00:11:06) preload more preload the hearts (00:11:07) contracting harder this could be a (00:11:09) situation such as pregnancy (00:11:12) and another thing is anemia anemia can (00:11:14) actually cause (00:11:16) higher contractile states there's other (00:11:18) things that can cause high outflow (00:11:19) states so high outflow states high (00:11:22) outflow states (00:11:24) could be things like these are a little (00:11:26) bit more uncommon but anemia (00:11:29) berry berry which is actually going to (00:11:30) be due to a thymine deficiency or av (00:11:33) fistulas these actually generate higher (00:11:35) outflow states your heart is not work (00:11:36) harder to keep pumping blood out into (00:11:39) the circulation so these are some of the (00:11:41) things there's a lot of things that can (00:11:42) create these hyperdynamic hearts which (00:11:44) increases the contractility and causes (00:11:47) higher amounts of velocity more blood (00:11:50) flowing through these channels through (00:11:51) the valves that's going to create (00:11:53) particular turbulence and murmurs these (00:11:55) are things to think about (00:11:57) okay (00:11:58) last but not least is going to be (00:12:00) something by which we said has nothing (00:12:02) to do with reynolds number it's actually (00:12:04) more particularly it's kind of an (00:12:06) isolated entity and this is going to be (00:12:08) when there is blood flow (00:12:11) across (00:12:13) incompetent valves (00:12:16) what kind of situation by which you (00:12:18) would have these incompetent valves (00:12:19) meaning that they're not providing a (00:12:21) good flow (00:12:22) it's pretty straightforward right let's (00:12:24) say here is your aortic valve it's not (00:12:26) doing a good job being able to prevent (00:12:27) backflow into the (00:12:29) aorta what is that called oh man these (00:12:31) are pretty easy right aortic (00:12:33) regurgitation you have this valve here (00:12:35) in the pulmonary valve it's supposed to (00:12:36) prevent backflow it doesn't this is (00:12:38) called (00:12:39) pulmonic regurgitation you're supposed (00:12:41) to have this valve here which is (00:12:42) supposed to prevent backflow into the (00:12:43) atria it doesn't this is called mitral (00:12:45) regurgitation and then last but not (00:12:47) least this valve is supposed to provide (00:12:49) prevent backflow into the right atrium (00:12:51) this is called tricuspid regurgitation (00:12:54) so any of these situations by which (00:12:55) there is blood flow across incompetent (00:12:57) valves really kind of puts you in a (00:12:58) category of any regurgitation murmur (00:13:02) because that will actually push blood (00:13:03) back into so for example think about (00:13:06) blood coming back into the pulmonary (00:13:08) from the pulmonary trunk into the right (00:13:10) ventricle when it flows across it's (00:13:12) going to bounce off the walls here and (00:13:14) produce turbulence (00:13:16) that is a turbulence of blood flow right (00:13:18) it has nothing to do with the things (00:13:19) that actually affect reynolds number (00:13:21) it's just there's going to be turbulence (00:13:23) of blood flow and that's because (00:13:24) whenever the blood is back flowing (00:13:26) whether it be from the pulmonary artery (00:13:28) into the right ventricle aorta into the (00:13:30) left ventricle it's going to bounce off (00:13:31) the walls and create a turbulence of (00:13:33) blood flow so that is the concept here (00:13:35) it's going to hit off these walls and (00:13:36) produce this turbulence that's going to (00:13:37) give you a (00:13:38) sound and that sound is going to be a (00:13:40) murmur so that's the big things to think (00:13:41) about all right we don't talked about (00:13:43) the physiology of murmurs which again (00:13:46) all comes down to the turbulence of (00:13:48) blood flow which is dependent upon the (00:13:49) reynolds number and those situations we (00:13:51) said increased velocity from (00:13:52) hyperdynamic states or from small (00:13:54) diameter orifices or channels will (00:13:57) increase the turbulence via the reynolds (00:13:59) number (00:14:00) or a decrease in viscosity will cause (00:14:02) the blood flow to move faster increasing (00:14:04) the turbulence and last but not least (00:14:06) something has nothing to do with the (00:14:07) reynolds number but whenever there's (00:14:08) blood flow crossing a competent valve (00:14:10) back into a chamber and the blood is (00:14:12) bouncing off the walls of those chambers (00:14:14) it creates a turbulence of blood flow (00:14:16) and precipitates murmurs we now (00:14:17) understand that let's go and talk about (00:14:19) some characteristics that we need to (00:14:21) understand about murmurs now all right (00:14:23) so let's talk about now the next thing (00:14:25) there's a lot of things up on the border (00:14:26) like oh my gosh there's like a million (00:14:27) things that we have to go over don't (00:14:28) worry it's i'm gonna make it really (00:14:30) simple because when we talk about (00:14:31) murmurs we have to come up with a system (00:14:34) to be able to remember a lot of these (00:14:35) it's difficult i'm not going to lie with (00:14:37) you i have difficulty in being able to (00:14:39) remember (00:14:39) all the different terms and buzzwords (00:14:42) that we have to be able to utilize for (00:14:44) our exams but i think i came up with a (00:14:46) good way for you guys to easily (00:14:47) categorize these in your head and (00:14:49) remember them so what i want to do now (00:14:51) is i want to talk about a couple things (00:14:53) all in one area here so i want to talk (00:14:55) about when we're talking about murmurs (00:14:57) we understand the physiology behind them (00:14:58) i want us to know now (00:15:00) where if i have someone who has aortic (00:15:02) stenosis aortic regurgitation yada yada (00:15:04) where am i listening on the chest that's (00:15:07) the first thing so location (00:15:09) second thing i want us to talk about is (00:15:11) that some murmurs it is super important (00:15:13) it helps you to differentiate from other (00:15:15) ones based upon where the murmur (00:15:17) radiates which is dependent upon the the (00:15:19) path of which the blood is flowing we'll (00:15:21) talk about that (00:15:22) then after we talk about that we'll go (00:15:24) over the quality there's particular (00:15:26) buzzword terms that we utilize to (00:15:27) describe a type of murmur is it blowing (00:15:30) is it machine like is it harsh or (00:15:33) rumbling so on and so forth (00:15:35) then we'll get into pitch so pitch is (00:15:37) important because it determines if we (00:15:39) listen with the bell of our stethoscope (00:15:41) or the diaphragm of our stethoscope and (00:15:43) we'll talk about that and then lastly (00:15:45) we'll talk about the intensity grading (00:15:46) the murmur because that's going to have (00:15:48) a clinical correlation (00:15:50) associated with it a little tidbit that (00:15:51) i want to teach you guys something is (00:15:52) very interesting all right so let's go (00:15:54) through that (00:15:54) location easy way to remember location (00:15:57) is the step-by-step process we're going (00:15:59) to go in this order all physicians earn (00:16:01) too much so aortic valve this is going (00:16:04) to be you come down and you listen at (00:16:06) the right second intercostal space (00:16:08) parasternal border so there's our first (00:16:10) rib second rib third rib so it has to be (00:16:13) right here second intercostal space so (00:16:15) again aortic valve will be at the right (00:16:18) second (00:16:19) intercostal space parasternal border (00:16:22) now the next one is the pulmonic valve (00:16:24) the pulmonic valve is (00:16:27) the left second intercostal space pretty (00:16:28) straightforward right so here we have (00:16:30) our left (00:16:31) second intercostal space and this is (00:16:33) going to be para (00:16:36) border boom we're nailing these herbs (00:16:39) point what the heck is herb's point (00:16:40) don't worry we'll talk about what herb's (00:16:42) point is a little bit later in these (00:16:43) we'll talk about why we're listening at (00:16:45) these areas and what we should be (00:16:45) listening for and types of murmurs that (00:16:47) could be present in just a second but (00:16:49) herb's point just come down one more so (00:16:51) now we're at the left third intercostal (00:16:53) space we're at the left (00:16:55) third (00:16:56) enter costal space parasternal border (00:16:59) then you come down again one more (00:17:00) tricuspid valve so tricuspid valve is (00:17:03) left fourth intercostal space (00:17:05) parasternal border (00:17:07) man this is not too bad right guys (00:17:09) and then mitral valve you would think oh (00:17:12) we come down one more no got to trick (00:17:13) you up a little bit here we do go down (00:17:15) to the fifth intercostal space but we (00:17:16) don't go parasternal border we go at the (00:17:18) midline level of the clavicle so i'm (00:17:20) going to drag this down here (00:17:22) about right here (00:17:24) that is going to be where i listen at (00:17:25) the mitral valve so i go left fifth (00:17:28) intercostal space definitely but it is (00:17:30) not parasternal border now it's at the (00:17:32) level of the mid clavicular line all of (00:17:34) these above were at the parasternal (00:17:36) border that's a simple way to remember (00:17:38) it now why do i want to remember that (00:17:40) here's why (00:17:42) if you're listening at the aortic valve (00:17:44) you're listening for things such as (00:17:46) aortic stenosis aortic regurgitation and (00:17:49) then also a co-arctic aorta all of these (00:17:51) are types of murmurs that you want to be (00:17:53) listening for so that's where you'll be (00:17:55) listening you'll hear the best types of (00:17:56) murmurs particularly aortic stenosis (00:17:58) they were to griegourgen corrected aorta (00:17:59) at the right second intercostal space (00:18:02) boom (00:18:03) what about pulmonic you guys are going (00:18:04) to be like oh this is he's so easy man (00:18:07) this would be pulmonic stenosis pulmonic (00:18:09) regurgitation and if you wanted to take (00:18:11) it to the next level we're not going to (00:18:12) talk about this in this lecture but asds (00:18:15) can also be heard in this area atrial (00:18:16) septal defects (00:18:18) all right herb's point you're like dude (00:18:19) i've never even heard of this bro don't (00:18:21) worry this is probably the most common (00:18:23) area that most people listen to they go (00:18:24) to this area they listen because it's a (00:18:26) good overview area that's what i want (00:18:28) you to remember herbs point as it's kind (00:18:29) of called the cardiology point because (00:18:31) what we do is we take the stethoscope (00:18:32) and i can hear almost everything i need (00:18:34) here in that one point and so it's good (00:18:35) for being able to tell me your s1 and s2 (00:18:38) i should be able to hear both s1 and s2 (00:18:40) in this area and it gives me a bunch of (00:18:42) different members the one that i really (00:18:44) want you guys to think about though (00:18:45) that's pretty good in this area is (00:18:46) hypertrophic obstructive cardiomyopathy (00:18:49) so this is actually one that i would be (00:18:50) listening for for hypertrophic (00:18:52) obstructive cardiomyopathy (00:18:54) okay tricuspid valve if i'm listening in (00:18:56) this area what kind of murmurs son of a (00:18:58) gun what should i be looking for (00:19:00) obviously tricuspid stenosis is an (00:19:01) obvious one right so i want to listen (00:19:03) for tricuspid stenosis i want to listen (00:19:06) for tricuspid regurgitation and there's (00:19:08) one more (00:19:09) the vsd (00:19:11) the ventricular septal defect (00:19:13) and then last but not least the mitral (00:19:16) valve at the left fifth intercostal i'm (00:19:18) listening for mitral stenosis mitral (00:19:20) regurgitation and one more called mitral (00:19:22) valve prolapse that's why it's so easy (00:19:25) once you identify the location (00:19:27) we'll go through all the different (00:19:28) things that helps to distinguish all (00:19:29) these different murmurs but we know the (00:19:31) locations now that's a good thing right (00:19:33) so we know the physiology we know the (00:19:34) locations (00:19:36) and they're actually relatively simple (00:19:38) the only ones that are a little bit (00:19:39) funky is the asd the hypertrophic (00:19:41) obstructive cardiomyopathy and the vsd (00:19:43) all the rest of them make sense so (00:19:45) that's it radiation (00:19:48) radiation is when you have this murmur (00:19:51) you want to think about the type of (00:19:52) murmur it is and you'll it'll all kind (00:19:54) of come together throughout the process (00:19:56) of this lecture but think about the path (00:19:58) by which that blood is flowing within (00:20:00) that murmur (00:20:01) so there's three that i really really (00:20:03) actually want you guys to remember that (00:20:05) are most important (00:20:07) this is (00:20:08) first one aortic stenosis (00:20:12) aortic regurgitation (00:20:14) and then we'll talk about another one (00:20:16) here in just a second which is called (00:20:18) mitral regurgitation these are the ones (00:20:21) that i want you guys to definitely (00:20:22) remember the radiation for because it's (00:20:24) helpful (00:20:25) aortic stenosis the whole process behind (00:20:28) aortic stenosis is there is a reduction (00:20:30) in forward flow the blood is trying to (00:20:32) go from the left ventricle (00:20:34) into the aorta right and then from the (00:20:36) aorta it would obviously follow up (00:20:37) through the carotids and the arms down (00:20:39) the lower extremities right (00:20:41) but the problem is when you're pushing (00:20:43) blood out it's a difficulty in getting (00:20:46) blood out of the heart so we would hear (00:20:49) this where you would hear it at the (00:20:52) right upper sternal border so right (00:20:54) second (00:20:55) intercostal space (00:20:58) so that's where you would hear it but (00:20:59) then when you're actually listening for (00:21:01) the murmur it's a problem where there's (00:21:02) an issue with forward flow (00:21:04) this would radiate though if you think (00:21:06) about the path of blood where it's (00:21:08) moving it is moving forward just very (00:21:10) reduced it's going to go up through your (00:21:13) carotids (00:21:14) so it's going to radiate to the carotid (00:21:17) that's a pretty straightforward one (00:21:18) right so it radiates to the (00:21:21) carotids and we'll put r for radiation (00:21:24) okay aortic regurgitation (00:21:27) and aortic regurgitation as blood is (00:21:29) flowing so let's do this in kind of a (00:21:30) different color here blood is back (00:21:33) flowing from the (00:21:35) aorta (00:21:36) down (00:21:38) into the left ventricle (00:21:39) okay it's coming backwards into the left (00:21:42) ventricle (00:21:44) think about this where do we hear this (00:21:45) we hear it at the right (00:21:47) second intercostal space we've already (00:21:49) established this (00:21:50) but when it radiates it's coming in the (00:21:52) direction of the flow so here think (00:21:54) about this you have the right secondary (00:21:57) cosplace here you're listening to the (00:21:58) aortic valve when blood is back flowing (00:22:00) it's back flowing this way (00:22:03) towards the left ventricle that's going (00:22:04) towards the left upper sternal border so (00:22:07) it's going to radiate to the left upper (00:22:10) sternal border we say maybe it's going (00:22:12) to be like the pulmonic valve area or (00:22:14) the herbs point area those are generally (00:22:17) where we're going to potentially hear it (00:22:18) so that's pretty cool right so the (00:22:20) aortic regurgitation murmur is you're (00:22:22) going to have it sounding at the right (00:22:24) secondary cost space but it will (00:22:26) actually radiate in the direction by (00:22:27) which it's flowing which is back into (00:22:29) the left ventricle which is the left (00:22:30) side of the heart left left sternal (00:22:32) border so that's important to want to (00:22:34) remember here radiation (00:22:35) all right mitral regurgitation this is a (00:22:38) problem where blood is supposed to be (00:22:39) going from the left ventricle up into (00:22:41) the aorta but it's not it's back flowing (00:22:43) into the (00:22:44) atria (00:22:45) so we would hear this where you would (00:22:47) hear this at the left fifth (00:22:49) intercostal space (00:22:51) mid clavicular line (00:22:53) but when it radiates think about this (00:22:55) so you're listening here for the actual (00:22:58) mitral regurgitation when you listen (00:23:00) there it's going to be pumping backwards (00:23:03) like it's actually going to be going (00:23:04) this way all right pumping back into the (00:23:06) left atrium so imagine left ventricle (00:23:07) here left atrial here it's going to be (00:23:09) pumping this way (00:23:10) that's going into the axilla (00:23:13) and so if it's pumping backwards into (00:23:15) the axle there'll be radiation of that (00:23:17) murmur into the axilla (00:23:20) that's not so bad right so these are the (00:23:22) ones that i don't want you to forget (00:23:24) don't forget mitral regurgitation (00:23:27) radiates to the axilla don't forget (00:23:29) aortic regurgitation radiates to the (00:23:31) left (00:23:32) sternal border and aortic stenosis (00:23:34) radiates to the (00:23:36) carotids (00:23:37) boom shakalaka we good (00:23:39) okay (00:23:40) quality (00:23:42) quality is a way that it's an annoying (00:23:44) one i think it's not like super (00:23:46) important but it's more of like a (00:23:47) memorization point unfortunately when we (00:23:49) talk about quality (00:23:51) it's a way that whenever they present (00:23:52) these in the clinical vignettes (00:23:54) that they may use a very specific (00:23:56) buzzword term they may use the term (00:23:58) called blowing or a (00:24:01) harsh type of sound or a rumbling type (00:24:03) of sound and so when you are a musical (00:24:06) or machine-like and those all have (00:24:08) particular patho-mnemonic types of (00:24:10) situations meaning that you hear that (00:24:11) term you think about this disease and so (00:24:13) we'll write these down so that you can (00:24:14) remember them in case they pop up that (00:24:16) may help you to think about the type of (00:24:17) murmur it is so quality wise it's (00:24:20) telling me the characteristics of the (00:24:21) murmur so the first one that i want you (00:24:23) guys to remember here (00:24:25) is going to be if you hear something (00:24:27) called a blowing (00:24:29) murmur or we also hear the term (00:24:31) sometimes musical so blowing or musical (00:24:35) you want to think about the term aortic (00:24:37) regurgitation or mitral regurgitation (00:24:40) because blowing murmurs are usually (00:24:42) regurgitation murmurs musical murmurs (00:24:45) are usually regurgitation members that's (00:24:47) the big thing to think about (00:24:48) the next one here (00:24:50) is if a patient has (00:24:52) what's called a harsh or rumbling type (00:24:55) of murmur so you hear that term harsh (00:24:58) or rumble (00:25:00) type of murmur this is particularly (00:25:03) indicative of aortic stenosis (00:25:06) and mitral stenosis (00:25:07) okay it's particularly indicative of (00:25:09) aortic stenosis and mitral stenosis (00:25:11) don't forget that so again you hear (00:25:13) blowing or musical (00:25:15) you think aortic regurgitation might (00:25:17) regurgitation you hear harsh or rumbling (00:25:19) type of murmur you think aortic stenosis (00:25:21) and mitral stenosis they correlate that (00:25:22) also with the location (00:25:24) and correlate that also with the (00:25:26) radiation of the murmur it's going to be (00:25:27) relatively easy right we're getting (00:25:29) there (00:25:30) the next one which is the one that you (00:25:32) definitely don't want to forget because (00:25:33) this will definitely be one that they (00:25:34) present in your pediatric types of mcqs (00:25:37) is that if you hear the term machine (00:25:39) like (00:25:40) so machinery or machine type of murmur (00:25:44) this is automatically patho mnemonic for (00:25:47) patent ductus arteriosus which is a hole (00:25:50) that exists between (00:25:52) you know there's where there's a (00:25:53) shunting of blood flow from the aorta (00:25:55) into the pulmonary artery throughout (00:25:57) sicily and diastole and it sounds like a (00:25:58) machine that's going off (00:26:01) these are very important qualities of (00:26:03) murmurs that we have to understand so we (00:26:04) got the location we got the important (00:26:06) radiation points and we got the (00:26:08) important qualities of the murmurs that (00:26:09) are very important all right so let's (00:26:11) talk about pitch so when we talk about (00:26:12) pitch we're talking about kind of like (00:26:14) this is going to determine whether we (00:26:15) listen with the bell of our stethoscope (00:26:17) or the diaphragm or stethoscope that's (00:26:18) kind of the big thing behind this so (00:26:20) when we talk about pitch i'll think (00:26:21) about a couple scenarios here and what (00:26:22) pitch actually really comes along with (00:26:24) it actually depends upon pressure (00:26:25) gradients and volume of flow across a (00:26:28) particular structure when we talk about (00:26:30) this first one let's talk about a vsd i (00:26:31) think this is a really good example to (00:26:32) start off with a vsd is a very important (00:26:36) one because when you think about the (00:26:37) flow it's going from the left ventricle (00:26:39) over to the right ventricle right that's (00:26:42) kind of the whole concept it's a high (00:26:43) pressure gradient there's a high (00:26:45) pressure (00:26:46) gradient (00:26:48) so when there's high pressure gradients (00:26:50) that are existing (00:26:52) this actually is going to give you a (00:26:53) very high pitch so whenever there's high (00:26:56) pressure gradient this gives you high (00:26:58) pitches (00:27:00) type of murmur (00:27:02) and high pitch murmurs are best heard (00:27:04) with the (00:27:05) diaphragm (00:27:07) of the stethoscope (00:27:10) so that is a big thing to remember (00:27:12) now this would be better right high (00:27:14) pressure gradients again you're thinking (00:27:15) about high pressure gradients this could (00:27:17) be with any kind of scenario but i think (00:27:18) a really good one to think about here is (00:27:20) ventricular septal defects so (00:27:21) ventricular septal defects there's a (00:27:23) high pressure gradient from the left (00:27:24) ventricle to the right ventricle but in (00:27:25) any kind of scenario where that kind of (00:27:27) pressure gradient exists where there's (00:27:29) not a large volume of flow across it (00:27:31) okay so it's high pressure gradients (00:27:33) with not a large volume because you have (00:27:35) a small septal defect not a large volume (00:27:36) of blood is going to be flowing across (00:27:38) the area so it's primarily the high (00:27:39) pressure gradient and not a large volume (00:27:42) of flow this is a perfect example in (00:27:44) those situations that give you high (00:27:45) pitches (00:27:47) okay best heard with the diaphragm of (00:27:48) the stethoscope (00:27:50) let's pick another example another (00:27:52) scenario here where you're going to (00:27:53) think about is let's say that you have (00:27:55) somebody who has (00:27:56) um mitral stenosis they got a really (00:27:58) really stenotic valve right so let's (00:28:00) pick an example here of mitral (00:28:02) stenosis (00:28:04) in mitral stenosis (00:28:07) they had this really really stenotic (00:28:09) valve and what happens is your left (00:28:11) atria is trying to increase the pressure (00:28:14) to push the blood from the atrium into (00:28:15) the ventricles right during diastole (00:28:18) but here's the thing the left atrium is (00:28:20) not a super high pressure system it's (00:28:22) going to try to increase its pressure to (00:28:23) push the blood down but when you're (00:28:25) going from an area of the left atrium (00:28:27) into the left ventricle in general the (00:28:29) pressure that you're going to be able to (00:28:30) generate (00:28:31) in this direction isn't going to be (00:28:33) super high (00:28:34) so we consider this direction by which (00:28:36) the flow and a murmur is actually being (00:28:38) precipitated we consider this to be a (00:28:40) low (00:28:41) pressure gradient it's just not a high (00:28:42) pressure system going from atrium to (00:28:44) ventricles in general are a low pressure (00:28:46) gradient (00:28:48) that's pretty common no matter what (00:28:49) right that should make sense when you go (00:28:51) from the atria (00:28:53) to the ventricles (00:28:54) that's not a super high pressure (00:28:56) gradient now when you go from the (00:28:57) ventricles into the aorta from the (00:28:59) ventricles into the (00:29:00) pulmonary artery those are high pressure (00:29:02) gradients but going from the atrium to (00:29:04) the ventricles are not high pressure (00:29:05) gradients they're lower (00:29:06) however (00:29:08) what we are trying to do though is the (00:29:10) left atrial pressure will try to (00:29:11) increase a little bit (00:29:13) and increase the flow across that valve (00:29:15) so we are going to try to increase the (00:29:17) blood flow (00:29:19) across that valve the best that we can (00:29:23) and so whenever there is a low pressure (00:29:25) gradient in combination (00:29:27) with a high amount of blood flow across (00:29:29) that valve because the left atrium is (00:29:31) trying to increase this pressure to push (00:29:32) the blood across that valve (00:29:34) this combination will give you a (00:29:38) lower pitch (00:29:40) okay so this is going to be a low pitch (00:29:43) because there's a low pressure gradient (00:29:45) and again you're trying to get blood (00:29:46) flow across that valve but it's just not (00:29:48) enough (00:29:49) in this situation this is best heard (00:29:51) with the (00:29:52) bell (00:29:53) of the (00:29:55) stethoscope (00:29:57) so don't forget that so when there is (00:30:00) high pressure gradients you hear it (00:30:02) better with the diaphragm because it's (00:30:04) going to give you a high pitch (00:30:05) if it's a low pressure gradient even (00:30:07) though there is trying to be more blood (00:30:09) that's flowing across that valve by the (00:30:11) left atrial pressure increasing it's (00:30:13) still going to be low pitch and that's (00:30:14) best heard with the bell of the (00:30:16) stethoscope the last scenario (00:30:19) is in someone who has something called (00:30:22) aortic stenosis (00:30:24) in aortic stenosis (00:30:28) in this situation (00:30:31) you have the left ventricle trying to (00:30:33) pump blood into the aorta across this (00:30:36) stenotic valve (00:30:38) if that's the case the left ventricle (00:30:40) whenever it generates pressures to push (00:30:41) into the aorta that's a high pressure (00:30:44) system so that system when you're having (00:30:46) aortic stenosis you're going to have (00:30:47) high (00:30:48) pressure gradients super high pressure (00:30:50) gradients (00:30:54) on top of that think about all the blood (00:30:56) flow that's moving across that valve (00:30:58) you're going to have to generate a lot (00:30:59) of pressure left ventricle is going to (00:31:00) have to generate a lot of pressure (00:31:02) increases pressure more than usual to (00:31:04) push as much blood flow as it can across (00:31:06) that valve and so there'll also be a (00:31:08) very large blood flow (00:31:11) across the valve (00:31:14) in that situation the combination of (00:31:16) high pressure and high blood flow is (00:31:19) going to really really increase the (00:31:21) pitch (00:31:22) to the point where we consider this to (00:31:24) be more of a harsh (00:31:26) terminology we call it harsh again going (00:31:28) back to the aortic stenosis (00:31:30) in those situations this is again best (00:31:33) heard with the (00:31:35) diaphragm (00:31:39) of the stethoscope (00:31:42) okay (00:31:43) that is an important thing to remember (00:31:45) you may also see this in another (00:31:46) situation not just aortic stenosis but (00:31:48) what if the left ventricle is pumping (00:31:49) tons of blood and a high pressure system (00:31:52) high pressure system from the left (00:31:53) ventricle to left atrium (00:31:54) in that situation that's a high pressure (00:31:56) gradient and on top that's a lot of (00:31:58) blood that's flowing backwards into the (00:31:59) atria you may also see this in (00:32:02) mitral regurgitation where you want to (00:32:04) be listening with the dye from the (00:32:05) stethoscope or if the aorta is just tons (00:32:07) of blood or back flowing in a high (00:32:09) pressure system from the order back into (00:32:10) the ventricles (00:32:12) that's going to be another situation so (00:32:13) you may also hear this in aortic (00:32:14) regurgitation thus supporting the fact (00:32:16) that you should listen to this during (00:32:17) what (00:32:18) with the diaphragm of the stethoscope (00:32:21) so these are the concepts that i want (00:32:22) you guys to understand here is that (00:32:24) we're looking for pitch the big thing (00:32:26) here is that if there's high pressure (00:32:27) gradients that causes a high pitch if (00:32:29) there's low pressure gradients that's (00:32:31) going to cause a low pitch again if (00:32:33) there's high pressure gradients plus a (00:32:34) lot of blood flow across a valve that's (00:32:36) going to produce very high pitches where (00:32:38) we call that harsh types of pitches (00:32:41) low pitches are best heard with what (00:32:44) the bell of the stethoscope high pitches (00:32:46) are best heard with the (00:32:47) diaphragm of the stethoscope that's (00:32:49) simple (00:32:50) okay (00:32:51) we got down location we got radiation we (00:32:53) got quality we got some of the pitch (00:32:55) concepts that we have to understand and (00:32:57) really it just comes down to high pitch (00:32:58) diaphragm low pitch bell that's it (00:33:00) intensity (00:33:02) when we talk about intensity this is (00:33:03) important for grading a murmur so we (00:33:05) utilize this to grade a murmur so we (00:33:07) have grades particularly from one all (00:33:10) the way to grade six and we say that (00:33:12) generally the higher it goes the worse (00:33:14) the murmur we'll see how that (00:33:15) technically is true with a couple of (00:33:17) exceptions (00:33:18) so how do we really grade these murmurs (00:33:20) so let's say that you're taking your (00:33:21) stethoscope you're listening to the (00:33:22) patient's chest you're listening for a (00:33:23) particular moment let's just say aortic (00:33:24) stenosis so you're listening here at the (00:33:26) right second intercostal space you're (00:33:28) trying to listen for a second and it's (00:33:29) just really really tough it's super (00:33:30) faint there may or may not be a murmur (00:33:33) kind of present it's tough to say so (00:33:34) it's it's difficult it's difficult to (00:33:36) discern let's say difficult is difficult (00:33:39) to discern (00:33:42) a murmur okay (00:33:44) very faint very faint type of armor (00:33:46) present that would be a great one (00:33:48) a grade two is where it's faint but it (00:33:52) can be heard so it's faint but it ca but (00:33:54) it can be heard with careful listening (00:33:57) with careful listening you listen a (00:33:58) little bit it's faint but okay i can (00:34:00) hear that (00:34:02) a third a grade three would be it's (00:34:04) super easily heard okay you place the (00:34:07) cetago stethoscope on the chest and it's (00:34:09) obviously heard oh that's definitely a (00:34:10) murmur okay grade four is it's loud it's (00:34:14) a loud murmur and they have when you (00:34:17) know whenever these murmurs occur (00:34:18) sometimes it causes the like a vibration (00:34:21) of the chest wall that whenever you put (00:34:23) your hand or your stethoscope on their (00:34:25) chest you can actually feel the (00:34:26) vibrations of the actual murmur against (00:34:29) the chest wall so they call it the (00:34:30) thrill the vibratory sensation (00:34:32) that is actually called a thrill and (00:34:34) sometimes that can be palpable with your (00:34:35) hand or with the stethoscope and so in (00:34:37) these patients grade four it's loud (00:34:39) murmur just like it is a you know a loud (00:34:41) murmur but they also have a palpable (00:34:43) throw present (00:34:46) for a grade five this is super loud and (00:34:49) they have a palpable thrill (00:34:52) they have a palpable thrill (00:34:54) but here's the thing (00:34:56) you can put the stethoscope like just (00:34:59) barely touching the chest it's barely (00:35:00) touching the chest (00:35:02) and you can still hear the murmur if you (00:35:04) have it on the chest and you're (00:35:04) listening and you have a palpable thrill (00:35:07) and it's there easily that's a great (00:35:08) fork but if you have let's say that you (00:35:10) just pick the stethoscope a little bit (00:35:11) where it's barely the rim of the (00:35:12) diaphragm is barely touching the chest (00:35:14) wall that could be considered to be a (00:35:16) grade five (00:35:17) okay so (00:35:18) stethoscope (00:35:23) barely on chest (00:35:27) okay that's going to be considered to be (00:35:28) a grade five and then grade six is where (00:35:31) the dang thing is so dang loud you have (00:35:33) a palpable thrill (00:35:36) but on top of this you can (00:35:39) hover (00:35:40) the stethoscope (00:35:43) over the chest (00:35:47) and still hear the murmur that's insane (00:35:49) you're hovering over the chest and you (00:35:52) hear that it's loud you you actually can (00:35:53) feel the vibratory sensations with your (00:35:55) hand or with your stethoscope off the (00:35:56) chest and you can still hear the murmur (00:35:58) with the seth go about the chest that is (00:36:00) a grade six (00:36:02) this is how we would grade murmurs now (00:36:03) why is all of this important well really (00:36:06) what's important to remember is that we (00:36:07) generally say for the most part that (00:36:10) grade (00:36:12) one to three (00:36:14) are likely to be there's a lower (00:36:16) likelihood of pathological murmurs so (00:36:19) it's potentially more but likely to be (00:36:21) benign (00:36:23) okay (00:36:24) whereas we say if it's grade three (00:36:27) or greater (00:36:29) particularly greater than grade three so (00:36:31) we sometimes we kind of like have it (00:36:32) right on that brink so grade three and (00:36:34) up (00:36:35) it's a higher likelihood of being (00:36:37) pathological (00:36:39) so actually we should say this let's say (00:36:42) grade less than three to be easy here if (00:36:44) it's less than three grade like one two (00:36:47) it's likely to be more benign if it's (00:36:49) three or above it's likely to be more (00:36:51) pathological and need further evaluation (00:36:54) there's one little exception to this (00:36:55) concept here where the grade less than (00:36:57) three and grade three plus usually we (00:36:58) say three plus odds pathological you (00:37:00) know grade less than three is benign (00:37:01) there's one exception particularly to (00:37:03) the grade less than three (00:37:05) you know if somebody has a uh (00:37:07) a vsd right they have a vsd (00:37:11) we would say (00:37:12) which would be the worst case vsd (00:37:15) so someone has a vsd (00:37:18) and it's a small let's put small vst (00:37:22) that means a small diameter (00:37:24) right a small diameter (00:37:26) if there is a small diameter of vsd that (00:37:29) means that there's going to be a higher (00:37:30) velocity of blood flow (00:37:32) across that vsd (00:37:34) if there's a higher velocity of blood (00:37:36) flow across that vsd that's going to be (00:37:37) a higher turbulence and a higher (00:37:38) intensity of the murmur so that'll (00:37:40) increase the (00:37:42) grade (00:37:44) of that murmur but it's a small vsd so (00:37:46) that's not as severe or pathological of (00:37:49) a vsd that would be an example example (00:37:51) if you have a big old honking vsd a (00:37:53) large vsd which is a bad situation (00:37:56) the murmur what happened to the murmur a (00:37:58) large vsd is a large diameter that means (00:38:00) a lower velocity a lower turbulence of (00:38:01) blood flow and a less intense murmur but (00:38:03) it's still a very significant type of (00:38:05) murmur it's a pathological murmur so (00:38:07) large vsds means a worse pathology but (00:38:09) the intensity of the murmur is lower (00:38:12) smaller vsds means less significant of a (00:38:15) pathological situation but higher (00:38:17) intensities of the murmur so don't (00:38:18) forget that as a particular exception (00:38:20) here okay ninjas we've done gone through (00:38:22) the location the radiation the pitch the (00:38:25) quality we've talked about the intensity (00:38:27) now that we've gone through that we've (00:38:28) really covered this in depth the next (00:38:30) part is super super important because (00:38:32) we're going to kind of put a lot of (00:38:33) stuff together and that's talking about (00:38:34) the timing of murmurs if it's systolic (00:38:37) diastolic continuous and we'll use some (00:38:38) particular types of murmurs and then the (00:38:41) configuration is it is it crescendo (00:38:44) decrescendo decrescendo is it hollow (00:38:46) styling all of these things we're going (00:38:47) to use all the terminology and keep kind (00:38:49) of repetitively coming back and talking (00:38:51) about location radiation quality pitch (00:38:54) and intensity let's talk about that all (00:38:56) right so let's talk about the timing and (00:38:58) configuration of murmurs this is a very (00:38:59) important part so (00:39:01) we want to understand what happens (00:39:03) particularly you know we understand if (00:39:05) we're listening for a murmur at a (00:39:06) particular location we can obviously (00:39:08) kind of identify as this aortic stenosis (00:39:10) is aortic regurgitation right i can (00:39:12) listen for radiation i can listen for (00:39:14) the quality is it blowing or is it harsh (00:39:16) i can also kind of determine the pitch (00:39:18) of it generally both of those are higher (00:39:20) pitches so diaphragm is going to be (00:39:21) better and then i can determine the (00:39:22) intensity is it grade three or above (00:39:24) likely grade three or above because (00:39:26) they're pathological (00:39:27) so with that being said (00:39:29) look the timing and then the (00:39:31) configuration of the murmur can also (00:39:33) help me to differentiate them so this is (00:39:34) where systolic diastolic continuous (00:39:37) murmurs come into play (00:39:39) all right so when we talk about these (00:39:41) the first thing that we have to think (00:39:42) about here is (00:39:43) when the ventricles go through a (00:39:44) particular stage right so we have the (00:39:46) first stage that they'll go through (00:39:47) which is ventricular (00:39:49) systole right so we'll have them go (00:39:51) through the ventricular system they're (00:39:52) gonna start contracting (00:39:54) so when the ventricles contract they (00:39:55) eject blood out of the heart (00:39:57) right and that would begin at what point (00:40:00) well we have s1 which is the closure of (00:40:02) the mitral in the tricuspid valve s2 (00:40:04) which is the closure of the aortic and (00:40:06) the pulmonary symmetry valve and then (00:40:08) back again here to s1 to start the cycle (00:40:09) all over again (00:40:11) from s1 to s2 is the ventricular systole (00:40:15) so we would say from this point here to (00:40:18) this point here would be (00:40:20) systole so this would be systolic murmur (00:40:22) so this is where we're going to be (00:40:23) talking about different types of (00:40:25) systolic (00:40:27) murmurs (00:40:29) and there's different ways that we can (00:40:30) categorize systolic murmurs we can (00:40:32) categorize them into what's called early (00:40:35) we can categorize them into mid (00:40:37) and we can categorize them into (00:40:39) holosystolic murmurs and we'll go over (00:40:41) all of those okay (00:40:44) the next thing is we have after (00:40:46) ventricular systole the ventricles have (00:40:48) to go into a relaxation phase so then (00:40:49) they have to start relaxing (00:40:51) and filling with blood (00:40:53) in this phase this starts at s2 so then (00:40:56) the closure of the aortic valve the (00:40:58) closure of the pulmonic valve and only (00:41:00) blood should be coming in (00:41:02) from the atria so this starts at s2 and (00:41:05) then continues until you get to s1 (00:41:07) that's ventricular diastole alright so (00:41:09) this is going to be the diastolic (00:41:11) murmurs and we'll talk about the (00:41:13) different types of diastolic murmurs (00:41:15) that we have here okay (00:41:17) so we have again ventricular systole (00:41:19) then we have ventricular diastole when (00:41:21) they're going through relaxation there's (00:41:23) one more type of murmur category that we (00:41:25) can have it's not just during systole (00:41:27) it's not just during diastole this bad (00:41:30) boy occurs during the entire time period (00:41:33) from systole (00:41:35) and into diastole what's this called (00:41:37) this is called a continuous murmur (00:41:40) continuous murmurs (00:41:43) and there's really one that we have to (00:41:44) talk about in that one but we'll go over (00:41:46) it okay so then you have the combination (00:41:48) of ventricular systole and ventricular (00:41:50) diastole that you'll be seeing these (00:41:52) murmurs okay so we got the different (00:41:53) types of murmurs systolic occurring from (00:41:55) s1 to s2 and then diastolic occurring (00:41:57) from s2 to s1 continuous occurring (00:41:59) throughout s1 all the way to the next s1 (00:42:02) let's talk about systolic first (00:42:05) so there's three different types of (00:42:06) systolic murmurs early (00:42:08) okay systolic murmurs mid-systolic (00:42:11) murmurs and holosystolic murmurs and (00:42:13) we'll talk about what each one of those (00:42:14) means (00:42:15) so early systolic murmurs okay here's (00:42:17) the ones that i really want you guys to (00:42:19) remember here there's two particular (00:42:21) ones that you guys can't forget here (00:42:23) the first one (00:42:25) is called aortic stenosis and we'll add (00:42:26) in another one here called pulmonic (00:42:28) stenosis so there's stenotic lesions the (00:42:30) second one that i want you to remember (00:42:32) here is called hypertrophic obstructive (00:42:34) cardiomyopathy and if you really want an (00:42:36) extra one to add on here you can even (00:42:38) add in a coarctation of the aorta can (00:42:40) also cause this too but i'm not super (00:42:42) concerned about this one i really want (00:42:43) you guys to remember (00:42:44) particularly aortic stenosis and (00:42:46) hypertrophic obstructive cardiomyopathy (00:42:49) so what happens in these types of (00:42:51) murmurs (00:42:53) okay whenever your ventricles are in (00:42:54) sicily they're just starting their (00:42:56) systole they're getting ready to (00:42:58) contract and push blood out of the heart (00:43:01) when they try to push blood out of the (00:43:02) heart in situations of aortic stenosis (00:43:05) and pulmonic stenosis the issue is with (00:43:06) the valve (00:43:07) if i have somebody who has a very very (00:43:09) rigid (00:43:10) and fibrotic type of calcified (00:43:14) immobile not very pliable valve (00:43:17) and i have to try to snap that valve (00:43:19) open so another way of looking at it is (00:43:21) imagine here (00:43:22) i have this valve looking like this so (00:43:24) here's the one leaflet here here's the (00:43:26) other leaflet here here's the opening (00:43:28) between it and what i want to do is i (00:43:30) would imagine that you guys would want (00:43:31) the valve to open up like this during (00:43:33) ventricular systole because if it's (00:43:35) opened up now it's easy for blood to (00:43:36) flow through that's not what happens an (00:43:39) aortic stenosis or pulmonic stenosis (00:43:42) what happens is these valves are rigid (00:43:44) and not very pliable so whenever the (00:43:46) left ventricle contracts to push blood (00:43:47) up it actually causes these valves to (00:43:50) bow (00:43:51) like this (00:43:53) so now this is where they would actually (00:43:55) look like during ventricular systole so (00:43:56) they go from here (00:43:58) and bow out like this (00:44:00) and that bowing (00:44:03) of the valve produces a very interesting (00:44:06) characteristic clicking sound okay so (00:44:08) imagine left ventricle contracting and (00:44:10) trying it's really best to open up the (00:44:12) aortic valve and it clicks because it (00:44:14) bows like that and then blood will start (00:44:16) squirting through it (00:44:17) that is going to produce this (00:44:18) characteristic type of clicking sound (00:44:20) that we hear right in the beginning (00:44:22) of ventricular systole right in the (00:44:24) beginning of ventricular systole after (00:44:26) s1 you'll have a ejection click (00:44:29) okay (00:44:30) this is what you would see in aortic (00:44:32) stenosis and pulmonic stenosis they have (00:44:34) an ejection click that's very important (00:44:39) after that happens blood is going to (00:44:40) start rushing through this area (00:44:44) a lot in the beginning so a ton of blood (00:44:46) will flow through and then less blood (00:44:48) will leave the ventricle less blood will (00:44:49) leave the ventricle out through the (00:44:50) aorta and then the actual intensity or (00:44:52) the volume of blood that's leaving will (00:44:53) decrease and so it'll actually be again (00:44:55) look like this a lot of blood will leave (00:44:58) through the left ventricle into the (00:44:59) aorta so the order starts getting really (00:45:01) filled and as that time goes by less (00:45:03) blood is leaving through the left (00:45:04) ventricle and into the aorta because (00:45:06) we're getting having less blood in the (00:45:07) left ventricle right as you contract and (00:45:09) contract less blood is going to be (00:45:10) leaving and so it gives this uprise from (00:45:13) blood squeezing out through the left (00:45:14) ventricle into the aorta (00:45:17) and then this down rise due to (00:45:19) less blood leaving the left ventricle (00:45:21) and going through the aorta this has a (00:45:23) very characteristic uprise and down rise (00:45:26) what do we call that (00:45:27) a crescendo decrescendo murmur this is (00:45:31) characteristic (00:45:32) and aortic stenosis and pulmonic (00:45:34) stenosis so you have this crescendo (00:45:39) de crescendo (00:45:44) de (00:45:46) crescendo (00:45:48) murmur that is important to remember (00:45:51) this is what you would see in aortic (00:45:52) stenosis and pulmonic stenosis you would (00:45:54) see this ejection click (00:45:56) plus (00:45:57) the combination of this crescendo (00:45:58) decrescendo murmur (00:46:19) you would not see this in hypertrophic (00:46:21) obstructive cardiomyopathy you wouldn't (00:46:22) see the click (00:46:23) here's what happens in hypertrophic (00:46:25) constructive cardiomyopathy (00:46:27) okay so let's actually write this down (00:46:28) here this is particularly only for (00:46:30) aortic stenosis and pulmonic stenosis (00:46:33) this one down here will be for (00:46:35) hypertrophic obstructive cardiomyopathy (00:46:38) now what happens in hypertrophic (00:46:39) obstructive cardiomyopathy is that their (00:46:41) interventricular septum is (00:46:43) asymmetrically hypertrophic so now i got (00:46:45) this hypertrophic (00:46:47) intraventricular septum (00:46:49) when the left ventricle contracts and (00:46:50) tries to squeeze blood out of the left (00:46:52) ventricle it's kind of just like aortic (00:46:54) stenosis (00:46:55) but i'm trying to squeeze blood through (00:46:57) this tiny little area here just like i'm (00:46:59) trying to squeeze blood through the tiny (00:47:01) little narrowing stenotic valve i'm (00:47:03) trying to squeeze it through this left (00:47:05) ventricular outflow tract and into the (00:47:07) aorta it's very narrow and it's tough (00:47:09) for me to squeeze all that blood through (00:47:11) and so what happens is a ton of blood is (00:47:14) going to rush through that area and then (00:47:16) less blood will leave through that area (00:47:18) as well and so it's going to produce (00:47:20) again this crescendo (00:47:24) de crescendo type of murmur because (00:47:26) again i'm going to squeeze the left (00:47:28) ventricle as hard as i can i'm going to (00:47:30) push as much blood through that narrow (00:47:31) area and that whenever the blood's (00:47:33) leaving a ton of blood leaves the left (00:47:35) ventricle into the aorta and feeds it (00:47:36) and then over time throughout the rest (00:47:38) of systole less blood will be leaving (00:47:39) the left ventricle so less blood will be (00:47:41) filling the aorta and again it produces (00:47:43) this classic crescendo (00:47:45) decrescendo type of murmur which looks (00:47:48) just like this but what's it missing (00:47:50) this has no ejection click that has no (00:47:53) ejection click so again for this one (00:47:54) you'll see a (00:47:55) crescendo (00:47:58) day crescendo (00:48:01) murmur (00:48:03) but again there is no ejection click (00:48:05) what's another thing (00:48:08) if you're listening for aortic stenosis (00:48:10) where would i be listening (00:48:12) right second intercostal space radiation (00:48:13) to the carotids so this would also have (00:48:15) an ejection click plus the crescendo (00:48:17) decrescendo at the right particularly (00:48:20) again pulmonic stenosis is very very (00:48:22) rare so we're going to just hold this (00:48:24) off right here it's very very rare so i (00:48:26) would focus more on the aortic stenosis (00:48:27) but for this one you would hear this at (00:48:29) the right (00:48:30) second intercostal space and it would (00:48:32) radiate to the carotids (00:48:36) in this example of crescendo decrescendo (00:48:39) without an ejection click for a (00:48:41) hypertrophic obstructive cardiomyopathy (00:48:43) this would be located where did we say (00:48:44) that you hear this best (00:48:46) herbs point so you can hear this at (00:48:48) herb's point (00:48:50) which is the left third intercostal (00:48:52) space does this radiate to the carotids (00:48:54) no (00:48:55) there's no radiation (00:48:57) and there's also other ways that we can (00:48:59) differentiate these two via specific (00:49:01) types of maneuvers but that's what i (00:49:03) really want you guys to remember here (00:49:04) okay (00:49:09) [Music] (00:49:20) we have that also again aortic stenosis (00:49:22) would be of a harsh type of murmur (00:49:25) hypertrophic obstructive cardiomyopathy (00:49:26) is also a harsh type of murmur so it's (00:49:28) not going to be the type of quality the (00:49:31) pitch they're both going to be high (00:49:32) pitched so they're both going to be (00:49:33) heard with the diaphragm of the (00:49:34) stethoscope and they're generally both (00:49:36) high grade okay high intensity so these (00:49:39) are things to be thinking about so we (00:49:40) kind of reviewed and recapped those (00:49:42) things if you really wanted to know the (00:49:43) extra little part of co-occupation of (00:49:45) the aorta how to differentiate these (00:49:47) this one has a systolic you know (00:49:48) crescendo decrescendo just like both hcm (00:49:51) and aortic stenosis i'm going to get rid (00:49:53) of pomonix donors just because it's (00:49:54) super super rare so aerodynamics know (00:49:56) this is the big one i want you to (00:49:56) remember for coordination of the order (00:49:58) the best way you can differentiate this (00:50:00) is this is heard at the left (00:50:02) posterior (00:50:04) hemithorax (00:50:06) that's a super obvious situation there (00:50:09) ain't listen for no murmurs of aortic (00:50:10) stenosis hypertrophic obstructive (00:50:12) cardiomyopathy in the left posterior (00:50:14) thorax you're not doing that you'll hear (00:50:16) that in coarctation of the aorta okay (00:50:18) so that's a big thing to think about and (00:50:19) also there's some other things with (00:50:20) cartesian therapy that's just past the (00:50:22) scope of this lecture i don't want to (00:50:23) get too much into but these are the big (00:50:24) ones i want to remember aortic stenosis (00:50:27) hypertrophic obstructive cardiomyopathy (00:50:28) based upon the early systolic ejection (00:50:30) murmurs again ejection click with aortic (00:50:33) stenosis not with hypertrophic (00:50:35) second intercostal space rights (00:50:36) parasternal border fraotic radius of the (00:50:38) carotids (00:50:40) hypertrophic herbs point no radiation (00:50:43) crescendo decrescendo for both of them (00:50:45) that is the important thing to remember (00:50:46) okay (00:50:47) now that we talked about that let's come (00:50:49) down for mid-systolic murmurs all right (00:50:50) so let's talk about mid-systolic murmurs (00:50:52) so in these situations here the biggest (00:50:54) big one that i really want you guys to (00:50:55) understand here is called mitral valve (00:50:56) prolapse and sometimes that can be (00:50:58) associated with a murmur so in mitral (00:51:00) valve prolapse (00:51:02) what's really happening in this (00:51:03) situation is that you have very you know (00:51:06) weak type of leaflets so there's what's (00:51:08) called maxometers degeneration it kind (00:51:09) of gets a lot of like deposition of (00:51:10) particular types of spongy tissue in (00:51:12) this valve and the valve leaflet is just (00:51:15) really weak all right so that's one (00:51:16) characteristic of mitral valve prolapse (00:51:18) is they have very weak mitral valve (00:51:21) leaflets (00:51:22) they're just super super floppy and easy (00:51:25) to be able to deform okay that's one (00:51:27) thing to think about (00:51:28) the second thing is that they have these (00:51:30) things you know they have the chordae (00:51:31) tendineae and they anchor them down to (00:51:33) the papillary muscles these are also (00:51:35) super weak so let's actually draw some (00:51:37) very weak types of chordae tendineae so (00:51:39) we'll draw them as kind of like they're (00:51:40) really they're not very taut they're not (00:51:42) very strong they're not really anchoring (00:51:43) the leaflets down they're just super (00:51:45) loose and chill and waxed so there could (00:51:47) also be (00:51:49) weak chordae tendineae okay and this (00:51:52) could be due to connective tissue (00:51:53) defects associated with like marfan (00:51:55) syndromes ehler-danlos syndrome stuff (00:51:56) like that (00:51:57) what happens (00:51:59) is that whenever the ventricles go into (00:52:00) their systole right they start (00:52:02) contracting and squeezing blood they (00:52:04) generate enough pressure that when we (00:52:06) want to close the mitral valve we want (00:52:08) the leaflets to come together seal and (00:52:10) prevent blood from backflowing into the (00:52:12) atria that's the whole purpose (00:52:14) whenever the blood hits the mitral valve (00:52:17) it causes the mitral valve leaflet (00:52:20) because it's super weak and the chordae (00:52:21) tendineae isn't really anchoring it down (00:52:24) imagine that thing just getting hit with (00:52:25) like a rock and just blowing back so (00:52:27) that very weak leaflet will blow back (00:52:30) into the actual left atrium so now (00:52:32) imagine this for a second where this (00:52:34) leaflet which was trying to be nice and (00:52:36) close to this one gets bowed back here (00:52:39) this poor leaflet so it gets bowed back (00:52:42) into the left atrium (00:52:43) that bowing back of that valve into the (00:52:46) left atrium causes a clicking sound so (00:52:49) you can kind of imagine i guess another (00:52:51) way of thinking about it is imagine here (00:52:53) i have the annulus which holds the (00:52:55) leaflets (00:52:56) okay (00:52:57) and here's the you know the one leaflet (00:52:59) here the anterior leaflet here and then (00:53:01) here's the posterior leaflet normally (00:53:03) it's like this right and it's anchored (00:53:05) by the chordae tendineae but in these (00:53:07) patients who have mitral valve prolapse (00:53:09) that leaflets very weak and when the (00:53:10) left ventricle contracts and pushes (00:53:12) blood to snap these leaflets together (00:53:14) instead of it snapping together this (00:53:15) poor thing just starts bowing (00:53:18) into the left atrium (00:53:20) and now again what's anchoring these bad (00:53:22) boys down what's supposed to be (00:53:23) anchoring them is the chordae tendineae (00:53:28) instead because it's not anchoring them (00:53:30) down the leaflets really weak the blood (00:53:31) will bow back what actually will bow (00:53:33) that mitral valve leaflet backwards and (00:53:36) now there's an open space between these (00:53:38) two leaflets where blood could easily (00:53:40) regurgitate back into the left atrium so (00:53:44) not only does mitral valve prolapse have (00:53:45) this click sound that they have so it'll (00:53:47) also produce a very important type of (00:53:49) click (00:53:50) but there may also be an associated (00:53:53) murmur present where blood can (00:53:55) regurgitate back what kind of murmur a (00:53:57) mitral regurgitation murmur could also (00:54:00) be present (00:54:02) so that's what it would be very (00:54:03) interesting here so what we see is we (00:54:05) see a click that occurs right like the (00:54:07) point of mid cystely so here will be my (00:54:09) ejection click and that's the bowing (00:54:11) that clicking is this part here where (00:54:13) the mitral valve bows (00:54:16) back into the left atrium that's the (00:54:17) click (00:54:19) but then also if we have the (00:54:21) regurgitation of blood flow due to not (00:54:23) having a poor seal you may also have a (00:54:26) regurgitation murmur that can also occur (00:54:29) after the ejection click and that's (00:54:31) important thing to remember and you (00:54:32) think about where would you have this (00:54:34) mitral valve prolapse with the murmur (00:54:37) like where would it be best audible (00:54:39) review it that's that left fifth (00:54:42) intercostal space (00:54:43) mid clavicular line does it radiate well (00:54:46) if there's the mitral regurgitation (00:54:47) murmur at will and it could potentially (00:54:49) radiate to the axilla (00:54:52) this would be high pitched this would be (00:54:53) a blowing type of quality you guys are (00:54:56) getting the point and it's pathological (00:54:57) so it'd likely potentially be like a (00:54:59) grade three or above so this is the (00:55:01) whole concept that we're continuously (00:55:02) repeatingly going through so we anchor (00:55:05) these types of things down in our brain (00:55:07) all right so that's the mitral valve (00:55:08) prolapse so an amid systolic ejection (00:55:10) click and if there's a murmur that (00:55:12) presents because the poor ceiling you (00:55:13) can get a regurgitation murmur like a (00:55:15) mitral regurgitation murmur that's an (00:55:17) important thing all right (00:55:19) the other thing is we'll talk about (00:55:20) maneuvers a lot later things that can (00:55:22) cause the click to come earlier murmur (00:55:24) to be longer click to come later murmur (00:55:26) to be shorter we'll talk about all those (00:55:28) things a little bit later (00:55:36) [Music] (00:55:58) all right the next situation that i want (00:56:00) you guys to remember is we can also have (00:56:02) mid-systolic murmurs without the click (00:56:04) and these are actually called (00:56:05) physiological murmurs so they're (00:56:07) physiological functional (00:56:10) and when i talk about these murmurs (00:56:12) there are particularly two reasons one (00:56:13) is you have a hyperdynamic circulation (00:56:15) so hyperdynamic circulation (00:56:19) or state is whenever your left ventricle (00:56:21) is just a clanging and a bang and it's (00:56:23) pumping out blood (00:56:24) through the left ventricle out into the (00:56:26) aorta and when it's flooding that blood (00:56:29) through the aorta imagine whenever that (00:56:31) blood is flooding through the aorta at a (00:56:32) high velocity that high velocity (00:56:37) is going to produce turbulence of blood (00:56:38) flow right you're going to get (00:56:39) turbulence of blood flow and if you get (00:56:42) increased turbulence of blood flow (00:56:43) that's going to precipitate murmurs it's (00:56:45) also going to cause these like aortic (00:56:46) valve which is flowing through to kind (00:56:48) of vibrate a lot because you're hitting (00:56:50) that valve with so much intensity and so (00:56:52) much velocity that when it gets hit (00:56:54) it'll actually vibrate a little bit (00:56:55) there'll be a turbulence of blood flow (00:56:57) from the high velocity and the high (00:56:58) velocity will actually vibrate (00:57:01) the valve (00:57:04) and that will produce a murmur that will (00:57:05) be audible (00:57:07) now this is usually due to hyperdynamic (00:57:09) states so what are some hyperdynamic (00:57:11) states we already talked about that (00:57:12) right so it could be fever (00:57:14) it could be sepsis (00:57:16) it could be exercise (00:57:19) it could be thyrotoxicosis because all (00:57:21) of these things are increasing your (00:57:23) sympathetic nervous system right they're (00:57:24) all increasing your sympathetic (00:57:26) nervousness it could be high volume (00:57:28) states like pregnancy (00:57:29) we talked about that one it could be (00:57:31) high outflow states where your body your (00:57:33) cardiac outputs were having to be higher (00:57:35) such as in berry berry (00:57:38) it could be in situations like an av (00:57:40) fistula (00:57:41) or even severe anemia (00:57:43) right we talked about all of these over (00:57:45) there with the physiology of murmurs but (00:57:46) it's the same concept when these murmurs (00:57:49) occur it actually starts at mid-systole (00:57:52) and then continues throughout the rest (00:57:53) of late systole all the way until we get (00:57:55) to the next heart sound so this starts (00:57:57) at so we have s1 (00:57:59) and then right after s1 which is the (00:58:00) closure of the mitral tricuspid valve a (00:58:03) little bit later we'll get our (00:58:04) mid-systolic murmur and it'll terminate (00:58:07) right at s2 and again we'll have s1 same (00:58:09) thing with the mitral valve prolapse (00:58:11) we'll have s1 right after s1 you get an (00:58:14) ejection click with a murmur that could (00:58:17) be present if there's a mitral (00:58:18) regurgitation then you get your s2 and (00:58:20) then your s1 (00:58:22) so that's what's happening in this (00:58:23) situation now there's one more thing (00:58:24) that you guys have to remember besides (00:58:26) hyperdynamic states and this is (00:58:28) important for your test which is called (00:58:29) the stills murmur (00:58:31) this is more important to kind of like (00:58:32) your pediatric patients we'll put (00:58:34) pediatrics (00:58:36) this is usually in young children okay (00:58:38) it's a benign finding so it's benign (00:58:40) again it's kind of supporting the fact (00:58:41) that it can be physiological or (00:58:43) functional it's not a pathological (00:58:44) finding and usually this is a grade (00:58:46) that's less than three so usually like (00:58:48) one to two (00:58:49) what happens in here is the ethiology (00:58:51) behind this we don't really know but (00:58:52) it's the same concept there's a (00:58:53) hypodynamic state in these young (00:58:55) children where there's a lot of blood (00:58:56) that's actually being flowing across the (00:58:58) aorta right a lot of blood flowing (00:59:00) across the aorta and again there's a (00:59:02) high velocity of blood flowing through (00:59:03) the aorta that's going to cause (00:59:04) turbulence turbulence will produce a (00:59:05) potential murmur and it's also going to (00:59:06) cause vibration of that aortic valve (00:59:09) in these situations one of the big (00:59:10) things for both of these is you can (00:59:12) modulate these murmurs we're not going (00:59:13) to talk about it later so we'll talk (00:59:15) about it now is you can modulate these (00:59:17) murmurs in a particular way (00:59:19) where you can increase the intensity of (00:59:21) a stills murmur (00:59:23) in one particular way and decrease the (00:59:25) intensity of a stills murmur in another (00:59:27) way (00:59:28) and it really comes down to venous (00:59:29) return if you want to increase the (00:59:31) intensity you want to increase the (00:59:32) venous return if you want to decrease (00:59:34) the intensity you want to decrease the (00:59:36) venous return so it's a simple concept (00:59:38) we increase venous return by having (00:59:39) someone squat down or having them lay (00:59:41) down flat and lift their legs we have (00:59:44) them reduce their venous return by (00:59:45) standing up quickly or by having them (00:59:47) valzava like they're bearing down to (00:59:49) take a poop and those situations that (00:59:51) can reduce your venous return the whole (00:59:53) concept if you increase venous return (00:59:55) you increase the volume of blood that's (00:59:56) being entering into the heart if you (00:59:58) have more blood in your heart and your (00:59:59) heart's already pounding it's going to (01:00:01) pound more blood through the aorta (01:00:03) that's more velocity that's more (01:00:05) turbulence and intensifying the murmur (01:00:07) if there's less blood volume this (01:00:09) heart's still contracting hard but (01:00:10) you're not pushing as much volume that's (01:00:13) less force less velocity and less (01:00:15) turbulence of blood flow decreasing the (01:00:16) intensity of the murmur that's one of (01:00:18) the big things to be thinking about for (01:00:20) these types of murmurs all right we (01:00:21) talked about mid-systolic murmurs really (01:00:23) well now let's go ahead and talk about (01:00:25) holosystolic murmurs all right so let's (01:00:27) talk about holosystolic murmurs so (01:00:28) holosystolic murmurs are different in (01:00:31) comparison to early and mid how its (01:00:33) holosystolic is occurring throughout the (01:00:34) entire systolic period so from s1 until (01:00:37) s2 there's going to be a murmur present (01:00:39) and so that's one of the big things now (01:00:41) there's two particular kinds of things (01:00:43) that can happen here one is there's a (01:00:44) regurgitation murmur or there's a vsd (01:00:47) that's what we've been thinking about (01:00:48) holes i like okay michael rieger truck (01:00:49) customer regards or vsd think about that (01:00:51) in your head that's the differential so (01:00:53) the first things first let's talk about (01:00:55) mitral regurgitation and tricuspid (01:00:56) regurgitation so mitral regurgitation or (01:00:59) tricuspid regurgitation in these (01:01:01) situations again what's happening the (01:01:03) ventricles are going to be in systole (01:01:04) they're going to be contracting when (01:01:07) they're contracting and they're starting (01:01:08) the contractile period right when the (01:01:10) left ventricle contracts to try to push (01:01:12) blood up into the aorta it's going to (01:01:15) squeeze blood back through these (01:01:16) incompetent valves (01:01:18) into the atria blood flow across an (01:01:20) incompetent valve will produce (01:01:22) precipitate a turbulence of blood flow (01:01:23) because it's going to bang off the (01:01:24) atrial chambers and cause a murmur (01:01:28) that murmur is going to occur without (01:01:30) any kind of clicking sound without any (01:01:32) kind of snapping sound or anything like (01:01:34) that it is going to be occurring (01:01:36) throughout the entire systolic time (01:01:38) period and we know that that's the (01:01:39) systolic time period because again (01:01:41) closure of the mitral and tricuspid (01:01:42) valve are supposed to occur at s1 (01:01:45) and then again (01:01:46) you have s2 which is when the aortic and (01:01:48) the pulmonic valve close which starts (01:01:50) the onset of diastole and then again we (01:01:52) go back to s1 so it has to occur between (01:01:54) s1 and s2 (01:01:56) but again it is holosystolic occurring (01:01:58) throughout the entire time period and (01:02:00) again the same thing that would happen (01:02:02) here with mitral regards would be the (01:02:03) same thing with tricuspid regurge you (01:02:06) have the right ventricle it's trying to (01:02:07) pump blood out into the pulmonary artery (01:02:10) but because we have this incompetent (01:02:12) valve we're rushing blood across the (01:02:14) incompetent tricuspid valve back into (01:02:16) the atria the right atrium causing blood (01:02:19) to hit the right atrium and cause (01:02:20) turbulence to flow and precipitate a (01:02:22) murmur that's the big thing and again we (01:02:24) can establish here with these that (01:02:26) mitral regurgitation would be best heard (01:02:28) at the left what (01:02:30) fifth (01:02:31) intercostal space (01:02:33) mid clavicular line and then it would (01:02:35) radiate where (01:02:37) it would radiate to (01:02:40) the axilla (01:02:42) this would be a very high pitched it (01:02:45) would be blowing in quality right you (01:02:47) get the point and it's going to be a (01:02:48) high grade if it's tricuspid (01:02:50) regurgitation that's relatively uncommon (01:02:52) but let's still mention it that would be (01:02:54) where that would be the left fourth (01:02:57) intercostal space (01:02:59) parasternal border and generally we (01:03:01) don't have any literature that supports (01:03:02) a particular radiation of this one but (01:03:05) again it might be a little bit more of a (01:03:07) higher pitch even though that side is a (01:03:09) little bit of a lower pressure system it (01:03:11) could be a variable pitch i would say (01:03:13) degrading is usually a little bit more (01:03:15) intensified though it's a higher grade (01:03:17) and again the quality of it is it'll be (01:03:19) more of a blowing type of mermaid (01:03:20) because it's a regurgitation murmur (01:03:22) all right and we'll talk about different (01:03:23) types of maneuvers that we can utilize (01:03:25) to particularly focus more on this one (01:03:28) because it's more common ways that we (01:03:29) can intensify or decrease the intensity (01:03:32) of mitral regurgitation murmurs okay (01:03:34) boom shakalaka we did that one (01:03:51) all right next one that we have to talk (01:03:52) about (01:03:54) vsd now with vsds these are very (01:03:56) interesting so ventricular septal (01:03:58) defects (01:03:59) all right but the problem with this one (01:04:01) is that when the left ventricle (01:04:02) contracts (01:04:03) you want it to pump blood out into the (01:04:05) aorta right that's the goal and it will (01:04:07) it'll still do that even with the vsd (01:04:09) because you're going from high pressure (01:04:10) to low pressure high pressure in the (01:04:11) ventricle to low pressure in the aorta (01:04:13) but guess what the left ventricle also (01:04:15) is higher pressure than the right (01:04:17) ventricle so when it's pumping blood out (01:04:19) into the aorta it's also pumping blood (01:04:22) across the ventricular septal defect (01:04:25) into the right ventricle (01:04:26) and whenever you do that that's going to (01:04:28) push blood here and cause this (01:04:30) turbulence of blood flow for two reasons (01:04:31) one is you're having to squeeze blood (01:04:34) through a small little tiny opening (01:04:36) within that septal defect that's a (01:04:38) higher velocity and that's going to (01:04:39) cause a increased turbulence (01:04:42) it's also a high pressure gradient so (01:04:44) it's going to produce a higher pitch but (01:04:47) also if i push blood across this area it (01:04:48) may bang up against the right (01:04:49) ventricular walls and cause more (01:04:51) turbulence and again precipitate murmurs (01:04:53) you get the point (01:04:54) this right here is still going to (01:04:56) produce a (01:04:57) murmur that occurs throughout the entire (01:04:59) systolic time period it's throughout the (01:05:02) entire systolic time period again it's (01:05:04) between s1 so s1 is the closure of the (01:05:07) tricuspid of the mitral valve that's (01:05:08) still going to close (01:05:10) and s2 as assuming that they have normal (01:05:13) mitral valves and normal tricuspid (01:05:14) valves this should close s2 is the (01:05:16) closure of the aortic and the pulmonary (01:05:17) similar valve and then again we get back (01:05:18) to s1 from s1 to s2 is systole so it has (01:05:22) to occur during systole and occurs (01:05:23) throughout that entire time period (01:05:26) big thing to think about with the vsd is (01:05:28) the actual intensity of the murmur is (01:05:31) dependent upon one what thing just to (01:05:33) remind you intensity (01:05:36) it increases with (01:05:38) decreasing (01:05:39) diameter (01:05:41) vsds so a decreasing diameter vsd will (01:05:44) cause higher velocity of blood flow so (01:05:47) remember that the smaller the vsd the (01:05:49) more intense (01:05:51) loud the vsd will be and so more audible (01:05:54) it will be the larger the vsd the larger (01:05:56) the diameter the less the velocity the (01:05:58) less the turbulence of blood flow and (01:05:59) less intense or loud the vsd will be (01:06:00) that's an important thing to remember (01:06:03) vsds though when you're listening for (01:06:04) these where are we particularly (01:06:06) listening for them they would listen (01:06:07) more particularly at what area the same (01:06:09) area is the tricuspid valve so you (01:06:11) particularly listen around the left (01:06:12) fourth (01:06:14) intercostal space okay parasternal (01:06:16) border so parasternal border (01:06:19) these are big things to be thinking (01:06:20) about my friends okay and again with a (01:06:23) ventricular septal defect this would be (01:06:24) more of a what type of heart sound if (01:06:25) you're comparing this from michael (01:06:26) regards because this is the more common (01:06:28) one mitral regurg versus the vsd this (01:06:30) would be more harsh (01:06:33) in nature whereas in patients with (01:06:35) mitral regurgitate we would consider (01:06:36) this to be more (01:06:38) blowing okay or musical (01:06:42) this one (01:06:44) has a radiation where (01:06:46) into the axilla this one generally there (01:06:48) isn't a particular like literature of (01:06:49) the base that says where exactly it may (01:06:51) radiate if it does radiate maybe it's (01:06:53) going to be a little bit more on like (01:06:54) the right lower sternal border but again (01:06:56) there's no literature to actually (01:06:57) support that (01:07:07) okay that's the big thing to think about (01:07:09) with your holosystolic murmurs okay (01:07:11) let's now move on to diastolic murmurs (01:07:13) so diastolic murmurs let's actually talk (01:07:14) about this on the graph here again s1 (01:07:17) begins the onset of ventricular systole (01:07:19) closure of the mitral valve and (01:07:20) tricuspid valve (01:07:21) s2 (01:07:23) is the closure of the aortic valve and (01:07:24) the pulmonary similar valve and that (01:07:26) indicates from here to here to the next (01:07:28) s1 this is ventricular diastole that's (01:07:30) the period when the ventricles are (01:07:31) relaxing and filling with blood right (01:07:34) okay there's two particular (01:07:36) differentials that you want to think (01:07:37) about with diastolic murmurs (01:07:39) aortic regurge which is the more common (01:07:41) one but you also want to think about the (01:07:42) associated one pulmonic regards we'll (01:07:43) we're gonna pretty much mention it but (01:07:45) think more particularly aortic reurge (01:07:47) and then mitral stenosis (01:07:50) or tricuspid stenosis but again think (01:07:52) more about mitral stenosis it's more (01:07:53) common okay so those are the two (01:07:55) differentials that we're going to write (01:07:56) down here (01:07:57) let's write down here first one (01:08:00) is going to be someone who has aortic (01:08:02) regurgitation pulmonic regurgitation but (01:08:05) again focus more on the aortic (01:08:07) regurgitation because it's way more (01:08:08) common (01:08:09) and aortic regurgitation what is (01:08:12) happening (01:08:13) this aortic valve is dooky it's not very (01:08:16) good at doing its job so when blood is (01:08:18) supposed to go from the left ventricle (01:08:20) out into the aorta it's supposed to go (01:08:21) out into the aorta and flow out into the (01:08:23) systemic circulation right (01:08:25) but whenever the aorta takes that blood (01:08:27) in it accommodates it it recoils it (01:08:30) smashes the blood (01:08:32) back down (01:08:33) towards the left ventricle (01:08:36) there's an incompetent and leaky valve (01:08:38) so blood is just going to flood (01:08:39) backwards and across that incompetent (01:08:42) valve into the left ventricle it's going (01:08:45) to bang up against the left ventricular (01:08:47) wall and produce turbulence of blood (01:08:49) flow which is going to precipitate a (01:08:50) murmur (01:08:53) if that happens when would this happen (01:08:54) this would happen right at the onset (01:08:57) of a ventricular dastly right at the (01:08:59) onset at s2 right after s2 boom you can (01:09:03) get the aortic regurgitation or pulmonic (01:09:05) regurgitation murmur (01:09:07) so when the blood flows back (01:09:09) against that across that incompetent (01:09:11) valve you will see this murmur and (01:09:13) here's where it's really interesting (01:09:14) it'll start off right here after s2 (01:09:17) you're going to see that as the blood is (01:09:18) flowing across more blood will flow (01:09:20) across in the initial time period right (01:09:23) so you'll have a high (01:09:24) volume (01:09:27) and early (01:09:28) diastole and then a low volume flowing (01:09:31) across (01:09:32) and the later phases of diastole okay so (01:09:36) a lot of volume is going to flow across (01:09:37) that actual aortic valve into the left (01:09:39) ventricle in the beginning phases and (01:09:41) then less volume will flow over and the (01:09:44) later phases so it'll kind of look (01:09:46) something like (01:09:47) this so it's a diastolic murmur (01:09:51) but it's decreasing in intensity (01:09:53) throughout diastole what do we call this (01:09:56) a diastolic decrescendo murmur so what (01:09:59) is this called this is called a (01:10:01) diastolic (01:10:05) decrescendo (01:10:07) murmur (01:10:10) now that is one important thing to (01:10:12) remember the other thing to remember (01:10:13) here (01:10:14) is not only is it diastolic decrescendo (01:10:17) is think about since aortic (01:10:18) regurgitations really want the one that (01:10:20) i want you to remember where would we be (01:10:21) listening for this one again we would be (01:10:23) listening at the right second (01:10:26) intercostal space parasternal border (01:10:27) where does it radiate (01:10:29) it radiates to the (01:10:31) where (01:10:32) left (01:10:33) upper sternal border left second (01:10:34) intercostal space generally (01:10:36) okay (01:10:38) the other thing is what's the quality of (01:10:39) it would you describe this as blowing (01:10:42) yes it's blowing or musical okay (01:10:45) and then again pitch it'd be very high (01:10:47) pitch and on top of that what else (01:10:50) it would also be a very high grade so (01:10:52) you guys get the point here with this (01:10:53) and this we get to say the same thing (01:10:54) about pulmonic regurgitation it's just (01:10:56) not very common so we commonly you just (01:10:58) think about aortic regurgitation so (01:11:00) again a diastolic decrescendo murmur (01:11:02) because again think about as blood is (01:11:04) flowing from the aorta into the (01:11:06) ventricle there's going to be more blood (01:11:07) that's flowing initially and then (01:11:08) eventually there's just less blood in (01:11:09) the aorta to come across into the left (01:11:11) ventricle and so the less volume (01:11:13) actually enters and so as less volume is (01:11:15) moving in there's less turbulence of (01:11:16) blood flow less velocity of blood flow (01:11:19) and again less turbulence less intensity (01:11:21) of the murmur as we go towards the (01:11:24) time period of beginning ventricular (01:11:25) systole (01:11:42) okay (01:11:43) next one we said aortic regurgitation (01:11:45) was the big one to think about for (01:11:46) diastolic murmurs you can also think (01:11:48) about pulmonic but the other thing we (01:11:50) said was what if it's not those what if (01:11:52) it's actually something like (01:11:55) mitral stenosis (01:11:57) or (01:11:58) tricuspid stenosis (01:12:00) with the emphasis being more on (01:12:02) mitral stenosis because it's way more (01:12:04) common trichosis is not too common (01:12:06) in these situations what happens is (01:12:08) something very interesting (01:12:10) you want blood during diastole so again (01:12:13) this was all happening during diastole (01:12:15) when the ventricles are supposed to be (01:12:16) filling with blood only from the (01:12:18) atria but instead these suckers are (01:12:21) getting filled by the pulmonary artery (01:12:22) and the aorta undesirably because of the (01:12:24) incompetent leaky aortic valve and (01:12:26) pulmonic valve (01:12:27) in this situation the valves here are (01:12:29) fine valves here are fine there's no (01:12:31) problems with those valves (01:12:32) and blood should only they should not be (01:12:34) coming this way okay this is not (01:12:36) happening no blood is back flowing from (01:12:38) the pulmonary artery or the aorta (01:12:41) in this situation we only want blood to (01:12:42) go from here to here right that's what (01:12:45) we want normally during diastole so when (01:12:47) the ventricles are supposed to be (01:12:48) relaxing and accommodating that blood (01:12:50) flow we only want them to be coming from (01:12:52) the atria (01:12:53) what if the blood flow isn't coming from (01:12:55) the atria because there's a very (01:12:57) stenotic and fibrotic and calcified (01:12:59) mitral or tricuspid valve oh man so in (01:13:02) this situation here here's what happens (01:13:04) take the mitral valve for example (01:13:06) here's your mitral valve (01:13:08) when you have your mitral valve like (01:13:10) this let's kind of draw it like this (01:13:13) we'll have it here and we'll have it (01:13:14) here as the mitral valves (01:13:17) okay (01:13:18) so here's your mitral valves (01:13:20) they're very very fibrotic and stenotic (01:13:23) right so we'll draw us like some some (01:13:24) fibrous tissue or you know (01:13:26) calcifications of these valves they're (01:13:28) very very stiff they're very calcified (01:13:30) what we want to do is we want to push (01:13:32) blood (01:13:33) and snap these valves open right so (01:13:35) generally what we would like to see in a (01:13:37) perfect world is we want to see a (01:13:39) situation like this where they would fly (01:13:41) open (01:13:42) and blood would easily flow down from (01:13:43) the atria into the ventricles (01:13:46) but these valves are super fibrotic (01:13:47) super stenotic super calcified and (01:13:50) they're very difficult to open (01:13:52) what happens is your mitral your uh your (01:13:55) atria contract as hard as they can and (01:13:57) drain and a lot generate a lot of (01:13:58) pressure to push blood through that (01:14:01) valve and pop it open (01:14:02) and so what happens is (01:14:04) in these situations here is when you (01:14:06) kind of like just crack these like old (01:14:09) fibrotic valves open it kind of makes (01:14:11) this snapping sound (01:14:13) and we call that sound that it makes (01:14:15) whenever you like quickly snap open the (01:14:17) mitral valve or the tricuspid of the (01:14:20) opening snap (01:14:21) and that's going to occur right at the (01:14:23) beginning of diastole so again if you (01:14:25) think about here you have s1 you have s2 (01:14:28) which is again the onset of ventricular (01:14:30) diastole because that's the closure of (01:14:32) the aortic valve and the pulmonary valve (01:14:33) those are closed no backflow (01:14:35) and we should have blood coming from the (01:14:37) atria (01:14:38) into the ventricles well what happens is (01:14:40) the blood is not wanting to come as (01:14:42) easily and so then the h3 have to (01:14:44) contract they have to kind of generate a (01:14:45) lot of pressure and snap open that (01:14:49) mitral valve or tricuspid valve (01:14:52) when it snaps it open just enough to (01:14:54) crack that opening enough to get blood (01:14:56) into the ventricles that is called the (01:14:58) opening snap (01:15:00) then think about it like once you open (01:15:02) it (01:15:02) you have a lot of blood waiting in the (01:15:04) atria to get down into the ventricles (01:15:06) once you open it and it took a lot of (01:15:07) time to (01:15:08) pressure and stress to open that valve (01:15:11) up once you open it a ton of blood is (01:15:13) going to flow down into the ventricles (01:15:15) very quickly (01:15:17) empty the atria and it's the same (01:15:19) concept there'll be a lot of volume (01:15:22) that'll cross the actual mitral valve or (01:15:25) tricuspid valve early (01:15:27) and then less volume because they're (01:15:29) starting to get empty (01:15:30) as it crosses the mitral valve later in (01:15:33) diastole (01:15:34) so then you get something like this (01:15:35) let's actually increase the intensity of (01:15:37) our opening snap let's bring it up a (01:15:38) little bit here opening stops right (01:15:40) there (01:15:41) now as a lot of volume of blood is (01:15:43) entering it's going to start off at the (01:15:44) highest peak high volume high velocity (01:15:46) right (01:15:48) it's going to be a lot of velocity and (01:15:49) then there's going to be a lower (01:15:50) velocity of blood okay as less blood is (01:15:54) actually present there's going to be (01:15:55) less blood that's flowing across that (01:15:56) area so now there's going to be a high (01:15:59) intensity moving towards a low intensity (01:16:02) holy crap that looks just like (01:16:06) aortic regurgitation and pulmonic (01:16:07) regurgitation doesn't it the only real (01:16:10) kind of difference here is that well (01:16:11) there's a couple differences here so (01:16:13) there's still a diastolic de crescendo (01:16:16) type of murmur let's actually kind of (01:16:18) separate these a little bit so we can (01:16:19) see the opening snap (01:16:20) so there's our opening snap right there (01:16:23) and then again right after that we have (01:16:25) the what is this (01:16:27) our diastolic (01:16:31) day (01:16:32) crescendo (01:16:34) we're murmur (01:16:39) but one of the big differences is that (01:16:41) you have an opening snap and the (01:16:42) diastolic day crescendo murmur you do (01:16:44) not have an opening snap and diastolic (01:16:46) or decrescendo are present in (01:16:49) aortic regurgitation and pulmonary (01:16:50) regurgitation that's one thing (01:16:52) second thing is we take into (01:16:54) consideration here that mitral stenosis (01:16:55) is the more common type of event here (01:16:58) mitral stenosis when we think about this (01:17:00) one it's going to be where where would (01:17:02) you hear it (01:17:03) left (01:17:04) fifth (01:17:05) intercostal space (01:17:07) mid-clavicular line (01:17:09) does it radiate there's actually none (01:17:10) that we didn't talk about radiation (01:17:11) there was no radiation particularly from (01:17:12) mitral stenosis okay good (01:17:14) the second thing is (01:17:15) not only is it that but also how do we (01:17:17) classify the stenosis well stenosis it (01:17:19) was going from atria to ventricles (01:17:21) that's a low pressure gradient but (01:17:22) there's a large volume of blood to try (01:17:24) and push across the valve early so that (01:17:26) would actually cause more of kind of a (01:17:28) unfortunately it's not generally enough (01:17:29) to get the pitch up high enough but it (01:17:31) is a low pitch but on top of that we (01:17:33) kind of just define any kind of like (01:17:35) mitral stenosis or tricuspid stenosis (01:17:39) or aortic stenosis we define those more (01:17:41) as like a kind of like a harsh or (01:17:42) rumbling type of sound you know we (01:17:45) actually give particularly from mitral (01:17:46) stenosis and tricuspid stenosis we use (01:17:49) the term a rumbling quality (01:17:52) so we prefer to use harsh for the aortic (01:17:54) stenosis (01:17:55) and pulmonic stenosis and we prefer to (01:17:57) use the rumbling terminology for the (01:18:00) mitral stenosis and the tricuspid (01:18:01) stenosis so we call this a diastolic (01:18:04) decrescendo (01:18:05) rumbling murmur for mitral and tricuspid (01:18:08) whereas this is a diastolic decrescendo (01:18:10) blowing murmur for (01:18:13) aortic and (01:18:14) pulmonic regurgitation (01:18:16) [Music] (01:18:31) okay we've covered the diastolic murmurs (01:18:34) let's move into the next one which is (01:18:35) the continuous murmurs all right so (01:18:37) let's talk about continuous murmurs (01:18:38) continuous murmurs are interesting in (01:18:39) the sense that they occur throughout the (01:18:40) entire systole and diastole right so (01:18:42) again if we were to take care of our (01:18:43) cardiac cycle here looking at the heart (01:18:45) sounds we have s1 closure of mitral (01:18:47) tricuspid valve onset of ventricular (01:18:49) systole s2 closure of aortic and (01:18:51) pulmonic valve onset of ventricular (01:18:53) diastole back into s1 (01:18:56) if it's a continuous murmur it's going (01:18:57) to have to occur throughout systole and (01:18:59) throughout diastole right so between s1 (01:19:01) s2 and between s2 to s1 now what would (01:19:04) be the particular reasons for that (01:19:05) whenever you hear (01:19:07) continuous murmurs you automatically (01:19:09) want to assume patent ductus arteriosus (01:19:11) pda so we'll call this patent (01:19:15) i'll be a good boy i'll actually write (01:19:16) this up peyton ductus (01:19:18) arteriosus but again we prefer to call (01:19:21) this we you know i like to say pda (01:19:24) not public to space and perfection but (01:19:26) paid ductus arteriosus (01:19:27) now what happens in patent ductus (01:19:29) arterios is that normally this has (01:19:31) happened in normal like fetal life there (01:19:33) is a little connection here so imagine (01:19:35) here you have the pulmonary artery (01:19:38) and the aorta there is this little like (01:19:41) connection here between the aorta and (01:19:44) the pulmonary artery and the whole (01:19:45) purpose of is whenever the baby is in (01:19:47) the amniotic fluid it's not breathing (01:19:48) and so we want not very much blood going (01:19:50) from the right ventricle to go to the (01:19:52) lungs so we divert it through that (01:19:54) little ductus arteriosus (01:19:57) into the aorta so that we bypass the (01:19:58) lungs (01:19:59) when you're born your left sided (01:20:01) pressures and throughout adulthood your (01:20:02) left hooded pressures are actually much (01:20:04) higher so your aortic pressure is much (01:20:06) higher than your pulmonary artery (01:20:08) pressure after birth so that's a big (01:20:10) thing that's one big thing to note is (01:20:11) that aortic (01:20:14) blood pressure not aortic aortic blood (01:20:17) pressure (01:20:18) aorta pressure (01:20:21) is much greater than the (01:20:24) pulmonary pressure and that honestly (01:20:25) does not matter at what point in time in (01:20:28) the cardiac cycle it's always higher (01:20:31) regardless if it's systolic (01:20:34) and diastolic that pressure is higher in (01:20:37) the aorta than the pulmonary pressure (01:20:39) so think about that for a second your (01:20:41) left ventricle pumps blood out (01:20:44) into the aorta when it goes into the (01:20:46) order obviously can go you know through (01:20:47) all the vessels all the branches of the (01:20:49) ord off the the branches off the aortic (01:20:52) arch down through the (01:20:53) descending aorta so and so forth but (01:20:55) then there's this other tube (01:20:57) where there's a high pressure in the (01:20:58) aorta so high pressure in the aorta (01:21:01) right in here (01:21:02) and then the pulmonary pressure is low (01:21:05) so then the pulmonary pressure (01:21:08) is low (01:21:10) blood can easily just flow from this (01:21:12) area (01:21:14) into this area (01:21:15) and that can happen during systole (01:21:18) and it can happen during diastole where (01:21:20) blood is just no matter what if blood is (01:21:22) in the aorta whether it's systole or (01:21:24) diastole it can continue to flow from (01:21:27) the aorta into the pulmonary artery (01:21:29) throughout systole and diastole because (01:21:31) as long as the pressure in the aorta is (01:21:32) greater than the pressure in the (01:21:33) pulmonary artery it doesn't matter as (01:21:34) long as their blood there's blood there (01:21:36) it's going to flow in that direction and (01:21:38) so what happens is this causes a (01:21:41) constant shunt (01:21:44) it causes a constant shunting of blood (01:21:45) if you will (01:21:47) from (01:21:50) aorta (01:21:52) to the pulmonary artery (01:21:55) via the patent ductus arteriosus (01:21:57) and that produces a continuous type of (01:22:00) murmur (01:22:01) so you would hear that during (01:22:03) systole (01:22:05) and you would hear that during diastole (01:22:08) now technically in this you would have (01:22:10) this continuous murmur as a very (01:22:12) interesting type of situation right and (01:22:14) actually what's interesting is usually (01:22:16) the intensity kind of increases (01:22:17) throughout systole because you're going (01:22:19) to have more of that blood shunting into (01:22:21) the (01:22:21) aorta and then eventually throughout (01:22:23) diastole (01:22:24) a less of that blood is shunting from (01:22:27) the aorta to the pulmonary trunk so it (01:22:28) kind of has like this in a way crescendo (01:22:31) during ventricular systole and kind of a (01:22:32) day crescendo during diastole but either (01:22:35) way it's kind of having this continuous (01:22:37) type of process that is occurring all (01:22:39) right so because there's this constant (01:22:41) shunt of blood from the from the again (01:22:42) the aorta into the pulmonary artery (01:22:44) during systole and diastole you get kind (01:22:46) of this nice little interesting type of (01:22:47) murmur here that you see continuous in (01:22:49) the sense that it's continuing to occur (01:22:51) during systole and continuing to occur (01:22:53) during diastole slight crescendo fashion (01:22:56) during between the ventricular systole (01:22:58) and then again slight decrescendo (01:23:00) fashion during the diastole what's (01:23:02) really interesting is where you would (01:23:03) hear this murmur and this is kind of the (01:23:05) one where it's just like super random (01:23:06) and that's why it's kind of easier to (01:23:08) remember in that sense (01:23:10) for patent ductus arteriosus you want to (01:23:12) listen on the left (01:23:14) kind of like infraclavicular region is (01:23:16) what we say so we say left (01:23:18) infra (01:23:21) infraclavicular area so left (01:23:23) infraclavicular (01:23:28) region (01:23:30) that's particular for the (01:23:33) pda so you want to listen to that left (01:23:35) infraclavicular area (01:23:37) okay so again here's your clavicle just (01:23:39) underneath the clavicle particularly is (01:23:41) where you're trying to listen for that (01:23:42) peyton ductus arteriosus it's a (01:23:43) continuous murmur (01:23:45) and here's another term that you can't (01:23:46) forget (01:23:47) not only is it continuous but we use the (01:23:49) term (01:23:50) it's machine like (01:23:53) it is a machinery or machine sounding (01:23:56) type of murmur that is continuous (01:23:58) throughout systole diastole left (01:24:00) infraclavicular region and it is machine (01:24:03) sounding okay (01:24:05) here's the next thing sometimes you can (01:24:07) hear this murmur (01:24:09) but you're listening on the right (01:24:11) infraclavicular region you're like is (01:24:13) this a pda (01:24:14) sometimes it's actually a very benign (01:24:16) finding and you want to have a (01:24:17) differential for that in that situation (01:24:20) where you find what's called a right (01:24:21) when you have right (01:24:23) infra (01:24:26) clavicular (01:24:28) a right infraclavicular murmur (01:24:32) that is continuous you want to think (01:24:34) about something called a (01:24:36) cervical (01:24:38) venous (01:24:39) hum (01:24:40) it is way more common that it's going to (01:24:42) occur on the right infraclavicular (01:24:44) region (01:24:45) less common that it does occur on the (01:24:46) left infraclavicular region let's say (01:24:48) though just just to kind of mess around (01:24:50) here let's say that you have this kind (01:24:52) of murmur that's present (01:24:54) this cervical venous hum (01:24:56) and it's on the left infraclavicular (01:24:57) region and you're like oh dang is this a (01:24:58) pda because it's continuous it sounds (01:25:00) somewhat machine like it's usually not (01:25:02) very loud as as intense and machine like (01:25:04) as a pda let's say that it's difficult (01:25:06) to differentiate it's a continuous (01:25:07) murmur here at the left infraclavicular (01:25:09) region what can i do to make me (01:25:11) definitely feel more comfortable that (01:25:13) it's likely a cervical venous hum in (01:25:15) comparison to a pda you can do a (01:25:16) particular maneuver what you can do is (01:25:19) you can have them flex their neck (01:25:23) when you flex their neck (01:25:25) and a patient with a cervical venous hum (01:25:27) the issue is the blood flow in the (01:25:28) internal jugular veins in this one (01:25:30) there's this kind of like continuous (01:25:31) blood flow through the internal jugular (01:25:33) veins and the turbulence within the (01:25:34) internal jugular vein is producing the (01:25:35) murmur if you have them flex their neck (01:25:38) you compress the internal jugular veins (01:25:41) or if you have them rotate their neck to (01:25:43) the side you compress the internal (01:25:45) jugular vein reducing the blood flow in (01:25:47) the internal jugular veins and that (01:25:48) would decrease the intensity to murmur (01:25:50) in a cervical venous human it would not (01:25:52) decrease the intensity to murmur a pda (01:25:55) man so this will decrease intensity (01:25:59) and the venous hum but it will not (01:26:02) increase the intense and not decrease (01:26:03) the intensity in the pda so again (01:26:06) continuous murmur please don't forget (01:26:09) pda due to a constant shunting of blood (01:26:11) from the aorta (01:26:12) into the pulmonary artery during systole (01:26:14) and diastole because its pressure is (01:26:15) higher it's heard in the left (01:26:17) infraclavicular region (01:26:18) it's also machine sounding (01:26:21) generally in this situation you may (01:26:24) think oh i hear a continuous murmur (01:26:26) around the right infraclavicular region (01:26:28) i think it could it be a pda (01:26:30) or let's say that you hear it on the (01:26:31) left infraclavicular region by some (01:26:34) potential chance and you think is this a (01:26:36) cervical venous hum or is this a pda i (01:26:38) don't know one's due to jugular venous (01:26:40) flow one is actually due to a patent (01:26:41) ductus arteriosus if i have them flex (01:26:44) their neck it'll compress their jugular (01:26:46) vein and reduce the intensity of the (01:26:47) murmur if it reduces the intensity of (01:26:49) mermaids or cervical venous hum if it (01:26:50) does not it is a pda (01:26:52) [Laughter] (01:27:02) boom shakalaka let's finish this up with (01:27:05) ways that we can change the intensity of (01:27:08) our murmur in senses that we can utilize (01:27:10) maneuvers or positions to increase the (01:27:13) intensity of the murmur decrease the (01:27:15) intensity of the murmur cause a click to (01:27:16) come early cause a click to come later (01:27:18) cause the murmur to be shorter causing (01:27:20) her to be louder we're gonna hit all (01:27:21) that let's do it all right so we've (01:27:23) really went pretty hard so far guys hang (01:27:26) in there with me we're almost there we (01:27:28) talked a lot about particularly the (01:27:30) physiology behind murmurs we talked (01:27:32) about the location the pitch the quality (01:27:34) the radiation the intensity of murmurs (01:27:36) we went over if they're in systolic type (01:27:38) of murmurs diastolic continuous what's (01:27:41) the configuration of the murmur we (01:27:43) really hit home on that but i think one (01:27:45) of the most important parts is that can (01:27:46) we do a particular maneuver or position (01:27:49) that changes the intensity of the murmur (01:27:51) to help me clinch the diagnosis let's (01:27:53) talk about that so the first one is (01:27:56) inspiration i think i kind of helped get (01:27:58) this in a way where it's easy to (01:27:59) remember (01:28:00) inspiration is one category (01:28:02) so inspiration when you take a deep (01:28:05) breath in you drop your inch of thoracic (01:28:06) pressure and when you drop your intro (01:28:08) thoracic pressure it creates the kind of (01:28:09) like vacuum effect that sucks blood into (01:28:11) the right side of the heart so you (01:28:13) increase right heart feeling so again (01:28:14) what happens with inspiration you drop (01:28:17) your intrathoracic pressure (01:28:19) because when you drop your intrathoracic (01:28:21) pressure by taking a deep breath in (01:28:24) that's going to (01:28:25) increase the venous return (01:28:28) if you increase venous return you (01:28:29) increase the right-sided filling (01:28:32) so all the murmurs on the right side (01:28:35) that are dependent upon that volume as (01:28:37) you have more blood on the right side of (01:28:38) the heart if you're pushing more blood (01:28:40) back into the atria and tricuspid (01:28:42) regurgitation that's going to increase (01:28:43) it if you're pushing more blood across (01:28:45) the tricuspid valve if you're pushing (01:28:47) more blood across the pulmonary valve (01:28:48) that's going to increase all the types (01:28:50) of right-sided murmurs so increasing (01:28:53) right filling increases the intensity (01:28:57) of (01:28:57) right (01:28:59) sided (01:29:00) murmurs (01:29:02) so that would infect which ones that (01:29:04) would alter the tricuspid stenosis (01:29:07) tricuspid regurgitation pulmonic (01:29:09) stenosis and pulmonic regurgitation boom (01:29:12) roasted let's move on to the next one (01:29:14) expiration (01:29:16) in expiration you actually are exhaling (01:29:19) it's going to do what to your (01:29:20) intrathoracic pressure increase the (01:29:22) intrathoracic pressure (01:29:23) when you increase the intrathoracic (01:29:25) pressure what you do is you actually (01:29:27) squeeze on the pulmonary vessels (01:29:29) so you increase your intra thoracic (01:29:32) pressure (01:29:33) and it squeezes on the pulmonary vessels (01:29:36) and that increases the venous return (01:29:38) particularly to the left side of the (01:29:40) heart so that increases left sided (01:29:42) filling (01:29:43) if you increase left side feeling now (01:29:45) you have more blood within the left (01:29:47) ventricle if there's more blood within (01:29:49) the left ventricle you can now increase (01:29:50) the blood flow across all these valves (01:29:52) or increase the regurgitation of volume (01:29:54) of blood across these valves that (01:29:56) increases the intensity of all (01:29:57) left-sided murmurs so that increases the (01:30:00) intensity (01:30:03) of all left-sided (01:30:05) murmurs (01:30:07) so that's one way that you can help to (01:30:09) differentiate between like pulmonic (01:30:10) stenosis and aortic stenosis aortic (01:30:13) regurgitation and pulmonic regurgitation (01:30:15) mitral stenosis tricuspisionosis you (01:30:17) guys get the point so this would affect (01:30:19) more the again mitral stenosis and (01:30:22) mitral regurgitation and aortic stenosis (01:30:25) aortic regurgitation boom good all right (01:30:28) next one (01:30:30) leaning forward what the heck does this (01:30:32) have to do with anything when you have a (01:30:34) patient lean forward what you do is you (01:30:36) bring their aorta and they already valve (01:30:39) closer to the chest wall so any type of (01:30:42) murmur or any kind of like abnormality (01:30:44) that is close to the order close to the (01:30:46) aortic valve is going to increase the (01:30:48) intensity of that murmur so if you lean (01:30:51) forward you bring (01:30:53) the aorta (01:30:55) and aortic valve (01:30:58) close (01:31:00) to the chest wall (01:31:03) and that will (01:31:04) increase the intensity (01:31:07) of those murmurs (01:31:09) that are close to the aorta and the (01:31:11) aortic valve what types of murmurs are (01:31:12) close to the aortic aortic valve (01:31:14) oh my gosh we're so good at this (01:31:16) aortic stenosis (01:31:18) aortic regurgitation (01:31:21) hypertrophic obstructive cardiomyopathy (01:31:22) believe it or not two (01:31:25) and one more (01:31:26) co-rectation of the order we never (01:31:27) really talked about that but again it (01:31:29) was a type of systolic ejection murmur (01:31:31) right early systolic murmur and again it (01:31:33) didn't have a click but it usually hurt (01:31:34) the left posterior hemi thorax and again (01:31:37) this one would also could be heard (01:31:39) easily if you had them lean forward i (01:31:41) would put more of an emphasis of leaning (01:31:43) forward on aortic stenosis and vertical (01:31:44) regurgitation though okay (01:31:47) what else (01:31:48) keep moving on keep moving on all right (01:31:50) so the next thing i want you guys to (01:31:51) think about (01:31:53) is something called the left lateral (01:31:54) decubitus position so the left lateral (01:31:56) decubitus position (01:31:58) is when you have a patient lay on their (01:31:59) side so you're having that you can (01:32:00) either have them lay supine and then you (01:32:02) put them on their side so they're laying (01:32:03) on their left side (01:32:05) and what you're doing is you're bringing (01:32:06) the mitral valve and even part of the (01:32:08) apex closer to the chest wall which will (01:32:11) increase the the audible since the (01:32:13) audible ability to adhere or increase (01:32:15) the intensity of abnormalities near the (01:32:18) mitral valve (01:32:20) so it brings (01:32:23) mitral valve (01:32:25) closer to the chest wall (01:32:29) and if you do that you're going to (01:32:30) increase the intensity of (01:32:33) the murmurs in that vicinity increase (01:32:35) the intensity (01:32:38) of (01:32:39) murmurs near the mitral valve so this (01:32:41) would include mitral stenosis (01:32:44) mitral regurgitation (01:32:45) and mitral valve prolapse man we good (01:32:49) all right so inspiration increase the (01:32:51) intensity of right side of murmurs (01:32:53) expiration increase the intensity of (01:32:54) left-sided murmurs leaning forward (01:32:56) bringing the aortic valve closer aortic (01:32:58) closer increase the intensity of aortic (01:33:00) stenosis and aortic regurge laying on (01:33:02) their left side increasing the intensity (01:33:04) of mitral stenosis mitral regards mitral (01:33:06) valve prolapse (01:33:07) okay the next one which is really high (01:33:09) yield (01:33:11) is squatting and passive leg raise what (01:33:14) does this do when you squat down (01:33:17) you squeeze out you actually contract (01:33:19) your muscles and squeeze on some of the (01:33:20) veins in the lower extremity and push (01:33:22) blood up to the heart (01:33:24) okay so when you squat or if you're (01:33:27) having a patient lay flat and you lift (01:33:28) their legs you're having blood drain (01:33:31) from their legs into their abdomen up to (01:33:33) their heart and again that helps to (01:33:34) increase venous terms but either way (01:33:35) these two mechanisms what they do (01:33:38) is they increase (01:33:40) venous (01:33:41) return (01:33:43) if you increase venous return you (01:33:45) increase what's called the preload to (01:33:47) the heart (01:33:48) right you increase preload of the heart (01:33:51) when you increase the preload of the (01:33:53) heart you're going to increase what else (01:33:57) this generally increases the intensity (01:34:02) of all murmurs (01:34:05) because you're going to have more stroke (01:34:06) volume so what happens is if you have a (01:34:08) higher preload you have a higher stroke (01:34:10) volume and so you're going to have more (01:34:11) blood that can flow across valves or (01:34:14) like in the stenotic in a forward way so (01:34:16) more blood flowing across the stenotic (01:34:18) lesion or more blood that can flow (01:34:20) backwards across a valve in a situation (01:34:24) of an incompetent valve during (01:34:25) regurgitation so what i want you to (01:34:27) remember is increased venous return (01:34:29) increases preload increase the stroke (01:34:31) volume which will cause more blood to (01:34:32) flow forward or more blood to flow (01:34:35) backwards so in a stenotic valve more (01:34:38) blood will flow across that and a (01:34:39) regurgitated valve or incompetent valve (01:34:41) more blood will flow across that it (01:34:42) increased the intensity of all murmurs (01:34:44) with two exceptions so i want you to (01:34:47) remember these two exceptions (01:34:49) so the exceptions to this (01:34:52) is what's called hypertrophic (01:34:53) obstructive cardiomyopathy and mitral (01:34:55) valve prolapse that's what i want you to (01:34:57) remember (01:34:58) increasing venous return increases (01:35:00) preload increases stroke volume (01:35:02) increases forward flow across the (01:35:03) sonatic valve and backward flow across a (01:35:05) regurgitant valve that increase the (01:35:07) intensity of all murmurs with two (01:35:08) exceptions hcm or hypertrophic (01:35:10) obstructive cardiomyopathy and mitral (01:35:12) valve prolapse let's explain why that is (01:35:14) an exception (01:35:16) because we it's easy to remember this (01:35:18) right (01:35:19) it's easy to remember this part (01:35:21) but then we have to make sense as to why (01:35:24) squatting increase the intensity of all (01:35:26) murmurs except these (01:35:28) okay (01:35:29) and hypertrophic obstructive (01:35:30) cardiomyopathy here's what i want you to (01:35:32) think about (01:35:33) you have in this situation here is your (01:35:35) hypertrophic obstructive cardiomyopathy (01:35:38) you have a increased venous return (01:35:42) all right (01:35:43) that means that there's going to be more (01:35:45) volume in the left ventricle what is (01:35:48) that called when there's more volume in (01:35:49) the left ventricle especially during (01:35:50) diastole there's what's called a (01:35:52) increase in left ventricular in (01:35:54) diastolic volume okay (01:35:57) in hypertrophic obstructive (01:35:59) cardiomyopathy their problem is they (01:36:01) have a asymmetric hypertrophy of their (01:36:05) septum so their septum's like this (01:36:07) it's bowing inwards and blocking this (01:36:10) left ventricular offal tract it's (01:36:12) difficult to get blood through that area (01:36:13) and that's causing a murmur (01:36:15) which type of murmur systolic injection (01:36:17) remember really which one early early (01:36:19) systolic murmur (01:36:20) now (01:36:21) if i have all of this volume that i'm (01:36:23) increasing venus return by squatting or (01:36:24) passive leg raises (01:36:26) i have more volume and what that's going (01:36:28) to do is that volume is going to try to (01:36:29) stretch and push down and mash down on (01:36:31) that dynamic obstruction (01:36:33) so what i'm trying to do by this (01:36:36) is decrease the intensity or decrease (01:36:38) the obstruction of that left ventricular (01:36:41) outflow tract so imagine now if i have (01:36:43) more blood i can stretch this this (01:36:45) actual (01:36:46) outflow tract out more and so it (01:36:48) decreases what's called the left (01:36:50) ventricular outflow tract obstruction (01:36:53) i know that's a lot but it's decreasing (01:36:55) that dynamic obstruction (01:36:57) if you decrease the dynamic obstruction (01:36:58) that means more (01:37:00) increased blood flow (01:37:02) across that area (01:37:05) and if there's an increased blood flow (01:37:07) across that area do you think it's going (01:37:08) to make as tense intense of a type of (01:37:10) crescendo decrescendo murmur now no (01:37:13) because i relieved their dynamic (01:37:15) obstruction which was causing their (01:37:17) crescendo decrescendo murmur if i have (01:37:19) more volume on stretching out the (01:37:20) dynamic obstruction relieving the (01:37:22) obstruction opening up that area for (01:37:24) more blood to flow through easily in (01:37:26) comparison to it normally (01:37:29) and so this will do what to the (01:37:30) intensity of the murmur (01:37:32) this will (01:37:34) decrease (01:37:35) the hypertrophic obstructive (01:37:37) cardiomyopathy murmur (01:37:40) so normally increased venous return from (01:37:43) squatting or passive leg raise increases (01:37:45) the intensity of all murmurs (01:37:47) except for hypertrophic obstructive (01:37:49) cardiomyopathy because it stretches out (01:37:51) the obstruction (01:37:52) opening up that left ventricular outflow (01:37:54) tract more blood can flow across that (01:37:56) area and it decreases the hypertrophic (01:37:59) obstructive cardiomyopathy murmur oh wow (01:38:02) okay what about mitrova prolapse (01:38:05) this is the next one (01:38:06) mitral valve prolapse we got to talk (01:38:08) about two scenarios (01:38:10) normally (01:38:12) what happens (01:38:13) and then when there is increased venus (01:38:16) return (01:38:17) okay normal mitral valve prolapse what (01:38:20) happens is you get something to click (01:38:22) right you'll get the click something (01:38:23) like this let's actually do a different (01:38:24) color let's do the click which happens (01:38:27) around mid systole right (01:38:29) so you get the click and that click (01:38:31) sound is due to the bowing or prolapsing (01:38:33) of the (01:38:34) leaflet into the atrium (01:38:36) then after that you get the what type of (01:38:39) murmur you get the regurgitation murmur (01:38:40) that can also present there okay now (01:38:43) here's where it gets cool (01:38:45) in a patient who has mitral valve (01:38:48) prolapse you increase their venous (01:38:49) return here's the way i like to remember (01:38:51) it it's i don't know why it just helps (01:38:52) me remember (01:38:53) if you increase venous return think (01:38:55) about the ventricle being more filled so (01:38:57) think about this being the space of the (01:38:59) ventricle so here's my ventricle (01:39:01) okay that's my ventricle with a little (01:39:03) space there so here i'll kind of stride (01:39:04) it a little bit for you here's my (01:39:06) ventricle (01:39:07) that's normal filling now what i'm going (01:39:09) to do is i'm going to fill it up more (01:39:10) because i'm increasing the venous return (01:39:12) [Music] (01:39:13) oh baby if i increase this bad boy (01:39:17) and i have it have more venous return (01:39:19) what happens now there's only a small (01:39:20) amount of distance for the click of the (01:39:21) murmur (01:39:23) uh oh (01:39:24) the click will come a lot later (01:39:28) and the murmur will be much shorter (01:39:31) now obviously this isn't why it happens (01:39:33) but it's easy to remember it this way (01:39:35) more volume (01:39:36) in this situation your left ventricle is (01:39:39) going to have a lot more volume it's (01:39:40) going to take a longer time for it to (01:39:42) contract and push all that blood against (01:39:45) the mitral valve to shut it so it just (01:39:47) happens a little bit later where the (01:39:48) comes later because now the left (01:39:50) ventricle is filled with all this blood (01:39:51) it has to contract and squeeze all that (01:39:53) blood it takes a little bit more time to (01:39:54) squeeze all that blood out of the heart (01:39:56) or close the mitral valve but an easy (01:39:59) way to remember that is more volume (01:40:03) there's less room for that click now (01:40:05) less room for the murmur so the (01:40:07) comes (01:40:08) later so we say the click (01:40:10) is later (01:40:12) and the murmur (01:40:15) is shorter (01:40:18) okay so what can we say whenever we have (01:40:20) someone squat or do a passive leg raise (01:40:22) it increases venous return which (01:40:24) increases preload increasing stroke (01:40:25) volume blood flow across the stenotic (01:40:27) valve blood flow across a regurgitated (01:40:29) valve (01:40:30) increasing the intensity of all of those (01:40:32) murmurs two exceptions hypertrophic it (01:40:35) relieves the obstruction to have more (01:40:36) venous return decreases the intensity of (01:40:38) the murmur mitral valve prolapse it (01:40:41) causes more volume takes a longer time (01:40:43) for the left ventricle to depolarize a (01:40:45) longer time before it actually causes (01:40:47) the mitral valve 2 prolapse in the (01:40:49) associated murmur and so the click comes (01:40:52) later and the murmur is shorter easy way (01:40:54) to remember it think about the ventricle (01:40:56) is the space between when the comes (01:40:58) if there's a larger ventricle meaning (01:41:00) it's more filled the click will come (01:41:01) later and the murmur will have to be (01:41:03) shorter which is going to make this (01:41:04) stuff a lot easier now all right so (01:41:06) let's talk about the next thing which is (01:41:07) the val zavas maneuver or standing (01:41:10) falzaf's maneuver is an interesting way (01:41:12) it's a it's a way of decreasing venus (01:41:14) return it's you know whenever you try to (01:41:15) poop you know you're trying to get (01:41:16) chocolate rain to flood from your (01:41:17) hershey highway when that situation (01:41:18) happens you're bearing down you're like (01:41:20) you're going to drop this bboy and when (01:41:22) you do that you close off your glottis (01:41:24) and increase your intrathoracic pressure (01:41:26) all right that's what you're doing (01:41:27) you're increasing your intrathoracic (01:41:28) pressure (01:41:29) when you increase your (01:41:31) intrathoracic pressure (01:41:34) from the valsava's maneuver (01:41:38) that is actually going to create less of (01:41:39) a vacuum effect to pull blood up into (01:41:42) the heart and to the right of the heart (01:41:43) so you're going to reduce the venous (01:41:44) return to the heart because you're (01:41:45) increasing intrathoracic pressures can (01:41:47) be harder to bring blood from your (01:41:48) inferior vena cava or super vena cava (01:41:50) into the heart because there's such a (01:41:51) high pressure inside of the chest things (01:41:52) like to go from areas of high pressure (01:41:53) low pressure if your chest and your (01:41:56) chest pressure is really high you're not (01:41:57) going to yank blood into the heart from (01:41:59) the inferior and superior vena cava (01:42:01) so because of that you get a decrease in (01:42:04) venous return (01:42:06) if there is a decrease in venous return (01:42:08) what does that do (01:42:09) decreasing venous return will actually (01:42:11) cause there to be less preload (01:42:13) if there's less preload that will (01:42:15) decrease stroke volume that means less (01:42:17) blood is across the stenotic lesion and (01:42:19) less blood is going to flow across the (01:42:20) incompetent valve and regurgitant lesion (01:42:23) that means that there's going to be a (01:42:25) decreased (01:42:28) intensity (01:42:30) of all murmurs (01:42:35) both the right and left-sided (01:42:37) with (01:42:38) two exceptions (01:42:41) and what is those exceptions the (01:42:43) exceptions for this situation here would (01:42:45) be hypertrophic obstructive (01:42:47) cardiomyopathy let's actually keep it (01:42:49) the same kind of consistent here that we (01:42:50) put hypertrophic obstructive (01:42:51) cardiomyopathy and mitral valve prolapse (01:42:55) okay so again big thing to think about (01:42:58) is in stan whenever you have someone (01:43:00) squatting or passive leg raise you (01:43:01) increase the intensity of all their (01:43:02) members because you increase their (01:43:04) venous return in val zava and standing (01:43:06) you increase their intrathoracic (01:43:08) pressure dropping their venous return (01:43:10) decrease the intensity of all murmurs (01:43:12) except for these why okay this should (01:43:14) actually be relatively easy now (01:43:16) because we're just repeating what we did (01:43:18) in this situation for hypertrophic (01:43:20) obstructive cardiomyopathy (01:43:22) you have a reduction in venous return (01:43:26) okay because of this process (01:43:28) when you have a reduction of venous (01:43:29) return you get less blood that's filling (01:43:31) into the ventricles (01:43:32) especially at the end of diastole so (01:43:34) there's a reduction in the left (01:43:35) ventricular in diastolic volume in (01:43:38) patients who have less of the volume in (01:43:40) the heart are they going to relieve the (01:43:43) left ventricular outflow tract (01:43:44) obstruction well there's less volume (01:43:46) no you're not going to have as much of (01:43:48) the blood to stretch out the heart so (01:43:49) you're not going to stretch out the (01:43:51) left ventricular outflow tract (01:43:53) obstruction (01:43:54) so imagine if there's a lot of volume (01:43:55) you'll stretch it out if there's very (01:43:56) little volume now the obstruction is (01:43:59) worse (01:44:00) so now i increase the left ventricular (01:44:02) outflow tract obstruction (01:44:04) now imagine having to squeeze blood (01:44:07) through this little area (01:44:09) oh my gosh very little blood is going to (01:44:10) flow through that area so there's going (01:44:12) to be decreased blood flow (01:44:17) across that area (01:44:20) and that is going to do what to the (01:44:21) intensity of the hypertrophic (01:44:22) obstructive cardiomyopathy it's going to (01:44:24) intense it like a mofo so you're going (01:44:26) to have a high intensity murmur so it's (01:44:28) going to increase the intensity of the (01:44:32) hypertrophic obstructive cardiomyopathy (01:44:34) murmur (01:44:35) all right we're pretty good now (01:44:37) microvap prolapse (01:44:39) is the next one so with mitral valve (01:44:40) prolapse we're going to talk about this (01:44:41) one nitro valve prolapse we have the two (01:44:44) scenarios here same thing we have the (01:44:45) normal (01:44:46) mitral valve prolapse there's no change (01:44:48) no maneuvers (01:44:50) and then we have whenever we're trying (01:44:52) to drop the venous return (01:44:54) now remember what happens in the normal (01:44:56) situation is you have again eventually (01:44:58) the left ventricle contracts bows the (01:45:00) leaflet of the mitral valve into the (01:45:01) atria and causes a click (01:45:03) and then an associated murmur okay (01:45:06) now (01:45:08) the left ventricle was filled (01:45:10) normally (01:45:13) in this situation now we're going to (01:45:15) fill it even less oh my gosh i don't (01:45:17) even know i can do this but they're (01:45:18) going to have a little ventricle right (01:45:19) there a little baby ventricle now it's (01:45:22) not filled very much and so because it's (01:45:23) not filled very much it's not going to (01:45:24) take a long time before it actually (01:45:26) generates enough pressure to close the (01:45:27) mitral valve (01:45:28) look what happens now to the injection (01:45:31) click it comes much earlier (01:45:33) it becomes much earlier now the murmur (01:45:37) is much longer right it's a (01:45:40) straightforward concept now if the (01:45:42) ventricle's smaller because they're not (01:45:44) filling it as much it's not going to (01:45:45) take a long time for it to be able to (01:45:47) contract that blood squeeze it up (01:45:49) against (01:45:49) to smash the mitral valve closed in this (01:45:52) case prolapse the mitral valve so that (01:45:54) click will come (01:45:55) earlier (01:45:57) so the click will come (01:46:00) earlier (01:46:02) dang markers the click will come earlier (01:46:04) and then what else will happen (01:46:06) not only will the click come earlier (01:46:09) but (01:46:10) the murmur will be longer (01:46:11) so the click will come (01:46:14) early (01:46:15) and the murmur (01:46:18) is longer (01:46:20) so to quickly submit that valzava (01:46:22) standing you reduce venus return reduce (01:46:26) the intensity of all murmurs with two (01:46:27) exceptions hypertrophic obstructive (01:46:29) cardiomyopathy you have less venous (01:46:31) return less (01:46:32) left ventricular end diastolic volume (01:46:34) you have more (01:46:36) left ventricular outflow attractive (01:46:37) obstruction because you're not expanding (01:46:38) or stretching out that obstruction (01:46:40) you're increasing the intensity of the (01:46:42) murmur (01:46:42) mitral valve prolapse (01:46:44) you're having less venous return less of (01:46:46) that volume of blood in the left (01:46:48) ventricle less time for the left (01:46:49) ventricle to contract and smash the (01:46:51) mitral valve closed or in this case (01:46:53) prolapse the mitral valve in (01:46:55) causing the click to come early and the (01:46:57) murmur to be longer and again think (01:46:59) about the little space there a little (01:47:01) ventricle the click has to come early (01:47:02) and now the murmur has to be longer (01:47:06) ah we done did it we're almost there (01:47:08) we're at the last part here which is now (01:47:10) the things that change after little (01:47:11) let's now talk about maneuvers such as (01:47:12) the hand grip maneuvers and a drug (01:47:14) called ammo nitrate all right so we're (01:47:16) at the last part guys all right we're at (01:47:18) hand grips what does this do what the (01:47:20) heck does this do so with hand grips (01:47:21) what you're doing is you're squeezing on (01:47:23) something right so you're squeezing on (01:47:24) something and you're increasing the (01:47:26) resistance of in the vessels right so (01:47:29) whenever you do the hand grip maneuver (01:47:30) what this does is this increases your (01:47:32) systemic vascular resistance when you (01:47:35) increase resistance that increases after (01:47:38) load right so it's going to increase (01:47:40) your afterload when you increase after (01:47:43) load (01:47:45) it makes it harder for the left (01:47:46) ventricle in this case we're talking (01:47:48) about left-sided murmurs it increases (01:47:51) the difficulty by which the left (01:47:52) ventricle has to pump blood out of the (01:47:54) heart so a high afterload actually drops (01:47:57) your stroke volume (01:47:59) if you drop stroke volume you decrease (01:48:01) the volume of blood that's leaving the (01:48:04) left ventricle (01:48:06) so i'm going to have a reduction in (01:48:08) forward (01:48:10) flow (01:48:10) you can think about right (01:48:12) why is that a particular problem (01:48:15) if i have a stenotic valve right i have (01:48:18) a patient who has what's called aortic (01:48:20) stenosis (01:48:21) their murmur is louder when there's (01:48:23) higher velocities of blood higher (01:48:25) volumes of blood that's flowing across (01:48:27) that stenotic valve right (01:48:29) if there's less velocity and less volume (01:48:32) of blood flowing across that stenotic (01:48:33) valve do you think the murmur's going to (01:48:34) be more intense or less intense less (01:48:36) intense and so it decreases the (01:48:39) intensity of that murmur (01:48:42) okay good (01:48:43) next thing (01:48:44) so this will cover this part here (01:48:47) the other thing that you need to (01:48:48) remember is that not only a reduction in (01:48:50) stroke volume causes less forward flow (01:48:53) but you can think about it the opposite (01:48:54) way (01:48:55) is that there is more blood (01:48:59) left (01:49:00) in the ventricles (01:49:02) because i didn't pump as much out and so (01:49:04) if there's more blood in the ventricles (01:49:06) that means that you can think about the (01:49:08) ventricles kind of being over filled (01:49:10) with blood because we didn't pump as (01:49:11) much of it out (01:49:13) if the ventricles are overfilled with (01:49:14) blood think about what that did to (01:49:16) hypertrophic obstructive cardiomyopathy (01:49:19) and what it did to mitral valve prolapse (01:49:21) what did it do to it guys well think (01:49:23) about that if you have more blood in the (01:49:26) ventricles for hcm what did that do you (01:49:28) had more blood it stretched out the (01:49:30) dynamic obstruction so that decreased (01:49:32) the left ventricular outflow tract (01:49:34) obstruction and that decreased the (01:49:36) intensity (01:49:38) of the murmur (01:49:40) it's not too bad (01:49:41) all right (01:49:42) what about mitrov prolapse (01:49:45) in mitral valve prolapse you cause the (01:49:47) ventricle to get filled larger and we (01:49:48) could use that diagram to make it easy (01:49:50) right the more you fill that ventricle (01:49:52) with blood (01:49:54) then the click will come later and the (01:49:56) murmur will be shorter you can also (01:49:58) think about it as the ventricle fills (01:50:00) with more blood it's going to take a (01:50:01) longer time for it to contract and push (01:50:03) all that blood out of the heart it's (01:50:04) going to take a longer time for it to (01:50:06) prolapse that mitral valve so the click (01:50:07) will come later and the murmur will be (01:50:09) shorter so in this situation you'll have (01:50:12) the click (01:50:13) come later (01:50:15) and the murmur (01:50:17) be shorter in duration (01:50:20) and the last thing to think about here (01:50:21) is actually another condition here and (01:50:23) this is actually kind of a lone wolf (01:50:25) associated with it mitral regurgitation (01:50:27) we never talked about this one but i (01:50:29) want you guys to think about it (01:50:30) and a patient has mitral regurgitation (01:50:32) think about (01:50:34) murmurs in the sense of an increase in (01:50:36) blood flow across a stenotic valve or an (01:50:38) increase in blood flow or backflow (01:50:41) across a incompetent valve causes a (01:50:44) murmur right (01:50:45) so if i have a regurgitant flow of blood (01:50:47) across an incompetent valve what do you (01:50:48) think that's going to do to the (01:50:49) intensity of that murmur i have more (01:50:51) volume of blood that i can pump (01:50:54) against (01:50:55) that actual left atria if there's an (01:50:57) incompetent mitral valve (01:50:58) it's going to increase the intensity of (01:51:00) the murmur and so this will increase the (01:51:02) intensity (01:51:04) of mitral regurgitation because i have (01:51:07) more blood that's flowing back into the (01:51:09) atria across that incompetent valve (01:51:12) okay (01:51:13) so we know (01:51:14) hand grip maneuvers increase afterload (01:51:16) which reduces the intensity of aortic (01:51:18) stenosis reduces the intensity of (01:51:20) hypertrophic obstructive cardiomyopathy (01:51:22) causes the click and mitral valve (01:51:24) prolapse to come later the murmur to be (01:51:26) shorter and increases the intensity of (01:51:28) mitral regurge you'd think we'd be done (01:51:30) right but we're not (01:51:32) okay (01:51:33) what about the aortic stuff (01:51:35) okay (01:51:37) in these hand grip maneuvers again we (01:51:39) increase the systemic vascular (01:51:41) resistance (01:51:42) if we increase the systemic vascular (01:51:44) resistance you increase the afterload (01:51:47) we got that down all right that makes (01:51:48) sense (01:51:49) if you increase the output here's the (01:51:51) next way i want you to look at it not (01:51:52) only is it reducing the stroke volume (01:51:54) but it's causing the pressure in the (01:51:56) aorta to be higher and that's the reason (01:51:58) for the lower stroke volume so you have (01:52:00) higher (01:52:01) aortic (01:52:02) pressures (01:52:04) if there's high aortic blood pressures (01:52:07) then that's okay as long as the (01:52:09) you know valve is functional right (01:52:11) you'll just have a drop in stroke volume (01:52:13) that's the whole problem is that (01:52:14) normally this will just cause a (01:52:16) reduction in stroke volume (01:52:18) but that's if you have a normal valve (01:52:20) if you have an incompetent or leaky (01:52:22) valve (01:52:24) guess why that is a problematic issue if (01:52:26) they have an incompetent valve (01:52:31) all that blood and that high pressure (01:52:34) vessel is going to flow backwards (01:52:37) into the left ventricle (01:52:39) and so you'll have an increase (01:52:41) backflow (01:52:43) a regurgitant flow back into the left (01:52:46) ventricle (01:52:47) and if that's the case that will (01:52:48) increase the intensity (01:52:51) of (01:52:53) aortic regurgitation (01:52:55) that's why having high afterload is not (01:52:57) a good thing that's why in patients who (01:52:58) have high orthotic regurgitation we (01:52:59) actually want to drop their afterload so (01:53:00) they have less of black flow across that (01:53:03) incompetent valve we'll talk about that (01:53:04) in this next step but (01:53:06) to recap (01:53:07) hand grips increase afterload (01:53:10) it does three things (01:53:12) one red reduces your stroke volume (01:53:14) reduces forward flow decrease intensity (01:53:15) of aortic stenosis causes more blood to (01:53:18) remain in the ventricle particularly (01:53:19) left ventricle stretches out the dynamic (01:53:21) obstruction decreasing hcm intensity (01:53:23) causes it to be overfilled within the (01:53:25) left ventricular taking a longer time to (01:53:26) depolarize contract and cause the mitral (01:53:28) valve prolapse click which it comes (01:53:30) later and the murmur's then subsequently (01:53:32) shorter and it causes more volume of (01:53:34) blood to get pushed across an (01:53:36) incompetent mitral valve causing a (01:53:38) mitral regurgitation member to be more (01:53:39) intense (01:53:41) it also increases afterload causing the (01:53:43) aortic pressure to be high which isn't a (01:53:44) problem if you have a good valve but if (01:53:47) you have an incompetent leaky valve then (01:53:49) you're going to have a massive backflow (01:53:51) of blood from the aorta into the left (01:53:52) ventricle which if you have aortic (01:53:54) regurgitation this will just increase (01:53:56) the intensity of it boom shakalaka (01:53:59) okay (01:54:01) oh and engineers before we pass out here (01:54:04) let's talk about um the last thing which (01:54:06) is how we can use something something to (01:54:08) actually reduce afterload and this is (01:54:09) ammo nitrate so ammo nitrate is a drug (01:54:12) and what this does is it actually causes (01:54:14) it'll cause vasodilation (01:54:17) okay so it'll vasodilate just like (01:54:18) whenever you do hand grips you (01:54:20) vasoconstrict which increases the (01:54:21) systemic vascular resistance right so (01:54:23) hand grips just cause vasoconstriction (01:54:25) so if we were to write that down here (01:54:26) hand grips all they do (01:54:28) is they (01:54:29) cause (01:54:31) vaso (01:54:33) constriction (01:54:35) and that increases systemic vascular (01:54:36) resistance with ammo nitrate you (01:54:38) vasodilate which does what (01:54:41) it (01:54:42) reduces systemic vascular resistance if (01:54:44) you reduce systemic vascular resistance (01:54:46) that reduces your (01:54:49) afterload is if you reduce your (01:54:52) afterload you increase your stroke (01:54:54) volume if you increase your stroke (01:54:56) volume (01:54:59) you increase your forward flow this is (01:55:02) going to be so easy now guys (01:55:04) if you increase your aortic flow in a (01:55:05) patient who has aortic stenosis that (01:55:07) means that more blood flow more velocity (01:55:09) is flowing across that aortic valve (01:55:12) if more blood is flowing across that (01:55:13) stenotic valve you're going to have an (01:55:15) increase in the intensity (01:55:18) of that murmur (01:55:22) boom (01:55:24) if you have a higher stroke volume that (01:55:26) means that you have (01:55:27) a decreased volume (01:55:30) of blood (01:55:33) in the ventricles remaining in the (01:55:35) ventricles because you're ejecting all (01:55:37) of it out (01:55:38) if you have very little blood within the (01:55:40) ventricles what did that do to the hcm (01:55:41) it's the exact opposite now right so for (01:55:44) hypertrophic obstructive cardiomyopathy (01:55:47) it's going to cause what to the left (01:55:48) ventricular outflow attract we have less (01:55:50) of it to stretch it out that's going to (01:55:52) increase the left ventricular outflow (01:55:54) tract obstruction and that's going to (01:55:56) increase the intensity of that murmur (01:56:00) boom (01:56:01) mitral valve prolapse (01:56:03) you're going to have less volume of (01:56:05) blood in the ventricle think about that (01:56:07) little diagram little little the filled (01:56:09) ventricle is going to cause the click to (01:56:11) come early and the murmur to be longer (01:56:14) or you can think about it being under (01:56:16) filled it's not going to take a long (01:56:17) time for the ventricle to contract and (01:56:18) prolapse that mitral valve causing it to (01:56:20) come early and the murmur will be (01:56:22) subsequently longer so the click will be (01:56:26) early (01:56:27) and murmur (01:56:30) will be (01:56:31) longer (01:56:34) next is again if you have someone who (01:56:36) has mitral regurgitation (01:56:39) you're going to have less volume of (01:56:40) blood in their left ventricle if there's (01:56:43) less volume of blood and they have an (01:56:44) incompetent or leaky mitral valve that (01:56:46) means that they can cause backflow into (01:56:48) that area but there's less volume of (01:56:50) blood less velocity of blood flow across (01:56:52) an incompetent valve that means it'll (01:56:54) decrease the intensity of that murmur so (01:56:56) in this situation you'll have a decrease (01:57:00) intensity (01:57:01) of the mitral (01:57:03) regurgitation (01:57:06) oh we're at the last part (01:57:08) in this last situation again we think (01:57:10) about ammo nitrate again it's going to (01:57:12) reduce systemic vascular resistance we (01:57:14) can look at in the sense of (01:57:16) increasing stroke volume right via the (01:57:18) reduction in afterload but the other way (01:57:20) we can look at this is high systemic (01:57:22) vascular resistance i'm sorry low (01:57:24) systemic vascular resistance lowers your (01:57:26) afterload (01:57:28) and what did that do to the aortic (01:57:29) pressure because again afterload is the (01:57:31) pressure that the left ventricle has to (01:57:32) overcome to push blood in the aorta if (01:57:35) the aortic pressure is really high that (01:57:36) means that the afterload's high if the (01:57:38) aortic pressure is low that means that (01:57:39) the after load is low (01:57:40) so it's going to lower the aortic blood (01:57:43) pressure (01:57:45) if you have (01:57:47) a competent valve (01:57:49) so if there's a competent valve what (01:57:51) will that do that'll increase your (01:57:53) stroke volume (01:57:54) but if you have a incompetent valve if (01:57:56) you have a competent valve that's not (01:57:58) going to be a problem blood won't (01:57:59) backflow and you'll be able to maintain (01:58:01) a good stroke volume okay (01:58:04) but if you have an incompetent valve (01:58:06) there may be some type of backflow if (01:58:08) there's an issue there right so if you (01:58:10) have a in (01:58:11) competent (01:58:14) valve (01:58:15) that could be an issue right there could (01:58:17) be backflow (01:58:19) but (01:58:21) if you compare this (01:58:23) to this situation where there was a high (01:58:25) afterload high aortic pressure (01:58:28) that means this pressure in this aorta (01:58:30) is dang near high and it is going to (01:58:32) flood down into the left ventricle blood (01:58:34) is going to flood down across that (01:58:35) incompetent valve causing an intensity (01:58:37) of that murmur way way more intense (01:58:41) if you have a low afterload (01:58:43) low aortic pressure the incompetent (01:58:45) valve even though it is present do you (01:58:47) think you're going to have as much (01:58:48) backflow if the pressure in this aorta (01:58:50) is lower (01:58:52) do you have as much backflow (01:58:54) no (01:58:55) because the pressure is lower because (01:58:56) you're going to be pushing a lot of (01:58:58) blood out (01:58:59) and there's going to be less of that (01:59:00) regurgitating flow back into the left (01:59:01) ventricle and so this will reduce (01:59:05) the backflow (01:59:06) and if you reduce the backflow (01:59:09) you reduce (01:59:11) the intensity (01:59:13) of the aortic regurgitation murmur (01:59:16) there's going to be less pressure in the (01:59:18) aorta and if there's an incompetent (01:59:20) valve there's going to be less backflow (01:59:22) because if there's high pressure it's (01:59:24) going to want to go to areas of low (01:59:25) pressure right but if there's not as (01:59:27) much high pressure in this area there's (01:59:29) not going to be as much blood back (01:59:30) flowing into the left ventricle as (01:59:32) compared to this situation there's high (01:59:33) afterload high aortic pressure (01:59:35) that's high pressure to low pressure (01:59:38) tons of blood will flow back into the (01:59:39) left ventricle because it's in a high (01:59:40) pressure system to a low pressure system (01:59:43) here you drop the afterload you drop the (01:59:45) aortic pressure not as much high (01:59:46) pressure to low pressure less backflow (01:59:49) less regurgitation and aortic regurg (01:59:52) ninja nurse before i pass out i thank (01:59:54) you guys so much for sticking along with (01:59:56) this video with me i hope it made sense (01:59:58) and i hope that you guys enjoyed it as (01:59:59) always until next time (02:00:01) [Music] (02:00:21) you