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227 Cards in this Set

  • Front
  • Back
intraembryonic cavity
formed by intercellular clefts in the lateral plate mesoderm, created by lateral folding and creates the future pleural, pericardial and peritoneal cavities
somatic mesoderm and splanchnic mesoderm layer
appear when intercellular clefts appear in the lateral mesoderm portion, occur when the plates are divided into two layers
splanchnic mesoderm layer
continuous with mesoderm of the wall of the yolk sac
intraembryonic cavity (body cavity)
the space bordered by the splanchnic and somatic mesoderm layer, loses connection with the extraembryonic cavity when the body of the embryo folds, forms the cavity extending from the thoracic to the pelvic region
somatic mesoderm
lines the intraembryonic cavity, become mesothelial and form the parietal layer of the serous membranes lining the ouside of the peritoneal, pleural and pericardial cavities
splanchnic mesoderm
form the visceral layer of the serous membranes covering the abdominal organs, lungs and heart
dorsal mesentery
point where the visceral and parietal layers are continuous with each other, it suspends the gut tube in the peritoneal cavity, initially it is a thick band of mesoderm running from the caudal limit of the foregut o the end of the hindgut
ventral mesentery
exists only from the caudal foregut to the upper portion of the duodenum and results from thinning of mesoderm of the septum transversum
mesentery
a double layer that provides a pathway for blood vessels, nerves and lymphatics of the organ
septum transversum
a thick plate of somatic lateral plate mesodermal tissue occupying the space between the thoracic cavity and the stalk of the yolk sac, does not separate the thoracic and abdominal cavities completely, communication through the pericardioperitoneal canals
pericardioperitoneal canals
the large openings found where the septum transversum does not separate the thoracic and abdominal cavity, act as a space where the lung buds grow into
lung buds
when they begin to grow they expand caudolaterally within the pericardioperitoneal canals, this causes the canals to shrink and the lungs expand into the mesenchyme of the body wall dorsally, laterally and ventrally
pleuropericardial folds
develop with lung buds, become part of the thoracic wall, appear as small ridges projecting into the primitive undivided thoracic cavity at first, form the pleuropericardial membranes
pleuropericardial membrane
contains common cardial veins and phrenic nerves, divide thoracic cavity into pericardial and two pleural cavities, forms the fibrous pericardium
components of the mesoderm after lung expansion
1. definitive wall of the thorax
2. pleuropericardial membranes-extensions of the pleuropericardial folds that contain the common cardinal veins and phrenic nerves
pleural cavities
are derived from the transformation of the pericardioperitoneal canals
divisions of the thoracic cavity
1. pericardial cavity
2. two pleural cavities
fibrous pericardium
formed from the pleuropericardial membranes
pleuroperitoneal folds/membrane
cresent-shaped folds that closes the opening between the pleural and peritoneal cavities, project into the caudal end of the pericardioperitoneal canals, by the 7th week they fuse with the mesentery of the esophagus and with the septum transversum, thus causing the separation of the thoracic and abdominal cavity
diaphragm formation
forms once the rim is established, myoblasts originating in the body wall penetrate the membranes to form the muscular part of the diaphragm
what structures derive the diaphragm
1. the septum transversum-forms the central tendon of the diaphragm
2. the two pleuroperitoneal membranes
3. muscular components from the lateral and dorsal body walls
4. the mesentery of the esophagus (where the crura develops)
3rd, 4th, and 5th cervical segments
grow into the septum
phrenic nerves
pass into the septum through the pleuropericardial folds, explains why expansion of the lungs and descent of the septum shift the phrenic nerves into the firbrous pericardium, supply the diaphragm with its motor and sensory innervation
diaphragm at the 6th week
at the level of the thoracic somites
repositioning of the diaphragm
caused by rapid growth of the dorsal part of the embryo compared with that of the ventral part, by the 3rd month some of the diaphragm is at the level of L1
superior vena cava
comes from the right common cardinal vein
ventral body wall defects
due to incomplete or improper folding or incomplete development of the body wall, bone, muscle and/or skin, failure of the ventral body wall to close
ectopia cordis
when the heart protudes through a sternal defect (cleft sternum or absence of the lower third of the sternum) and heart lies outside the body
omphalocele
herniation of abdominal viscera through an enlarged umbilical ring, failure of bowel to return after physicological hernia (which is normal during the 6th to 10th week), covered amnion, 59% cardiac, 40% neural tube, INC in alpha fetoprotein
gastroschisis
herniation of abdominal viscera through the body wall into the amniotic cavity, lateral to umbilicus usually right side, not covered by amnion which leads to damage, not associated with other defects or chromosomal abnormalities like omphaloceles, INC in alpha fetoprotein, volvulus otherwise prognosis excellent
cleft sternum
ventral body wall defect that results from lack of fusion of the bilateral bars of mesoderm responsible for formation of this structure
Cantrell pentalogy
a defect that involves both the thorax and the abdomen
bladder and cloacal exstrophy
defects in the pelvic region resulting from a lack of closure of the body wall
diaphragmatic hernia
failure of one or both pleuroperitoneal membranes to close the pericardioperitoneal canals, abdominal viscera herniates here, 90% left side, a large defect associated with a high rate of mortality from pulmonary hypoplasia and dysfunction (hidden mortality), 1/2000 births
parasternal hernia
occurs when a small part of the muscular fibers of the diaphragm fails to develop, found in anterior portion of the abdominal wall, enter chest between the sternal and costal portions of the diaphragm
esophageal hernia
thought to be due to congential shortness of the esophagus, upper portions of the stomach are found in the thorax, stomach is constricted at the level of the diaphragm
respiratory diverticulum (lung bud)
forms at 4 weeks old, it appears as an outgrowth from the ventral wall of the foregut, along the gut tube
TBX4
determines the location of the bud along the gut tube, expressed in the endoderm of the gut tube at the site of the respiratory diverticulum, induces formation of the bud and the continued growth and differentiation of the lungs
endoderm and lung
origin of the epithelium of the internal lining of the larynx, trachea, and bronchi as well as that of the lungs
splanchnic mesoderm and the lung
is the origin for the cartilaginous, muscular, and connective tissue components of the trachea and lungs
tracheoesophageal ridges
two of them, separates the foregut from the lung bud after the diverticulum expands caudally, these fuse form the tracheoesophageal septum
teacheoesophageal septum
divides the forgut dorsally into the esophagus and ventrally into the trachea and lung buds
laryngeal orifice
maintains communication of the respiratory primordium with the pharynx, changes in shape from a sagittal slit to a T-shaped opening due to rapid proliferation of mesenchyme
mesenchyme of the 4th and 6th pharyngeal arches
is the origination point for the cartilage and muscle of the larynx
thyroid, cricoid and arytenoid cartilages
fromed from the mesenchyme of the two pharyngeal arches, gives the shape of the laryngeal orifice
laryngeal ventricles
a pair of lateral recesses caused from the vacuolization and recanalization of the lumen (caused by proliferation of the laryngeal epithelium), these recesses are bounded by folds of tissue that differentiate into the false and true vocal cords
larynx in a 12 week embryo
epiglottis/supraglottis formed from the 4th pharyngeal arch, vocal cords and arytenoid swelling from 6th pharyngeal arch
purpose of laryngeal development
to separate the airway and esophagus, larynx separates the trachea and pharynx (esophagus)
vagus nerve
CN X, innervate all the laryngeal muscles
superior laryngeal nerve
innervates derivatives of the 4th pharyngeal arch
recurrent laryngeal nerve
innervates derivatives of the 6th pharyngeal arch
lung bud gives rise to what?
trachea and two lateral bronchial buds
bronchial buds
enlarge at the 5th week and form right and left main bronchi, right then forms three secondary bronchi and the left two secondary
6th week embryo and lungs
segments of the primitive lobes form, 10 segments on the right and 8 on the left
8 week embryo and lungs
segments divide further, pleuroperitoneal folds separate the lobes to form major and minor fissures
pericardioperitoneal canals
spaces for the lungs, become more narrow as the lung buds expand into the cavity, lie on each side of the foregut
primitive pleural cavities
formed from the pleuroperitoneal and pleuropericardial folds separating the pericardioperitoneal canals from the peritoneal and pericardial cavities
visceral pleura
derives from the mesoderm covering the outside of the lung
parietal pleura
derives from the somatic mesoderm layer covering the body wall from the inside
pleuropericardial folds
separate the pericardial and pleural cavities
pleural cavity
space between the parietal and visceral pleura
tertiary (segmental) bronchi
form from the further development of the secondary bronchi, ten in the right and 8 in the lef, these form the bronchopulmonary segments of the adult lung, by the end of the 6th month, 17 generations of subdivisions have formed, six more formed during postnatal life
what regulates branching
epithelial-mesenchymal interactions between the endoderm of the lung buds and splanchnic mesoderm that surrounds them, involve FGF family
pulmonary artery development
grow caudally from the aortic sac positioning themselves next to the bronchial branches, arterial branches completed by 16 weeks, arterioles and capillaries continue to proliferate/grow for several years after birth
pseudoglanular period
5-16 weeks, branching has continued to form terminal bronchioles, no respiratory bronchioles or alveoli are present, bronchial branching completes
canalicular period
16-26 weeks, each terminal bronchiole divides into 2 or more respiratory bronchioles, which in turn divide into 3-6 alveolar ducts, alveolar ducts open to 10-16 alveoli, respiratory bronchioli/alveolar ducts form
recognition of respiratory bronchioli
by thinning of cuboidal epithelial cells into thin, flat cells capable of gas exchange
terminal sac period
26 weeks to birth, terminal sacs (primitive alveoli) form and capillaries establish close contact
alveolar period
8 months to childhood, mature alveoli have well-developed epithelial endothelial (capillary) contacts
respiratory bronchioles
cuboidal in shape, allow for respiration to occur when change to thin, flat cells, intimately associated with numerous blood and lymph capillaries
terminal sacs (primitive alveoli)
surrounding spaces of the bronchioles and capillaries, i.e. surround thin, flat cells
type I alveolar epithelial cells
line terminal sacs, become thinner, allows surrounding capillaries to protrude into the alveolar sacs, forms blood-air barrier
mature alveoli
not present before birth
type II alveolar epithelial cells
produce surfactant
surfactant
a phospholipid-rich fluid capable of lowering the surface tension at the air-alveolar interace, phospholipids + surfactant proteins (SP-A, SP-B, SP-C, SP-D), measure lecithing/sphingomyelin ratio in amniotic fluid, ratio > 1.9, then phosphatidylglycerol (which comes from phosphotidylinositol) is present = low risk for respiratory distress syndrome
purposes of surfactant
decreases surface tension, reduces collapse of alveoli, DEC pressures required to expand lung, controls fluid balance in alveoli, keeps them dry
fetal breathing movements
begin before birth and cause aspiration of amniotic fluid, important for stimulating lung development and conditioning respiratory muscles, when respiration begins at birth, most of the lung fluid is resorbed
postpartum breathing
bring air into the lungs, growth of lung primarily to an increase in the number of bronchioles and alveoli (formed during the first 10 years of postnatal life)
esophageal atresia
abnormaliites in partitioning of the esophagus and trachea by the tracheoesophageal septum, may allow gastric contents or amniotic fluid to enter the trachea and cause penumonitis and pneumonia
tracheo-esophageal fistulas TEF
occurs when the esophagus and trachea are attached, associated with other birth defects (cardiac abnormalities), component of the VACTERL association, complication is polyhydramnios (bec. amniotic fluid does not pass to the stomach and intestines)
Syptoms of TE fistula
may present with excess salivation/drooling, choking, inability to pass feeding catheter into stomach, X-ray shows dilated upper esophageal pouch, INC air in abdomen and stomach, diagnosis by bronchoscopy
Type III TEF
most common, occurs 86% of the time, occurs when the upper portion of the esophagus ends in a blind pouch and the lower segment forms a TEF, affects amniotic fluid volume
H-type (V-type) fistula
forms an H shaped fistula in which there is communication of esophagus with the trachea at one point, does not present with esophageal atresia
isolated esophageal atresia
no TEF forms, just two esophageal atresias
tracheal stenosis/agenesis
vascular compromise to the developing trachea, shrinking of the trachea
congenital laryngeal cleft
very rare, deficiency in the separation of the larynx from the hypopharynx, symptoms include aspiration, choking, weak voice
shape of larynx in infants
CROUP, funnel shape in infants, cylindrical in adults
respiratory distress syndrome (RDS)
cause: surfactant deficiency (causing INC surface tension, collapse (atelectasis) of lungs, INC alveolar fluid), ventilator induced trauma, hypoxia, acidosis (damage to capillary endothelial cells, leakage of proteinaceous fluid “hyaline membranes”)
occurs: after 23 weeks gestation, potentially viable
20% of deaths in newborns
hyaline membrane disease (HMD)
AKA of RDS, hyaline membrane consists of protein, dead epithelial cells, fibrin clot formation
treatment of RDS or HMD
surfactant treatment (DECes surface tension within mins/hrs.), at 72 hours pulmonary macrophages will appear, other complications include infection, ventilator damage, oxygen toxicity, INC lung fluid from other causes such as PDA
Dochdalek type congenital diaphragmatic hernia
most common and sever, 80-85% left sided, abdominal organs migrate into the left chest wall, heart pushed over to the right, moderate-severe lung hypoplasia of left lung, mild hypoplasia of right lung
morgagni type congenital diaphragmatic hernia
parasternal defect, incomplete muscularization of the diaphragm, so significant pulmonary hypoplasia, mild or no respiratory distress
hypoplastic lung
leads to smaller airways, alveoli and pulmonary vascular bed, DEC gas exchange surface area
hypoxemia
INC constriction of pulmonary blood vessels, pulmonary vascular resistance and pulmonary artery pressures, a right to left shunting of blood
ectopic lung lobes
arise from the trachea or esophagus, formed from additional respiratory buds of the foregut
congential cysts of the lung
formed by dilation of terminal or larger bronchi, gives honeycomb appearance to lung, these structures normally drain poorly and lead to chronic infections
when is the vascular system established
during the middle of the third week when the embryo is no longer able to satisfy its nutritional requirements by diffusion alone
where are cardiac progenitor cells
lie in the epiblast lateral to the primitive streak, they then migrate through the streak in a sequential cranial -> caudal order, proceed toward the cranium and position themselves rostal to the buccopharyngeal membrane and neural folds residing in the splanchnic mesoderm, then induced by the pharyngeal endoderm to form cardiac myoblasts, blood islands also appear to form blood cells and vessels
cardiogenic field
horseshoe-shaped endothelial tube composed of cardiac myoblasts
pericardial cavity
the intraembryonic cavity over the cardiogenic field
dorsal aortae
blood islands that appear bilaterally, parallel and close to the midline of the embryonic shield
growth of the brain and the position of the heart tube
causes the buccopharyngeal membrane to be pulled forward while the heart and pericardial cavity move first to the cervical region and finally to the thorax
heart tube
angiogenic cell clusters coalesce to form right and left endocardial tubes, embryo folds cephalocaudally and laterally, endocardial tubes fuse via programmed cell death (PCD) forming a continuous tube with an inner endothelial lining and an outer myocardial layer
where does venous drainage occur in the heart tube
at the caudal pole
where does blood get pumped out of
the first aortic arch into the dorsal aorta at its cranial pole
dorsal mesocardium
a fold of mesodermal tissue that attaches the tube to the dorsal side of the pericardial cavity
transverse pericardial sinus
created by the disappearance of the dorsal mesocardium, connects both sides of the pericardial cavity, suspends the heart in the cavity by blood vessels at its cranial and caudal pole
proepicardium
formed from the mesothelial cells on the surface of the septum transversum, is near the sinus venosus and migrate to the heart to form epicardium, rest of epicardium comes from mesothelial cells from the outflow tract (cephalic end)
three layers of the heart tube
1. endocardium-forms the internal endothelial lining of the heart, surrounded by cardiac jelly which separates it from the myocardium
2. myocardium-forms the muscular wall
3. epicardium or visceral pericardium-covering the outside of the tube, responsible for formation of the coronary arteries, including their endothelial lining and smooth muscle
creation of the cardiac loop
caused by the bending of the cephalic portion (ventrally, caudally and to the left) and the caudal portion (dorsocranially and to the right), start at day 23 with a series of expansions, constrictions and folds, completed by day 28, normal is folding to the left
five dilations of the heart tube (cephalic -> caudal, ventral -> dorsal)
1. aortic roots-remains outside the pericardial cavity after looping
2. bulbus cordis-divided into truncus arteriosus, conus cordis and trabeculated part of the right ventricle
3. primitive ventricle
4. primitive atrium-goes inside the pericardial cavity after looping
5. sinus venosus-remains outside the pericardial cavity after looping
what does the formation of the cardiac loop create
1. normal position of heart chanber
2. changes a single circuit system into an assymetrical system -> pulmonary and systemic circulations
atrial portion
initially a paried structure outside the pericardial cavity, forms a common atrium and is incorporated into the pericardial cavity
atrioventricular junction
forms the atriventricular canal, connects the common atrium and the early embryonic ventricle
bulbous cordis
narrow, proximal end of bulbus forms the trabeculated part of the right ventricle
conus cordis
will form the outflow tracts of both ventricles, midportion of bulbus
truncus arteriosus
distal part of the bulbus, will form the roots and proximal portion of the aorta and pulmonary artery
primary interventricular foramen
junction between the ventricle (left) and the bulbus cordis (which eventually makes the right), externally indicated by the bulboventricular sulcus
primitive left ventricle
formed from the primitive ventricle when it is trabeculated
primitive right ventricle
formed from the proximal third of the bulbus cordis when it is trabeculated
sinus venosus
initially on the dorsal end in association with the septrum transversum, in the middle of the 4th week (24 day) it receives venous blood from the right and left sinus horns and gives it to the atria, entrance shifts to the right venous return caused by left to right shunts of blood (35 days), IVC, SVC and coronary sinus all open into here, contains crista terminalis (conducting fiber tract SA node to AV node)
right vitelline vein
becomes the IVC
right anterior cardinal vein
becomes the SVC
left sinus horn
coronary sinus and oblique vein of the left atrium
right sinus horn
blends into the right posterior wall of the right atrium becoming the smooth area sinus venarum
pulmonary veins
come from the smooth portion of the left atrium
where do sinus horns receive blood from
1. vitelline or omphalomesenteric vein
2. umbilical vein
3. the common cardinal vein
when is the right umbilical vein and left vitelline vein obliterated?
fifth week,
when is the left common cardinal vein obliterated
10 weeks, mostly due to the fact that venous drainage occurs entirely on the right side now
what remains of the left sinus horn after the 10th week
oblique vein of the left atrium and the coronary sinus, empty into the sinus venosus
sinuatrial orifice
entrance of the right horn into the right atrium, flanked on each side by right and left venous valves
septum spurium
caused by the fusion of the right and left venous valves dorsocranially
right venous valve and its formation of great vessel valves
superior portion is obliterated, inferior portion forms the valves of the IVC and coronary sinus
crista terminalis
forms the dividing line between the original trabculated part of the right atrium and the smooth walled sinus venarum which originates from the right sinus horn
when are the septa formed
27th to 37 days
theories of cardiac septa formation
1. two actively growing masses (endocardial cushions) approach each other until they fuse, dividing the lumen into two separate canals
2. one actively growing mass that makes its way to the other end
3. does not envolve cushions, occurs when the atria and ventricle grow while a narrow ridge does not forming a septa, such a septa never completely divides the original lumen, closed secondarily by neighboring proliferating tissues
endocardial cushions and formation of cardiac septa
splanchnic mesoderm, addition of neural crest cells in the conotruncal area or AV region, play a role in formation of septa and valves and cardiac defects
AV and conotruncal area
help in formation of the atrial and ventricular (membranous) septa, the atrioventricular canals and valves and the aortic and pulmonary channels
septum primum
thin membranous septa, first portion is a small sickle shaped crest that grows in the roof of the common atrium into the lumen, extend toward the endocardial cushions in the AV canal, perforations made in the upper portion through cell death
ostium (foramen) primum
opening between the lower rim of the septum primum and the endocardial cushions, closed with further development of the endocardial cushions on the end of the septum primum
ostium (foramen) secundum
coalescence of the perforations found in the septum primum, maintains right and left shunt bypassing the pulmonary circulation
septum secundum
second crest fold formed, a thick muscular septum forms to the right of the septum primum, never forms a complete partition, only overlapping the ostium secundum
oval foramen
forms by incomplete closure of the septum secundum maintaining a right to left shunt, foramen ovale closes right after birth
closure of the foramen ovale
DEC in right atrial pressure from occlusion of placental circulation and INC left atrial pressure due to INC pulmonary venous return, a functional closure at birth, anatomical closure at 3 months when the septum primum and septum secundum fuse
pulmonary vein
develops as an outgrowth of the posterior left atrial wall, to the left of the septum primum, gains connections with veins of the developing lung buds, eventually formes the smooth walled part of the adult atrium, eventually 4 enter the left atria
AV endocardial cushions
appears at the superior and inferior borders of the Av canal, project into the lumen and fuse, results in a complete dicision of the canal into right and left AV orifices by end of 5th week
bulbo(cono) ventricular flange
` separate the bulubus from the left ventricle, terminates at the end of the 5th week
lateral AV endocardial cushions
appear on the right and left borders of the canal,
formation of AV valves
after fusion of cushions, orifice is surrounded by proliferations of mesenchymal tissue, bloodstream hollows out tissue on the ventricular side of the proliferations forming valves connected to the wall by muscular cords, muscular cords replaced with dense connective tissue, connected to papillary muscles by chordae tendinae
truncus swellings (ridges)
forms aorticopulmonary septa dividing truncus into aortic and pulmonary channels, lie on the right and left superior wall, right swelling grows distally and to the left while the left grows distally and to the right (growth toward the aortic sac), left and right twist around each other (to make sure that the correct outflow tract is lined up with the correct ventricle)
conus swellings (ridges)
forms the outflow tracts of the right (anterolateral) and left (postereomedial) ventricles, develop along the right dorsal and left ventral walls, unite with the truncus septum
neural crest cells and partitioning of the truncus arteriosus and conus cordis
contributions to both swellings to form CT and smooth muscle of the aorticopulmonary septum
partitioning of the primitive ventricle
end of the 4th week, muscular intervetricular (IV) septum develops midline on the floor of primitive ventricle from merging medial walls of the two ventricles, IV foramen between free edge of muscular IV septum and fused AV cushions allows for communication between the two ventricles, eventually closes through outgrowth of inferior AV cushions
interventricular forman
above the muscular portion of the interventricular septum shrinks once the conus septum is made
expansion of the primitive ventricles
due to growth of the myocardium on the outside and continuous diverticulation and trabecula formation on the inside
membranous IV septum
formed from complete closure of the IV foramen
1. right and left bulbar ridges
2. inferior AV cushions
semilunar valves
two pairs, visible as small tubercles found on the main trunucs swelling, tubercules hollow out at their upper surface and form the valves, neural crest cells contribute to the formation of the valves
pacemaker of the heart
initially in the caudal part of the left cardiac tube, later sinus venosus assumes this function, incorporated into the right atrium, replaced with pacemaker tissue and forms SA node at base of interatrial septum
bundle of His
derived from cells in the left wall of the sinus venosus, and cells from the AV canal
vasculogenesis
one form of blood vessel development, vessels arise by coalescence of angioblasts, makes major vessels like the dorsal aorta and cardinal veins
angiogenesis
another form of blood vessel development, vessels sprout from existing vessels, forms remainder of vessels
vascular endothelial growth factors (VEGF)
pattern the system of vessel formation
aortic arch arteries
arise from the aortic sac (expansion of cranial end of the truncus arteriosus), ventrally and connect to the left and right dorsal aortae dorsally
aortic arches
six pairs originate in aortic sac (the 5th though sometimes never forms or forms incompletely the regresses) and terminate in right and left dorsal aortae, give arterial supply to each of the pharyngeal arches
adult arterial system
develops from aortic arches 3, 4 and 6 (these develop asymmetrically and make major contributions) and the right and left dorsal aortae, aortic arches 1 (disappear by day 27, before arch 6 is made), 2 and 5 disappear
brachiocephalic artery
the right horn of the aortic sac
aortic arch
the left horn of the aortic sac
arch 1
gives rise to maxillary artery
arch 2
gives rise to hyoid and stapedial arteries
arch 3
common, external and part of the internal carotid artery
arch 4
left: part of the arch of the aorta
right: most prosimal segment of the right subclavian
arch 6
left: left pulmonary artery and the ductus arteriosus
right: right pulmonary artery
recurrent laryngeal nerves
left: nerve hooks where the ligamentum arteriosum is
right: moves up and hooks around the right subclavian
vitelline arteries
initially a number of paired vessels supplying the yolk sac, form the vessels in the dorsal mesentery of the gut (celiac, SMA, IMA)
derivation of coronary arteries
1. angioblasts formed elsewhere and distributed over the heart surface by migration of the proepicardial cells
2. epicardium
inflow tract remodeling
1. above the diaphragm-remodeling begins with a shift to the right of the venous return
2. below the diaphragm-
vitelline system below the diaphragm
gives rise to the liver sinusoids (including the ductus venous), the portal system (portal vein, SMV, IMV and its components) and a portion of the IVC, carries blood from the yolk sac to the sinus venosus
right umbilical vein below the diaphragm
disappears and the left umbilical vein anastomoses with the ductus venous, originates in the chorionic villi and carry oxygenated blood to the embryo from the placenta
cardinal veins
drain the body of the embryo proper, form the main venous dranage system of the embryo initially
how does oxygenated blood from the placenta reach the heart
via the single umbilical vein and the ductus venosus
ductus venosus
direct communication between the left umbilical vein and the right hepatocardiac channel, bypasses the sinusoidal plexus of the liver
ligamentum venosum
obliterated left umbilical ductus venosus
anterior cardinal veins
drain the cephalic part of the embryo
posterior cardinal veins
drain the rest of the embryo
common cardinal veins
joining of the anterior and posterior cardinal veins before reaching the sinus horn
subcardinal veins
drain the kidney
sacrocardinal veins
drain the lower extremities
supracardinal veins
drain the body wall by way of the intercostal veins, taking over the function of the posterior cardinal veins
left brachiocephalic vein
created by the anastomosis between the anterior cardinal vein
left superior intercostal vein
receives blood from the second and third intercostal spaces, comes from the left posterior cardinal vein
superior vena cava
formed by the right common cardinal vein and the proximal portion of the right anterior cardinal vein
left renal vein
formed from the anastomosis between the subcardinal veins
left gonadal vein
also forms from the subcardinal veins
left common iliac vein
comes from the anastomosis between the sacrocardinal veins
azygos and hemiazygos veins
come from the right and left supracardinal vein
fetal circulation
well oxygenated blood returns from the placenta via the umbilical vein, half passes through the hepatic sinusoids, other half bypasses the liver and goes through the ductus venosus, into the IVC (right to left shunt), blood goes into the right atrium, then most through the foramen ovale into the left atrium (right to left shunt) into the left ventricle and out the ascending aorta, best oxygenation to head, neck and upper limbs, small amount of blood from the right ventricle enters pulmonary trunk, some goes to the lungs but most passes through the ductus arteriosus into the aorta (right to left shunt), umbilical arteries return blood to the placenta for re-oxygenation
where does oxygenated blood meet non-oxygenated blood in fetal circulation
1. liver
2. IVC
3. right atrium
4. left atrium
5. ductus arteriosus
saturation levels of blood in the umbilical arteries that goes back to the placenta
58%
neonatal circulation
at birth, the three shunts that permitted most of the blood to bypass the liver and the lungs cease to function, the foramen ovale, ductus arteriosus, ductus venosus and umbilical vessels are no longer needed
how are the unnecessary fetal circulation shunts obliterated
1. aeration of the lungs provides a dramatic fall in vascular resistance, causes INC in pulmonary blood flow -> INC of lest atrial pressure above that in the right atrium -> closing of the foramen ovale
2. constriction of the ductus arteriosus
3. constriction of the ductus venosus
4. constriction of the umbilical vessels
fetal remnants
1. and 2. umbilical arteries -> internal iliac arteries and medial umbilical ligaments
2. umbilical veins -> ligamentum teres of liver
3. ductus venosus -> ligamentum venosum
4. ductus arteriosus -> ligamentum arteriosum
5. foramen ovale -> obliterated
lympathic system
appears later than the circulatory system, 5th week, may form from mesenchyme in situ, two jugular, two iliac, one retroperitoneal and one cisterna chyli
dextrocardia
folding to the right, heart lies on right, resulting in mirror image of the heart
isolated dextrocardia
associated with other severe cardiac anomalies
dextrocardia with situs inversus (inversion of the all viscera)
not associated with sever cardiac defects, normal physiology, slight risk of heart defects
heterotaxy
where sidedness is random in the organs, some reversed some not, classified as laterality sequences
probe patency of the foramen ovale
incomplete anatomical fusion of septum primum and septum secundum, present in approx. 25% of the population, of no clinical importance
ASD (atrial septal defects)
2:1 femal to male prevalence, can be ostium secundum defects (most clinically significant ASD), cor triloculare biventriculare (common atrium), or ostium primum defects
ostium secundum ASD
characterized by a large opening between the left and right atria, caused by either excessive cell death and resorption of the septum primum or by inadequate formation of the septum secundum, may cause intracardiac shunting from left to right
cor triloculare biventriculare
complete absence of the atrial septum, is always associated with serious defects elsewhere in the heart
ostium primum ASD
partially fusion of AV canal, defect in atrial septum, usually combined with a cleft in the anterior leaflet of the tricuspid valve
tricuspid atresia
obliteration of the right AV orifice, characterized by the absence or fusion of the tricuspid valves, symptoms include patency of the oval foramen, ventricular septal defect, underdevelopment of the right ventricle and hypertrophy of the left ventricle
endochondral cushions and heart defects
cushions play a role in ASD, VSD, transposition of the great vessels, tetralogy of Fallot , if cushions fail to fuse results in persistent atrioventricular canal
conotruncal cushions and heart defects
neural crest cells cause both heart and craniofacial defects in the same individual
transposition of the great vessels (TGA)
failure of the aorticopulmonary septa to develop in a spiral fashion (so aorta lines up with the right ventricle and the pulmonary trunk leaves with the left), leads to cyanosis, complete TGA is incompatible with life if there is no associated septal defect or patent ductus arteriosus (allows for connection between the arch of aorta and pulmonary arteries
persistent truncus arteriosus
no formation of the AP septum, a single arteriole vessel leaves the heart giving rise to the aorta and pulmonary trunks, usually accompanied by a defect in the IV septa, cyanosis
teratology of fallot
failure of outflow tract openings to align with ventricles, cyanosis, most freq. occurring of the conotruncal regions, four classic findings
1. overriding aorta that arises directly over the septal defect
2. pulmonary stenosis
3. rt. ventricular hypertrophy bec. of higher pressure on the right
4. IV septa defect
ventricular septum defects
most common cardiac defect, occurs in about 25% of children with congenital heart disease, occurs through failure of the membranous IV septum to form or muscular VSD which arises from single or multiple perforations in the muscular IV septum
acyanotic congential cardiac anomalies
1. anomialies of the aortic arches
a. right arch of aorta
b. double arch of aorta
c. retro-esophageal right subclavian artery
2. coarctation of aorta
usually acyanotic congenital cardiac anomalies (left right shunts)
1. persistent ductus arteriosus
2. interatrial septal defects
3. interventricular septal defects
cyantoci congenital cardiac anomalies (right left shunts)
1. complete transposition of great vessels
2. truncus arteriosus communis
3. teratology
patent ductus arteriosus
a ductus arteriosus that does not close, can be isolated or accompany other heart defects
coarctation of the aorta
occurs when the aortic lumen below the origin of the left subclavian artery is narrowed
retro-esophageal right subclavian artery
near where the left subclavian is, must cross the midline and posterior to the esophagus to reach the right arm, does not usually cause problems with swallowing or breathing though
double aortic arch
the right dorsal aorta persists, forms a junction with the left arch of the aorta and a vascular ring is present that surrounds the trachea and esophagus and commonly compresses the structures
right aortic arch
arch of the aorta is on the right side bec. left is obliterated, can cause swallowing complaints
interrupted aortic arch
caused by obliteration of the 4th aortic arch on the left side, combined with an abnormal origin of the right subclavian