DIP Episode 176 - USMLE Step 1 Cardiology Review Series 6 (Cardiac Embryology)

Okay welcome my name is divine I'm a resident this is episode 176 of the Divine Intervention Podcasts and in this podcast I'm going to be continuing a comprehensive USM list of one cardiology review series so this will be series six and this will actually be the cardiac embryology podcast as promised and then one thing I'll go ahead and say is I'm actually attaching a slide it's just a simple like two slides literally to this podcast so you can download it at the bottom on the website and basically the thing I'm gonna I just showed diagram as I promised in the prior cardiac podcast that details the pathophysiology behind the tetralogy of the low this is just a diagram of always used to explain that concept to people and it has really helped a lot of people have that idea sticking their minds very well okay so let's jump right into cardiac embryology right so the thing is I will make another podcast hopefully in the future that details like the embryology like how you go from like essentially like D zero to like D like D 21 or something like that I'll do that later but basically to describe the embryology of the heart let's kind of study on week four right and easy way to remember that is week four right four chambers the heart has four chambers so that's just a nice way to keep that in mind so the thing is basically right there are these body four days that occur prior to week four right and after all those body four days have happened there is a street blood vessel that forms that street blood vessel will eventually become the heart and it's actually formed in the ventral portion of the body right so it's formed in the anterior body wall and the thing is this blood for this blood vessel blood actually flows in it in a cordal to cranial direction so it flows from the bottom to the top okay so it should essentially make sense right for doing with a straight tube that's

ultimately going to become the heart the most cordal structure should be like a blood returning structure like a vein right a structure that returns blood to the heart like a vein and really the embryology for this is the sinus venosus now on the flip side it should also make sense that the most cranial structure should be like some kind of blood removing structure right some kind of blood removing structure like an auto right and it so happens that the embryologic name for this is the truncus arteriosus okay so sinus venosus kind of like a vein truncus arteriosus kind of like an auto although the thing is the thing that I guess maybe throws in a little wrench here is that the beginning of the truncus arteriosus actually has a special name and it's known as the Bobus cordus the Bobus cordus is just almost like a subset of the truncus arteriosus is the very beginning of it and then we have the future hfuture ventricle they are like derived from the primitive hf and ventricle so the thing is as the heart tube again as this straight tube develops right the primitive hf the primitive ventricles they get larger right and the way they actually get larger is by assimilating nearby structures right the way I kind of think about it is almost like a gentrification sort of thing it's like okay you know what I want to expand my property by binds or on the properties and kind of bringing them on them I umbrella that's essentially what happens with the primitive hf and ventricles they get bigger by just assimilating their close cousins right so the primitive hf the incorporate some part of the sinus venosus into the adult final literature right and one thing that actually helps here that again occasionally your friends at the MBA me we throw on the USML exams is that the lumina of the primitive hf prior to that assimilation of the sinus venosus it's purely rough but the lumina pri

or to the lumina of that sinus venosus itself prior to assimilation into the primitive hf is purely smooth so the thing is that the assimilation of some parts of the sinus venosus is the primary mechanism behind us observing why you may have like rough walled and smooth walled regions of the hf right the rough walled regions of the hf those are your pectinit muscles the smooth walled regions those are your that's the those are the parts that are derived from the incorporated sinus venosus when really pretty much the same thing happens in the ventricles although the only difference is that the structure that is assimilated is the Bobus cordis right we again remember the Bobus cordis I said was the beginning of the truncus arteriosus now the thing is as that heart tube again that straight tube gets bigger and bigger a specific kind of fold in occurs some people call it cardiac looping and essentially the each area remember I said blood flow at least in that straight tube blood flowed in a cuddle to cranial direction right the thing is that each area that we at some point cuddle before doing the way that makes them like posterior and superior okay so posterior and superior the way I remember that is PSA and then the other one is the other one so post each of four posterior and superior and then the ventricles remember again the other things that ultimately squared blood right from from the heart so they were the most cranial part of this business that I talked about earlier right so the ventricles they were at some point cranial that you do for the way that makes them anterior and inferior okay so each year for the way that makes them posterior and superior ventricles for the way that makes them anterior and inferior right so it should actually then make sense to you why arteries live from the front wall of the heart in an adult because again remember these arteries drai

n ventricles right and then kind of like the reverse case is what obtains for veins so now that we've kind of talked about how the heart is set up let's talk about how blood flows in utero so let's talk about this in steps right so let's talk through like a couple of steps here so step one essentially is the ultimate source of oxygen for the fetus is the placenta right and the deoxygenated blood is delivered you know the placenta the placenta gives blood to the umbilical arteries that's step one and then in step two when the umbilical arteries pick up this blood I mean sorry wait let me back up for a second here let me collect my thoughts so the thing is the placenta is where gas exchange occurs in the fetus through that out there now the thing is that blood the deoxygenated blood that makes its way to the placenta to get oxygenated comes there through the umbilical arteries that's a pretty very high eautonom and then after the blood gets oxygenated it gets taken away in step two via the umbilical veins right so umbilical veins they have the highest oxygen tension of all the blood vessels in the body so the obelical veins picks up that blood right on that blood automatically flows to the IVC right but the thing is as the blood flows to the IVC the blood in the ovul in the obelical vein actually bypasses the portal circulation right remember the portal circulation deals with blood from the lower body right so um an important shot is taken by the obelical veins essentially as it routes blood all the way to the IVC this shot is known as the doctors venoses the thing is your friends at the mbmed may put sinus venoses as an answer choice don't fall for that right and then in step three the blood in the IVC again I'm trying to bring this up into discrete steps so that you can follow this thing up very closely so in step three the blood in the inferior vein akeva it actually

flows into the right each and then he goes through the four men ovale more on that later to the left each and then from the left each on that blood flows to the left ventricle and then from the left ventricle to the asin in the order and from the naysan in the order to the rest of the body now that's IVC blood let's talk about SVC blood in step four so the thing is blood from your upper body already drains into the right each room through the SVC now this blood actually does not take the pathway of the foramen ovale for the most part okay doesn't take the part of the foramen ovale for the most part it goes from the right each room so SVC blood comes into the right each room and then after that it goes into the right ventricle and then it enters the pulmonary artery and the thing is you may say oh divine shouldn't this go to the lungs it actually does not because remember when a kid is in uterus right this kid's lungs essentially don't work right and it belongs in our working that's like a hypoxic condition well hypoxia causes pulmonary viso constriction so that viso constriction makes it essentially impossible for blood to make its way to the lungs right so the thing that happens is that the blood in the pulmonary artery actually finds its way to the part of the aorta that is distal this is very high yield that is distal to the arch distal to the aortic arch and the way that the blood from pulmonary artery makes its way to the part of the aorta that is distal to the aortic arch is through another shantunas the doctors arteriosus now the thing is for purposes of understanding is actually can a high yield to know that the blood that comes into the heart through the IVC again I've kind of mentioned this already but I think repetition always helps right the blood that comes into the heart through the IVC and the blood that comes in through the IVC they actually don't mix

until you get to that region as I've mentioned already until you get to the region of the aorta that is distal to the aortic arch so what's the use of not letting them mix in the heart when they are ultimately gonna mix just outside the heart maybe like why don't we just mix early and then let's get this over with well think about this for a second the mix in outside the mixin of this blood the IVC IVC blood they mix outside the heart distal to the aortic arch the thing is if you really think about it right the aortic arch itself it gives rise to blood vessels that feed the brain and the name the brain is very important in development uses a ton of oxygen right brain is very important needs high oxygen tension so that it can function properly and it can develop properly after your brain receives oxygen rich blood the body is like okay fine we can mix things after that so essentially the reason the pathophysiological reasoning behind the IVC and the IVC blood mixing distal to the arch is so that you can give the brain more oxygen rich blood so that proper development can happen so what are the things that then happen after a baby is born right after a baby is born the umbilical arteries close okay the umbilical arteries become the medial so medial with an L at the end the medial on the ligaments okay and then give the umbilical arteries close and then there's no more blood returned from the placenta right the umbilical vein the doctors and also those both close as well right remember that the umbilical vein becomes the ligamentum teres okay and then the um the doctors venosus becomes the ligamentum venosus okay so please don't mix those up and then the thing is the high pressures that develop in the left heart right the left side of the heart that actually pushes the form and ovale shot and then that's what gives rise to the fossa ovales in the adult now the thing is

the high pressures that you see in the left heart the ultimately get transmitted to the order right so if those high pressures now exist in the order that shunt that existed the doctors at the urges were blood flowed from the pulmonary artery to the other that shunt actually reverses because again there are much higher pressures in the order blood then flows from the order to the pulmonary artery through that uh through that uh doctor satiriosus although one of the things that also happens is that instead of the hypoxia right that's existing when the kid is in utero right you know there's an oxygen tension when the kid gets born right so that high level that high oxygen tension one thing it actually does is that it actually causes the release it inhibits the production of first the glandins but on the flip side it also encourages the production of uh catecholamine's like no repinephrine and then that causes constriction of the doctor satiriosus so that it kinks off and then becomes the ligamentum arteriosus so again let's uh summarize some uh fiddle adult structural derivatives because this is something that we test all the time on exams right so when the right hand left remember there's one on bilicovina and two on bilicol arrows right so when the right hand left on bilicovina's close right they form the migiel with an L at the end on bilicol ligaments okay and then when the on bilicovina closes the on bilicovina becomes the ligamentum teres of the liver when the doctor's venusus closes it becomes the ligamentum venusus when the foreman ovali closes it becomes the façade ovalis and then when the doctor's arteriosus closes it becomes the ligamentum arteriosus and again these are all floridly high-yield things to know for purposes of the exam so now let's talk about how the actual heart develops right let's talk about how the actual heart develops so the thing is the h

eart actually for the most part starts out as kind of like a two-chimber tube okay starts out as a two-chimber tube with like a primitive atrium primitive ventricle okay now the thing is this two-chimber heart ultimately becomes a four-chimber heart okay by each of septition so you basically like put a septum between the two between the atrium so they can form a right and a left atrium and this actually happens between weeks four and six and then also you have a ventricular septition which happens between weeks five and seven now the first thing that happens is separation of the atro ventricular canal right essentially it's basically the region between the primitive atrium primitive ventricles right so you separate the atro ventricular canal into like two parts right now we'll essentially serve as the right and left sides of the heart right so around the area of the atro ventricular canal you just develop the heart into a right side and a left side okay and the way this happens is you actually have ingruth of tissue from the walls of the heart tube and the thing is these tissue ingruths they have a special name they're known as endocardial cushions okay and it's actually very high to know for purposes of the US and the US depot exam that these endocardial cushions are derived from neurocress cells okay and people that have Down syndrome the most common cardiac anomaly we have is something called an endocardial cushion defect now after this actually I may have been spoken a little earlier so I said that the first thing that happens is that you separates the atro from the ventricles okay and again when you separate the atro ventricular I guess maybe I didn't make it very clear let me make it very clear so you separate the atro from the ventricles so that means the separation that comes between should be a canal that divides the atrium from the ventricles right aka the a

tro ventricular canal and the atro ventricular canal is derived from neurocress cells right because it's the endocardial cushions that makes that happen so essentially it's almost like from the right and left sides of the of the heart tube you have this infording of tissue that like ingruths of tissue and then they divide the atro from the ventricles so the next step that then happens is that okay you're like okay I got to divide the atro into two right so the thing is if you're dividing the atro into two you need to fulfill two requirements you can just divide the right and left atrium are willingly you actually need to divide it in a way that makes sense so what is the way that makes sense well the way that makes sense must fulfill two conditions right the first condition is you want to build a wall between both atro but you also still want to maintain some communication for oxygenated blood movement purposes right so you still want oxygenated blood to be moved between the right atrium and the left atrium and then you also want to have a mechanism in place so this is the second criteria you need to have a mechanism in place to close that wall when the child is born so that you don't keep having communications between the right atrium and the left atrium okay the thing is the dividing wall between both atro is actually made by two that I'm going to discuss right now actually so let's talk about this process and again this is one of those areas where you know you want to kind of pay close attention maybe listen to this a couple of times so that it kind of sticks in your brain well right and I mean obviously I'm just going to say it right right off the bat right if I press the hands issues with this atro septition that's an ASD remember ASD white fixed plate S2 hard sound easy pz on exams so what happens in step one right informing the C3 of septor right again pay atte

ntion to these terms the thing is in step one again I want to chunk you down into steps so in step one you have a septum that grows down towards the endocardial cushions remember I said those are the cardio cushions from the atro ventricular canal so you have a septum that grows down towards the endocardial cushions from the top this septum right it's the first septum it's known as septum primer now the thing is the septum primer meaning actually does not completely grow down to the endocardial cushions it doesn't grow all the way down so there's some leftover space between the bottom of the septum primer and the endocardial cushions this leftover space where the septum primer essentially does not grow down to is what's known as the foramen primer okay foramen primer foramen primer just means first hope now for purposes of understanding something I'll describe later the septum primer is actually very thin remember that write that down somewhere the septum primer is actually very thin so now let's jump to step two so for step two over time right epaptosis actually starts happening in the upper part of the septum primer and as epaptosis happens you actually form a new hole this new hole notice it's the second hole that is forming so it's known as the foramen secondum foramen secondum for second hole the thing is after this epaptosis occurs and you form the second hole the foramen secondum the lower part of the septum primer actually grows to reach the endocardial cushion this sequence of events I mean it should hopefully make some sense right because if you had complete downgrowth of the septum primer before the epaptotic event that happens at the top that will essentially prevent any kind of right to left heart communication right and obviously the videos will die under those circumstances so that's what happens in step two now in step three as the septum primer keeps

growing down to reach the endocardial cushions again keep this thing is almost like a time lapse series of events so as the septum primer as it keeps growing down a new septum actually grows to the right of it okay so the septum primer is growing down to cover over the area that was the foramen primum okay and then a new septum begins to grow to the right of the septum primer because this is the second septum it's known as the septum secondum now it is super high yield to know that this septum secondum is actually much thicker than the septum primer okay the septum secondum is much thicker than the septum primer okay and the thing is this septum secondum that grows again it grows to the right anatomically of septum primer it actually grows about halfway down the distance that is covered by the septum primer so it effectively covers over the foramen secondum i'll see that again we have the septum primer form right it grows down but it doesn't grow all the way down to the indocharya cushions so there's a space left behind that's known as the foramen primer after that the upper part of the septum primer has some hipoptosis happen to form a second hole that's known as the foramen secondum and then after that hipoptosis happens the lower part of the septum primer grows all the way down to the indocharya cushions now as that growing all the way down is happening a second septum is forming to the right of the septum primer it's known as the second as the second septum or the septum secondum now the septum secondum only grows halfway down it grows from top to bottom it only grows halfway down so it essentially covers over the foramen secondum right it covers over the foramen secondum so if you're following along with my explanation you say hmm divine when this block of communication between the right and left sides of the heart well hold your horses there is actually an expla

nation for this right so what's that explanation the thing is if you think about it the right side of the heart in utero receives blood from the placenta and the upper and lower extremities right so really a ton of blood flows into the right side of the heart on the flip side the actual only source of blood for the left side of the heart is blood that's coming from the lungs which is very menial skull right so the thing is the pressures on the right side of the heart vastly exceed the pressures on the left side of the heart when a child is in utero and remember I said a few moments earlier that the septum primer is thin while the septum secondum is thick again I'll see that again the septum primer is thin while the septum secondum is thick so the thing that happens is that the higher pressures on the right side of the heart actually push down like they are strong enough to push down the septum primer which effectively allows not to almost flow like in a valve-like mechanism from the right side of the heart to the left side of the heart okay just the way to illustrate this is almost like take one take one of your hands and have your your index finger pointed like the index finger for like your left hand pointing down the index finger for your right hand pointing up and then let your like your fingers like the tips of your fingers overlap each other right the septum primer is thin the septum secondum is thick so the thing is if the pressures on the right side of the heart are very high that pressure is high enough to push down the septum primer and that will create some space for blood to zip right past from the right each arm to the left each arm okay so this valve-like mechanism that now exists okay is what is known as foramen oval okay this valve-like mechanism that exists is what is known as foramen oval because again the septum secondum when he grows down it actual

ly covers over the area that is known as the foramen right so that area is gone right but the thing is it can be opened periodically by the high pressures in the right each arm those high pressures can pound down on the septum primer and that will is temporary not all the time temporary that's why it's a valve okay that will temporary pull the septum primer and the septum secondum apart so that blood can flow from the right each arm to the left each arm this valve-like mechanism is what is known as the foramen oval so if you think about it when the pressure situation is kind of reversed and birth right where you have higher pressures on the left side of the heart lower pressures on the right side of the heart well the thing is those higher pressures on the left side they actually push down on the foramen oval right and this essentially shuts off the valve right and then the foramen oval receives a new name at this point aka the forsa vales so it should hopefully make some sense that the foramen ovale contains only tissue that is derived from the thin septum primer right so this should again actually make sense and help you understand why the forsa ovales is thin relative to the remaining parts of the dividing walls between the two each in the adog between the right each arm and the left each arm so let's talk about how we found the interventricular septum this one is a lot easier right so the interventricular septum kind of like we had for the each right we need to divide the ventricle into two parts okay remember the right ventricle actually feeds the pulmonary artery and the left ventricle actually feeds the other right remember the other is a much larger blood vessel so with these two different outflow trucks right it should make sense that there should be some kind of divisor between not just the right ventricle and the left ventricle but there should also be a di

visor between the a-order and the pulmonary arteries okay so all the pulmonary artery because it's one thing so let's again chunk this down into some steps of it essentially created myself so in step one the thing that happens is you have your muscular interventricular septum grow from the bottom up okay and this is probably a good time to look at the graphic that I post that I'm posting with this podcast because it kind of highlights the key events here as well right so you have a muscular interventricular septum it grows from the bottom up and divides up a part not all a part of the right of a part of the ventricles and then in step two you have a septum that grows from top to bottom remember the muscular interventricular septum grew from bottom to top in step two you have a septum that grows from the top to bottom and that septum actually works in a nifty way the first thing it does is it actually divides the a-order and the pulmonary trunk okay that's why it should make sense that it should be known as the a-order colp pulmonary septum and then after he has divided the a-order and the pulmonary artery from each other it keeps proceeding downwards even more to divide the rest of the ventricle the thing is the portion of the a-order colp pulmonary septum that actually divides the ventricles is what's actually known as the membranose interventricular septum and it's actually again very high yield to know for the purposes of step one that the a-order colp pulmonary septum is derived from neurocress cells you may see the vine you keep saying it's very high yield it's very high yield it's very high yield let me tell you this of all the embryology that's tested on the USM list step one probably the highest yield is cardiac embryology neuroembryology and then GI but cardiac embryology is probably the highest yield of them all that's why I'm like I'm literally making a pod

cast just on cardiac embryology okay so do not forget the aortic colp pulmonary septum is actually derived from neurocress cells now it is actually very again very high of understanding to keep in mind that the aortic colp pulmonary septum actually grows down in exactly the same longitudinal axis as the most preventive ventricle septum so they essentially meet like perfectly in the midline when you don't meet perfectly you begin to have a lot of problems arising like the tetralogy of fallon remember in my last cardiac podcast I promised I think it was either the last one of two podcasts before that oh I will I will give you a diagram that explains this whole tetralogy of fallon business or here's the time again it's attached at the bottom of this podcast you can download it on the website so the tetralogy of fallon already is essentially like a very important sanonic congenital hard defect that has for clinical findings right and again everyone marises this pulmonary stenosis overriding the order VSD right so like a ventricle septal defect from the membranous part of the inward interventricular septum and then right ventricle hypertrophy right and then so let me see oh these are such disparate findings but actually if you again understand the diagram that I'm adding at the end of this podcast and you understand what I guess maybe I have described in the prior podcast I kind of like describe the diagram in words in the preceding podcast you will actually see that all these things were observing they are really not unrelivened in any way shape or form they are actually derivatives of one central problem and the thing is it's actually much easier to remember the four findings in tetralogy of fallon if you understand it beyond the line pathophysiology and again remember four findings right that's why it's called a tetralogy in the first place and what is this on the line

problem the on the line problem is that the uricopulmonary septum fails to meet the musculine ventricular septum in the center as it should the thing that happens is that the uricopulmonary septum is actually displaced off to the right once you understand this like literally like every other thing that relates to tetralogy of fallon just makes perfect sense in your mind right and again I'm kind of like harping on this because it kind of illustrates a concept that I talked about when I made a podcast is one of my older podcasts that I call the central dogma of studying where I talk about strategies that I suggest for people to think about when they're setting up a study plan studying for exam studying in med school the thing is it's very easy to fall into a pattern of oh I'm just going to memorize this code and move on with my life in med school the thing is it actually makes more sense to try to understand what you're doing because if you understand the material on your first pass through that material and they make multiple passes you will almost invariably do really well in med school that is essentially what I did all through my med school days I understood the material on the first pass had like a slow nice first pass where I understood the material and then I just made repeated passes prior to any exam and then obviously I also started focusing on test strategy especially when I jumped into the world of step one step two's against step three so again this diagram kind of illustrates everything I've talked about because again if you're the thing I described here as APF the theoretical pulmonary septum it grows down is displaced to the right well that will not develop the pulmonary trunk and the yoder very well right so the yoder will get more space than it should get aka over writing the yoder and the pulmonary trunk will get less space than it should get aka pulm

onic stenosis right and if the pulmonary trunk is the most then the right ventricle will need to work harder to send blood through it aka you have right ventricular hypertrophy right and then because the ueric pulmonary septum is not meeting the muscular and ventricular septum nicely in the center they essentially are convoluted like this between the right and the left ventricle which is the VSD so hopefully this makes some sense and I mean I've essentially talked about the rest of the findings and the trilogy of following the other podcast but let me just maybe wrap this wrap up this podcast by essentially maybe saying a few more things here real quick right so the thing is people that have the trilogy of fallow right they have you know high pressures in the pulmonary system from cyanosis so the thing is blood actually flows from the right ventricle to the left ventricle through the VSD so because blood is flowing from the right to the left ventricle the blood that is making its way to the yoder from the left ventricle itself is not purely oxygenated it's actually a mixture of oxygenated and the oxygenated blood so this is actually why the trilogy of fallow is a cyanotic defect now the other like congenital defects like trunkus arteriosus transposition of the grid vessels yada yada actually describe those in cardiology I believe series five so I've already essentially talked about that so I'm not going to see that anymore so I'm going to go to head on pause here because I don't know I feel like cardiac embolies one of those things where you just want to be that leave that be the only topic you cover so that people can again have them to like listen to the podcast again understand it and go from there and then as I do at the end of every podcast I offer 101 tutoring for the USML is step one step two ccans step three exams and also step two cs and then I tutor for the

pre clinical medical exams 30th shelf exams and then if you're a med student applying to residency so like an ERAS application or a college student applying to med school so an AMCA application I don't offer like 101 coaching for this right so like mock interviews personal statement writing and editing editing applications rec letters again I've worked with people on those things and again the vast majority of people have worked with they've all much that their first choices and then if you you know there's this thing I do call longitudinal tutoring where if you're a first second of 30 a med student I tutor you for like your block exams or your shelf exams but at the same time I tutor you for your upcoming USML exam and again the vast majority of people have done this with they've done very well they've proceeded to do very well on their USML tests it's almost like preparing for step one or step two cc over a long time period and then I also do this thing called a USML booster course where it's like 10 hours for step two cc or step three or 20 hours for step one although if you want a longer period for any of these exams I can essentially design a longer course for you but that's more than a keyspi case basis you just need to request it for me so these booster courses they're good for people at the end of the dedicated periods or people that you know feel like the knowledge base is pretty good so you just want someone to you know kind of put everything together for you in a very high-yield fashion like the most no things for the exam you can review them in a very short time period that's essentially what I do with those booster courses and then some people again I've kind of talked with me about like divine your course like your full-on course for step one or your full-on course for step two cc or your full-on course for step three how can I participate in that well h

ere's the deal here's the deal if you have at least five people that can attend the course if you can band you up a group of five and send me an email then we can try to arrange a 14-D period where I can essentially do like a course that covers essentially most of what you'll see on step one or step two ck or step three okay it just needs a group of five people and a physical location so if you can get a group of five people and a physical location then we can take care of that and then if you have a college student buddy that needs to learn from like Gen CAM, OEM Physics, Bio CAM, Physiology, Histology, Opportunity for all those things so have a wonderful rest of your day God bless you all seeing the next podcast thank you

Week four (4) $\rightarrow$ Four chambers.

Sinus venosus (caudal/inferior end).

Bulbus cordis.

Endocardial cushions, Aortopulmonary septum, and Membranous interventricular septum (via the aorticopulmonary septum).

High pressures in the left heart push down on the septum primum, causing it to seal against the septum secundum.

Tetralogy of Fallot (TOF).

Primitive atrium, primitive ventricle, and parts of the sinus venosus.

Umbilical arteries $\rightarrow$ Medial umbilical ligaments; Umbilical vein $\rightarrow$ Ligamentum teres; Ductus venosus $\rightarrow$ Ligamentum venosum.

The right side receives blood from both the placenta (high flow) and the upper/lower extremities, while the left side's only source is the lungs (low flow).

Septum primum (forms foramen primum); Septum secundum (grows to cover the foramen secundum).

Aortopulmonary septum.

1) Muscular IV septum grows bottom-up; 2) The aortopulmonary septum grows top-down, meeting the muscular septum.

Primitive atrium, primitive ventricle, and parts of the sinus venosus.

Umbilical arteries $\rightarrow$ Medial umbilical ligaments; Umbilical vein $\rightarrow$ Ligamentum teres; Ductus venosus $\rightarrow$ Ligamentum venosum.

The right side receives blood from both the placenta (high flow) and the upper/lower extremities, while the left side's only source is the lungs (low flow).

Septum primum (forms foramen primum); Septum secundum (grows to cover the foramen secundum).

Aortopulmonary septum.

1) Muscular IV septum grows bottom-up; 2) The aortopulmonary septum grows top-down, meeting the muscular septum.