Full transcript
0:05Hello everybody and welcome to our
0:07module on cardiac embryology.
0:09About 3 weeks after the egg is
0:11fertilized, the primitive heart develops
0:13in the embryo. And one thing you should
0:15be aware of is that the primitive heart
0:17develops as a straight tube which will
0:18eventually fold and become the structure
0:21that you know in the adult. And all the
0:23different bulges on the tube have names
0:24and you need to know what the names are.
0:26So let's go over them now. So at the top
0:28of the tube is a structure called the
0:29truncus arteriosis. Below that is the
0:32bulbous cortis. We then have a bulge
0:34called the primitive ventricle followed
0:36by another section down at the bottom
0:37here called the primitive atrium. And
0:39then finally at the very bottom we have
0:40a structure called the sinus venosis
0:42which has two horns as you can see in
0:44this picture on the screen.
0:47The truncus arteriosis has the word
0:49artery in its name. And that can help
0:51remind you that in the adult heart, the
0:52truncus arteriosis develops into the
0:54aorta which supplies all our arteries
0:57and also into the pulmonary artery which
0:59has the word artery in its name. The
1:01bulbous cortis develops into the smooth
1:03portions of the left and right
1:04ventricle. I'll show you a picture of
1:06those in a minute. [snorts] The
1:07primitive ventricle develops into the
1:09tbaculated portions of the left and
1:11right ventricle. The primitive atrium
1:13develops into the tbeculated portions of
1:15our atria. And finally, the sinus
1:17vinosis develops into the right atrium
1:20and coronary sinus. And here I've zoomed
1:22in on the sinus vinosis so that I can
1:25show you that the right horn develops
1:27into the smooth portion of the right
1:28atrium. This is called the sinus
1:30venarum. And the left horn develops into
1:32the coronary sinus. And an easy way to
1:34remember this is that the coronary sinus
1:35drains blood from the left ventricle.
1:37Therefore, it comes from the left horn.
1:39The smooth right atrium comes from the
1:41right horn. And then finally, I'll
1:42mention structures in the embryo called
1:44the cardinal veins. These are the
1:46structures that form the SVC and the
1:48IVC. The vennea do not come from the
1:50heart tube. The cardinal veins will
1:52eventually connect to the right atrium
1:54and form the SVC and IVC. The superior
1:57vennea comes from the right common
1:58cardinal vein and the right anterior
2:00cardinal vein and the inferior vennea
2:02comes from posterior cardinal veins.
2:05Here's a picture of the adult heart and
2:06I just want to point out to you that in
2:08the adult heart you have these bumpy
2:09sections. Those are called the
2:10tbaculated portions of the chambers. You
2:13also have these smooth sections up here.
2:15And the reason some portions are
2:16tbaculated and some are smooth is
2:18because they derive from different
2:19embryologic structures. And the smooth
2:22portions are generally found where the
2:24heart connects to other vessels. So for
2:25example, you can see smooth sections
2:27here right below the aortic valve. You
2:29can also find smooth portions below the
2:31pulmonic valve and near the connections
2:33to the vennea and pulmonary veins in the
2:35atria.
2:37So I mentioned this before but the
2:38primitive heart tube will fold and
2:41become the adult heart that we know.
2:43This process is shown on the screen
2:45here. And if you want to understand how
2:47this happens in three dimensions, go to
2:49YouTube and Google heart embryology and
2:51you will find an old video that shows a
2:53beautiful cartoon of how this happens in
2:55three dimensions. Now at the same time
2:57that the heart is folding inside of the
2:59heart, walls are being built. walls
3:02between the left and right ventricles,
3:03walls between the left and right atria,
3:06and even a wall that separates the
3:08pulmonary artery from the aorta. So, in
3:10the next few slides, we're going to talk
3:11about how all of those walls form while
3:13the heart is folding, like is shown on
3:14the screen here. Let me briefly mention
3:17a process that occurs in the embryo
3:19called cardiac looping. The heart tube
3:21loops at about four weeks of gestation
3:23and this establishes the normal left
3:25right orientation of the heart in the
3:27chest. You may know that your heart is
3:28normally found on the left side of your
3:30chest and that's because of the process
3:31called cardiac looping. This process
3:34requires psyia and dininin and I discuss
3:37both psyia and dininin in videos in the
3:39cell biology section. But psyia are
3:41modal structures and dionin is an
3:44important modal protein and they need to
3:45function normally for the heart to
3:47orient correctly in the chest. If psyia
3:50and dinin are abnormal, this can lead to
3:52dextrocardia. This is when the heart is
3:54found on the right side of the body.
3:55This is an X-ray of a patient with
3:57dextrocardia. Note that the heart is
3:58located on the right side of the chest,
4:00not the left side where it should be.
4:02And dextrocardia is seen in cartagonar
4:04syndrome, which is part of the disorder
4:06called primary siliary disanesia. And I
4:08discuss both of these things in videos
4:10in the cell biology section. Now let's
4:13talk about the formation of the
4:14ventricular septum. This is the wall
4:17that will eventually separate the left
4:19ventricle from the right ventricle. So
4:21initially the ventricle is a single
4:23chamber that will be divided and it's
4:24rare but sometimes children are born
4:26with a single ventricle. This is a
4:28severe form of congenital heart disease.
4:30There's an outgrowth of the ventricular
4:32chamber which will eventually form the
4:34pulmonary artery and aorta and it has a
4:36septum dividing it and that septum will
4:38divide this outflow into the pulmonary
4:40artery and aorta. So the first step in
4:43this process is that a structure called
4:45the muscular ventricular septum begins
4:47to form. That's shown in blue here. This
4:49forms at the bottom of the ventricle and
4:51grows upward towards the outflow section
4:53of the ventricle. Next, what happens is
4:56that the membranous septum forms. The
4:58way this happens is the aortical
5:00pulmonary septum begins to twist. You
5:02may know that the pulmonary artery and
5:04aorta twist around each other. So, this
5:06happens in the embryo. The aortical
5:07pulmonary septum twists and then it
5:09fuses with the muscular septum and forms
5:12this green portion of the
5:13interventricular septum called the
5:15membranous septum. After this step,
5:17structures called the endocardial
5:19cushions appear and they will separate
5:21the right and left atria and the right
5:23and left ventricle. And the final result
5:25is that you have a single septum
5:27separating the left ventricle from the
5:28right ventricle. And if you know the
5:31names of the structures in the embryo
5:33that form the ventricular septum, then
5:34it's easy to understand ventricular
5:36septal pathology. There are a number of
5:38forms of ventricular septile defects and
5:41some of them are called membranous. This
5:43is the most common type. Others are
5:44called muscular. And the reason they are
5:46named this way is because this
5:48represents the structures from which
5:50they derive in the embryo. I mentioned
5:52the endocardial cushions before. Those
5:54are these two yellow squares I've shown
5:56on my little drawing here. And these are
5:58very important structures in the embryo.
6:00They contribute to several cardiac
6:02structures in the adult. They contribute
6:04to development of the atrial septum, the
6:06ventricular septum. They also contribute
6:08to development of the AV valves which
6:10are the mitro and tricuspid valves and
6:12also the so-called semi lunar valves
6:14which are the aortic and pulmonic
6:16valves. And sometimes children are born
6:18with a form of congenital heart disease
6:20called endocardial cushion defects.
6:22These are also sometimes called atrio
6:24ventricular canal defects or atrio
6:26ventricular septile defects. And these
6:28defects involve several different parts
6:31of the heart in the adult. They can
6:32involve the atrial septum and involve an
6:35atrial septile defect. They can also
6:37include a VSSD and they can also include
6:39valvular mal formations. And this type
6:41of embryologic heart defect is common in
6:44children in Down syndrome which I talk
6:46about in the video in Down syndrome in
6:47the genetic section. I also mentioned
6:49before an important structure called the
6:51aortical pulmonary septum. It's also
6:53sometimes called the spiral septum. If
6:55you look at this picture at the bottom
6:56of the screen in the embryo, the
6:58ventricle has a single outflow tract,
7:00but the aortical pulmonary septum will
7:02divide it into the aorta and the
7:04pulmonary artery. And it's very high
7:06yield for you to know that proper
7:07formation of this septum requires neural
7:09crest cells. This may seem strange since
7:12neural crest cells play such a big role
7:13in development of the nervous system.
7:15But they also play a role in developing
7:17this septum that divides the pulmonary
7:19from the aorta. These cells migrate to
7:22areas in the primitive heart tube called
7:24the trunkal and bulbar ridges. If you
7:27look over at the drawing on the right
7:28side of the screen here, there are
7:29ridges between the truncus arteriosis
7:31and the bulbous cortis. The neural crest
7:33cells migrate there and then they form
7:35this septum which separates the aorta
7:37and pulmonary arteries and as I
7:38described earlier it fuses with the
7:40intraventricular septum to help form the
7:43membranous ventricular septum. If this
7:46septum does not form normally that can
7:48lead to a number of congenital heart
7:49defects. Transposition of the great
7:51vessels can be caused if this septum
7:53fails to spiral normally. tetrology of
7:56flow can be caused if this septum is
7:58formed in a skewed manner and a
8:00persistent truncus arteriosis can
8:02develop if there is partial or
8:03incomplete septum development and I talk
8:05about all of these disorders in another
8:07video but I just want to mention here
8:08that they all derive from abnormal
8:10formation of the aortical pulmonary
8:12septum now let's talk about how the
8:14atrial septum forms this is the wall
8:16that separates the right atrium from the
8:18left atrium this process begins with the
8:21endocardial cushions at the base of the
8:23atrial chambers and the septum primum
8:25which is a structure that forms at the
8:27top of the atrial chambers. The septum
8:29primum will begin to grow downward
8:31toward the endocardial cushions. The
8:33tricky part about this process is that
8:35as it is growing downward, a hole opens
8:38up in the back of the septum. That's
8:40this hole right here. This is called the
8:42framcundum. So once the framcundum opens
8:45up, you now have two holes between the
8:47atrial chambers. You have the framcundum
8:49up at the top and you have the fram
8:51primum down at the bottom. The septum
8:54primum will eventually fuse with the
8:55endocardial cushion as I've shown here
8:57in my drawing. This will eliminate the
8:59fram primum. It will leave only the
9:01framcundum as a communication between
9:04the two atrial chambers. A new structure
9:06will then form called the septum
9:08seccundum. This will grow downward and
9:10cover the framcundum.
9:12At this point, you have a situation
9:14where the septum primum shown in blue
9:16here functions like a valve. Pressures
9:18in the fetus are very high in the right
9:20atrium. So it will push this septum
9:22primum to the right and allow blood to
9:24flow between the two chambers as I've
9:26shown with my black arrow here. And this
9:28opening between the two chambers formed
9:30by the septum primum functioning as a
9:32valve is called the framan o valley. At
9:35the time of birth the framan o valley
9:37should close. If you look at the bottom
9:38right side of the screen here at the
9:39time of birth pressures in the left
9:41atrium become very high. This will push
9:44the septum primum against the septum
9:46seccundum and they should seal together
9:48and eliminate the framino oval. However,
9:50in about 25% of adults, this doesn't
9:53occur normally and they are left with
9:54what's known as a PFO or Payton fraal.
9:57This is caused by failure of the framino
9:59valley to close after birth. It's caused
10:01by the septum primum and secundum
10:03failing to fuse together. And in my
10:05practice when I perform transophageal
10:07echo cardiograms, I frequently identify
10:09a PFO. They're found in one out of every
10:11four patients. This is a picture of a
10:13PFO by transissophageal echo cardiogram
10:16shown in the screen. This is the right
10:17atrium here. This is the left atrium.
10:19Here you can see this flap which has an
10:21opening between it that allows blood to
10:23travel from the left atrium to the right
10:25atrium or from the right atrium to the
10:27left atrium depending on the pressures.
10:29I'll finish this video by talking about
10:31the fetal circulation and how that
10:33circulation changes at the time of
10:35birth. The key to understanding the
10:37fetal circulation is to remember that
10:39physiologically there is very high
10:40resistance to flow in the lungs. The
10:42lungs are filled with amniotic fluid and
10:44it's very difficult for blood to flow
10:46through them in the womb. This is okay
10:48for the baby however because oxygen is
10:50coming from the mother by way of the
10:52placenta. The umbilical veins contain
10:54oxygenated blood. Now interestingly the
10:57partial pressure of oxygen in the blood
10:59in the umbilical veins is relatively low
11:01about 30 millm of mercury. However, this
11:03results in a saturation of hemoglobin of
11:06about 80%. And that's because fetal
11:08hemoglobin has a strong affinity for
11:10oxygen. That oxygenated blood from the
11:13placenta and the umbilical veins travels
11:15straight to the right atrium. It
11:16bypasses the liver via a structure
11:19called the ductus venosis. This is
11:20because the liver is relatively
11:22unimportant in the fetus since the
11:24mother is performing many of the
11:25metabolic roles of the liver. Once the
11:28blood gets to the heart and the right
11:30atrium, it can bypass the lungs via the
11:32framino valley which we previously
11:34discussed. This is shown in this slide
11:36at the top right of the screen. The
11:38famino valley is here and it allows
11:40oxygenated blood to bypass the lungs.
11:42The blood doesn't want to go to the
11:43lungs because resistance to flow is
11:44high. So it will bypass the lungs, go
11:46through the framino valley and travel to
11:48the left atrium. Now some blood,
11:50especially blood from the head of the
11:52fetus will still get to the right
11:54ventricle. In other words, it won't go
11:55through the framino valley. If you look
11:57at this picture on the right side of the
11:59screen here, blood coming from the head
12:00may go straight down and through the
12:02tricuspid valve and enter the right
12:04ventricle. But there's a second bypass
12:06structure for the lungs called the
12:07ductus arteriosis. This is shown in this
12:10picture here. It connects the pulmonary
12:11artery to the aorta. So once again, this
12:13allows blood to bypass the lungs. If you
12:16remember that resistance to flow in the
12:18lungs is very high in the womb, then
12:20it's easy to remember that the major
12:22change at birth is that pulmonary
12:24resistance falls. The baby takes a
12:26breath of air. This starts to remove
12:28fluid from the lungs and the lungs fill
12:30with air and the resistance gets much
12:32lower. This allows a rush of blood to
12:35travel from the right ventricle and
12:36pulmonary artery through the lungs. This
12:39leads to more blood in the left atrium
12:41and it raises the pressure in the left
12:42atrium so that it becomes higher than
12:44the right atrial pressure. This is going
12:47to close the framinal oval in most cases
12:49so that it becomes the fossal. Like I
12:52showed you before when pressure in the
12:53left atrium becomes high it pushes that
12:56septum primum against the septum
12:58seccundum and the two structures fuse
13:00together. The ductus arteriosis the
13:02other bypass of the lungs will also
13:05close. In udo you have relatively low
13:08oxygen tension in the ductus arteriosis
13:10and you have lots of prostaglandins
13:12around coming from the placenta. This
13:14maintains the patency of the ductus
13:16arteriosis. At birth the oxygen content
13:19of the blood in the ductus arteriosis
13:21rises because the lungs start to work
13:23and the level of prostaglandins fall
13:25because you lose the placenta. And these
13:27are the two major triggers for closure
13:29of the ductus arteriosis.
13:32So at the bottom of the screen, I've
13:33highlighted the key physiologic changes
13:36between in uterero and at birth and
13:38these are very high yield for you to
13:39know for step one of your boards. So the
13:42resistance to flow through the lungs,
13:43the pulmonary vascular resistance is
13:45very high in uterero but falls at the
13:47time of birth. The pressure in the right
13:49atrium is very high in uterero. This is
13:52what drives blood across the framino
13:54valley. And at birth, the pressure in
13:56the right atrium falls because blood
13:58begins flowing into the right ventricle
13:59and through the lungs. In the left
14:01atrium in uterero the pressure is
14:03relatively low but at birth there is a
14:05rush of blood coming through the lungs.
14:07This raises the pressure in the left
14:08atrium and seals the famino valley
14:11closed.
14:12And then the final topic that I'll
14:14mention in this video is that the
14:15placenta has a low resistance to flow
14:18and in uterro this helps to keep the
14:20left atrial pressure low. Remember that
14:22the left atrium pumps blood into the
14:24left ventricle and in uterro the left
14:27ventricle has a very easy time moving
14:29blood into the aorta. That's because the
14:31aorta is connected to the placenta which
14:33is a very low resistance structure. So
14:35it's easy for blood to move from the
14:37left ventricle to the aorta and
14:38therefore it's easy for blood to move
14:40from the left atrium to the left
14:41ventricle and this helps to keep the
14:42left atrial pressure low in the baby in
14:44the womb. Now at birth when the placenta
14:47is lost there's a rise in peripheral
14:49resistance. This is one of the
14:50physiologic changes that occurs at
14:52birth. This leads to a rise in systemic
14:54blood pressure. Basically the afterload
14:56on the left ventricle goes up and the
14:58blood pressure rises. This leads to a
15:00rise in left ventricular pressure and
15:01this in turn contributes to the rise in
15:04left atrial pressure that occurs at
15:06birth and helps to close the framan
15:08valley. And that concludes our video on
15:10cardiac embryology.