Cardiovascular Formation of Endocardial Tubes

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  • Formation of Endocardial Tubes

    • Signals from the endoderm cause splanchnic mesodermal cells in cardiogenic plate to aggregate in 2 longitudinal angioblastic cell clusters ventrolateral to the neural plate

    • Clusters canalize  2 endocardial (EC) tubes

    • At the same time, outflow & inflow tracts form

      • Outflow (dorsal aortae)

        • Connected w/ EC tubes before folding begins

        • As a result of folding, dorsal aortae forms 1st aortic arch

      • Inflow (sinus venosus)

        • Receives blood from 3 paired vessels (common cardinal, vitelline, & umbilical veins)

    • Primitive Heart Tube

      • Cephalic folding – 2 EC tubes into thoracic region

      • Lateral folding – 2 EC tubes close together  fuse to form 1 heart tube

      • Day 21: tube elongates & develops dilations & constrictions

      • Day 22: Thick mass of splanchnic mesoderm invests fused EC tubes & differentiates into 2 layers

Splanchnic Mesoderm
Myocardium Cardiac Jelly

Heart muscle Layer of acellular matrix (GAGs & matrix proteins) separates

myocardium & heart tube


-Substrate for cell migration in cardiac septation & valve


-Accumulates to form EC cushion @ AV jxn & in outflow


-Stimulates endothelial cells to migrate into the cushion

matrix where transform to mesenchyme to form fibrous

basis of mitral & tricuspid valves

      • Serous Epicardium (visceral pericardium) derived from dorsal mesocardium (derivative of foregut splanchnic mesoderm)

      • Heart tube bulges into pericardial cavity attached via dorsal mesocardium

      • Dorsal mesocardium ruptures

        • Forms transverse pericardial sinus

        • Heart tube is suspended in pericardial cavity anchored cranially by dorsal aortae & caudally by vitelloumbilical veins

    • By day 21/22 heart begins to beat – but ineffective

      • Blood ( above) enters in sinus venosus & exits via dorsal aorta

  • Cardiac Looping (Day 23)

    • Cardiac tube is constrained at the sinus venosus by the septum transversum, & at truncus region by its connection w/ the aortic arches

    • Free to move between these constraints – bends upon itself & to the R to form the bulboventricular loop

      • Bulbus cordis moves inferior, anterior & to the R

      • Primitive ventricle moves to the L

      • Primitive atrium & sinus venosum move superiorly & inferiorly – now located dorsal & cranial to the ventricle

    • Causes: probably multifactorial involving asymmetrical distribution of actin bundles, pressure of cardiac jelly, cell deformation, & hemodynamic factors

  • Development of the conduction system

    • Modified myocardial cells

    • Nodal tissue develops in sinus venosus w/in R atrium & condenses at entry of SVC as SA node, & near R AV orifice as AV node

    • AV node development accompanied by the appearance of a bundle of specialized conducting cells, bundle of His, that sends 1 branch into R ventricle & 1 branch into L ventricle

      • Must avoid this pathway during repair of VSD

  • Early Circulatory System

    • Inflow and Outflow from Heart

      • Outflow Track: truncus opens into aortic sac from which arise the aortic arches that in turn open into the paried dorsal aortae (formed in paraxial mesoderm & unite from behind heart to level of L4)

      • Inflow Track: sinus venosus receives paired umbilical, vitelline, and common cardinal veins

    • Vitelline Circulation

      • Vitelline arteries arise from the dorsal aortae & bring blood to yolk sac & future gut

        • In Adult: celiac, superior, & inferior mesenteric arteries

      • Blood returns to heart via vitelline veins

        • In Adult: portal & hepatic veins

    • Umbilical circulation

      • Umbilical arteries arise from dorsal aortae & conduct 50% of cardiac output to placenta

      • Oxy blood returns to heart in umbilical vein

    • General Circulation

      • Blood distributed by dorsal intersegmental branches of dorsal aortae to neural tube & somites, & by lateral segmental arteries to developing kidneys & gonads

      • Blood returns to heart via ant. & post. cardinal veins that join to become common cardinal v.

  • Heart Tube Remodeling Starts

    • Up to ~ day 24 sinus venosus = centrally located and there is bilateral symmetry

    • Sinus venosus shifts to the R (1st asymmetric event in embryo)

    • Sinoatrial orifice gradually shifts to the R until sinus venosus communicates only w/ R atrium

  • Formation of Definitive Atria

    • Incorporation of sinus venosus (SV) into the R atrium

      • R & L horns of SV receive blood via common cardinal, vitelline, & umbilical veins

      • As heart undergoes looping and IA septum forms, entrances of SV shift to R atrium

      • Result of LR shunts, R horn enlarges & L horn shrinks

        • L horn remains as coronary sinus of heart

        • R horn is incorporated into R atrium

        • All blood returning to heart via IVC, SVC & coronary sinus enters R atrium

      • Incorporated SV forms smooth walled sinus venarum of definitive R atrium

      • R venous valve of SA orifice forms crista terminalis, valve of the IVC and valve of the coronary sinus

      • The original embryonic R atrium becomes pectinate auricular appendage

    • Embryonic L atrium = greatly expanded by incorporation of primitive pulmonary vein and its branches.

      • Pulmonary vein tissue smooth-walled part of definitive atrium

      • Embryonic L atriumauricular appendage

  • Partitioning of the Heart (4th-7th weeks)

    • Artioventricular canal

      • At day 28, a common atrium communicates w/ a common ventricle through a single AV canal

      • Endocardial cushions (accumulation of cardiac jelly) form on dorsal & ventral walls of AV canal (day 35), fuse (day 42), and divide the single canal into 2 (R & L AV canals)

      • Adherons (proteoglycan particles) produced by myocardial cells accumulate in EC cushion tissue

        • Induce overlying endothelium  mesenchyme  migrate into cardiac jelly

        • Mesenchymal cells participate in formation of definitive mitral & tricuspid valves

      • EndothelialMesenchymal transformation also occurs in proximal bulbus cordis, but NOT in primitive atrium or ventricle.

        • Prevented by inactivation of transforming growth factor – β3

    • Interatrial Septum Formation

      • Primitive atrium divided into R & L atria by formation of IA septum

      • Septum primum (sickle shaped) grows from roof of atrium toward EC cushions;

        • Foramen primum = opening btwn lower edge of septum primum & AV cushions

          • Gets progressively smaller & is obliterated when septum primum fuses w/ fused AV cushions

        • Before foramen primum is completely obliterated, genetically programmed cell death creates perforations in septum primum, which coalesce to form the foramen secundum.

          • Blood continues to flow from R to L to avoid loading pulm. circ.

      • Septum secundum appears to the R of septum primum & overlaps foramen secundum.

        • Opening btwn lower edge of septum secundum & fused AV cushions = foramen ovale.

      • Blood flows RL via foramen ovale & btwn overlapping edges of septum secundum & septum primum into L atrium (blood only flows RL)

      • Persistent part of septum primum below foramen secundum = valve of foramen ovale

        • In postnatal life valve of foramen ovale=floor of fossa ovalis, overlapping edges of septa fuse to form limbus of fossa ovalis

    • Interventricular Septum Formation

      • Muscular IV septum results from dilations of ventricles on each side of it. Grows actively toward but does not read fused AV cushions leaving IV foramen

      • Membranous IV septum completes septum

        • Derived from AV cushion tissue that fuses w/ aorticopulmonary septum & muscular IV septum

      • Cavitation of ventricular walls  trabeculae carneae, papillary muscles, & chordae tendineae

    • Partitioning of Bulbus Cordis & Truncus Arteriosus

      • Aorticopulmonary Septum

        • Derived from neural crest mesenchyme

        • Divides bulbus cordis & truncus arteriosus into ascending aorta & pulmonary trunk

        • Fuses w/ AV cushions to help form membranous IV septum

        • Formed by fushion of ridges that appear in bulbus & truncus (spiral fushion)

      • Neural crest cells migrate to form:

        • Tunica media of ascending aorta & pulmonary trunk

        • CT of leaflets of aortic & pulmonary valves (form at base of bulbus)

      • Bulbus cordis forms the:

        • Trabeculated part of R ventricle (primitive ventricle  trabeculated L ventricle)

        • Conus arteriosus in R ventricle

        • Aortic vestibule in L ventricle

  • Development of Veins Associated w/ the Heart

    • L & R ant. cardinal veins (drain blood from brain) anastamose & blood is shunted to the R ant. cardinal vein

      • L ant. cardinal vein disappears below anastomosis

      • Portion of L ACV above anastomosis becomes L brachiocephalic vein; portion of R ACV above anastomosis become R brachiocephalic vein

      • Portion of R ACV below anastomosis is SVC

      • All blood returning from head, neck, & upper limbs enters SVC

    • Posterior Cardinal Veins disappear (mostly)

      • Terminal portion of R PCV forms azygous vein

    • R umbilical vein, L umbilical vein, & L vitelline vein btwn liver & sinus venosus disappear

    • R vitelline vein btwn liver & sinus venosus become IVC

  • Aortic Arches

    • First: forms due to folding (day 22-24)

      • largely disappears, remainder forms maxillary arteries

    • Second: develops from angioblasts that migrate from surrounding splanchnic mesoderm

      • largely disappear, remainder form stapedial arteries

    • Third: appear as 1st arch regresses (day 28)

      • develop from angioblasts that migrate from surrounding splanchnic mesoderm

      • form common carotid and proximal portion of internal carotid arteries

        • *[distal internal carotids form by cranial portions of dorsal aortae]

    • Fourth: appear as 1st arch regresses (day 28)

      • develop from angioblasts that migrate from surrounding splanchnic mesoderm

      • L – forms the arch of the aorta (connect the ventral & dorsal aorta)

      • R – forms proximal part of the R subclavian artery

        • *[distal part from R dorsal aorta & R 7th intersegmental artery]

    • Fifth: absent in 50% of embryos;

      • regresses completely – no known contributions

    • Sixth: forms as 2nd arch regresses (day 29); gives branches to lungs

      • R & L proximal portions  R & L pulmonary arteries

      • R distal portion disappears

      • L distal portion  ductus arteriosus (ligamentum arteriosus in adult; shunt connecting aortic arch to pulmonary artery to prevent lungs from being overworked)

  • Fetal Circulation

    • Umbilical vein carries oxy blood from placenta  fetus

      • 80% shunted through ductus venosus  IVC (to avoid liver)

      • IVC also conducts deoxy blood from lower trunk, lower limbs, & liver

    • IVC blood enters R atrium & almost all is shunted  L atrium through foramen ovale

      • Mixes w/ deoxy blood from lungs (small amount)

    • Enters L ventricle & ascending aorta (distributed to heart, head, neck, & upper limbs immediately – remainder continues along aorta)

    • SVC receives deoxy blood from upper body

      • Enters R atrium (mixes w/ small amount of IVC blood left over)

      • Flows into R ventricle & on to pulmonary trunk

      • Only a small amount enters lungs (b/c high pulmonary resistance)

        • Most flows through ductus arteriosus to descending aorta to return to placenta via umbilical arteries (40% of blood in descending aorta to placenta)

        • Some small amount goes to lower limbs & lower trunk

    • Patency of ductus arteriosus & ductus venosus in the fetus is maintained by prostaglandins (PG)

      • Can take NSAIDS to block PG synthesis if born w/ patent one

  • Changes at Birth

    • First Inspiration:

      • Opens up pulmonary vascular bed (blood in pulmonary trunk enters lungs)

      • Pressure in ductus arteriosus drops (constricts minutes after birth)

      • Lots of blood entering L atrium through pulmonary veins ( L atrial pressure)

    • Cutting of Umbilical Cord:

      • No more blood entering body via umbilical vein

      • Reduces blood entering R atrium ( R atrial pressure)

    •  L atrial pressure +  R atrial pressure = L atrial pressure >> R atrial pressure

      • Valve of foramen ovale pushes tightly against septum secundum

        • Functionally closes foramen ovale

      • Adherence of septum primum to edge of septum secundum is secure by

        • Intially: fibrin deposits

        • Replaced by: fibrous CT over several months

  • Congenital Defects

    • Most frequent group of serious malformantions, w/ an incidence of around 8/1000 live births

    • Etiology:

      • Single gene defects

      • Chromosomal abnormalities (10%) – e.g. Down syndrome, trisomies 18,13

      • Environmental factors – e.g. thalidomide, rubella, anti-convulsant drugs, high EtOH intake

      • Unknown – regarded as multifactorial – produced by a genetic predisposition acting w/ unknown environmental factors

    • Most vulnerable period of cardiovascular dvlpmnt = 3rd-7th wk

    • 80% of CV malformations due to: ASD, VSD, pulmonary & aortic stenosis, Fallot’s tetralogy, persistent ductus arteriosus, coarctation of aorta, abnormalities of position

    • Atrial Septal Defects (ASD)

      • Result in mixing of oxy & deoxy blood

      • Can lead to (all due to blood moving to the R because of pressure on the L):

        • Pulmonary hypertension

        • R ventricle & pulmonary trunk enlargement

        • Heart failure

      • Probe Patency of foramen ovale:

        • Incomplete adhesion btwn overlapping edges of septum primum & septum secundum

        • Usually not clinically significant (high pressure in L atrium would force it closed)

      • Secundum ASD:

        • Patent fossa ovalis caused by:

          • Excessive resorption of septum primum

          • Defective formation of septum secundum

      • Endocardial cushion defect w/ primum ASD:

        • Incomplete fusion of AV EC cushions preventing proper fusion of septum primum w/ them

        • Persistent foramen primum

        • Often associated w/ abnormal mitral valve & VSD

        • Often occurs in Down’s Syndrome

    • Ventricular Septal Defects (VSD):

      • Most common type of cardiac defect (25%)

      • Membranous VSD:

        • Defect in formation of membranous part of septum

        • Caused by failure of muscular portion of IV septum to fuse w/ free edges of cushions

      • Muscular VSD:

        • Caused by cavitation of myocardial tissue during formation of muscular septum

    • Abnormal Division of Truncus Arteriosus:

      • Persistent Truncus Arteriosus:

        • Failure of truncal swellings to grow

        • Single artery arises from both ventricles above the VSD (pulmonary & systemic blood mix)

          • Distall divide into aorta & pulm. trunk by incomplete septum

    • Transposition of Great Vessels:

      • Aorta arises from R ventricle & pulm. trunk arises from L

      • Failure of truncoconal swellings to grow in normal spiral directions

      • Associated w/: VSD & Patent Ductus Arteriosus

      • Associated symptoms allow survival (oxy blood to reach the body)

    • Tetralogy of Fallot:

      • Most common cause of blue baby

      • Conus septum develops too far anteriorly (causes a large aorta & a small stenotic pulm. trunk)

      • Characteristics (4):

        • Pulmonary stenosis

        • VSD of membranous portion (septum too far anterior)

        • Overriding aorta (straddles the VSD)

        • R ventricular hypertrophy (shunting blood L  R; pulmonary stenosis   R ventricular pressure  walls expand)

    • Aortic or Pulmonary Stenosis:

      • Thickened aortic or pulmonary valve (narrowed)

      • Causes abnormally high pressure in L or R ventricle

        • Wall of ventricle becomes hypertrophied (stenosis of valve restricts flow)

        • Causes heart murmur

        • Narrowing can be mild, but often worsens w/ growth

        • If severe, symptoms may develop, or heart may show evidence of strain

          • Valve may require treatment to open it

    • Malformations of Great Arteries:

      • Persistent Ductus Arteriosus:

        • 10% of CVS malformations in infancy

        • Normally functionally closes w/in a few days after birth, anatomically closes w/in a few wks

        • Often associated w/ premature birth & rubella

        • Blood flows from aorta to pulmonary artery

      • Coarctation of Aorta:

        • 10% of major CVS malformations

        • Narrowing of aorta, usually proximal to ductus arteriosus

        • When ductus closes, blood reaches lower part of body through collateral pathways

          • Scapular anastomosis (connects w/ intercostal arteries, blood flows into thoracic aorta)

          • Internal thoracicsuperior epigastricinferior epigastricfemoral a.

        • Should always be suspected in young adults w/ hypertension

          • Femoral pulses reduced & delayed

          • Enlarged intercostal arteries

    • Abnormalities of Position

      • Dextrocardia (apex of heart on the R):

        • Primitive heart tube folds to the L (instead of to the R)

        • Mirror image of normal

        • Occurs in situs inversus (all organ systems reversed)

Cardiac Development Timeline

Summary of Embryonic Derivatives

Respiratory and GI Tract

  • Overview

    • Gut forms from folding of endoderm & splanchnic mesoderm ventrally (transverse & cephalocaudal) during wk 4

    • Layers

      • Endodermepithelial lining of resp. system & gut tube except lower anal canal, & glandular tissue

      • Splanchnic mesodermmuscle, vessels & CT & visceral layers of serous membranes, pleura, pericardium & peritoneum

      • Somatic mesodermparietal layer of those membranes & contributes to body wall

      • Ectodermlower anal canal epi.

        • neural crest cellsenteric plexus & support cells of PNS

    • Extent: begins as tube bounded by stomodeum & buccopharyngeal membrane at cranial end, cloacal membrane & proctodeum at caudal end, suspended btwn dorsal & ventral mesentery


  • Larynx, Trachea and Bronchi

    • Derivation

      • Begins as diverticulum of foregut

      • Endoderm forms epi. and glands of larynx, trachea, bronchi, and lungs

      • Mesodermsmooth muscle, CT, cartilage (except for laryngeal cartilage & muscle that come from pharyngeal arches)

    • Development

      • Respiratory diverticulum: develops wk 4 in floor of pharyngeal endoderm caudal to 4th pouches, surrounded by splanchnic mesoderm, elongates & enlarges into R & L lung buds

      • Separation of trachea & esophagus: tracheoesophageal ridges/folds develop and fuse to form tracheoesophageal septum

        • Creates laryngotracheal tube separate from foregut

        • Communication w/ foregut maintained at laryngeal inlet

        • Process requires sonic hedgehog protein (shh)

      • Development of Larynx: develops at cephalic end of resp. diverticulum (endodermint. lining; mesoderm of 4th & 6th pharyngeal archescartilage & muscle)

        • 2 swellings develop – epiglottal & arytenoid  epiglottis & laryngeal cartilages

        • laryngeal orifice: slitT shaped opening

        • prolif. of laryng. epi.temp. occlusion of lumen

          • wk 9-10 recanalization, formation of ventricles, true & false vocal folds

        • grows rapidly in first 3 years after birth

        • Derivatives of 4th innerv. by sup. laryngeal n. & 6th innerv. by recurr. laryngeal n.

    • Clinical Correlations

      • Definitions

        • Atresia=absence of normal opening or absence of normally patent lumen

        • Fistula=abnormal passage from an organ to the body surface or btwn organs

        • Abnormalities in amounts of amnionic fluid:

          • Polyhydraminos=excessive amount of amnionic fluid

            • Due to: GI abrnomalities w/ inadequate swallowing (duodenal/esophageal atresia) or other dvlpmntl anomalies

            • Results in: maternal complications due to abdominal swelling & fetal complications such as impaired uteroplacental perfusion

          • Oligohydraminos=deficient amount of amnionic fluid (deficient fluid to vitrually none)

            • Due to: faulty dvlpmnt of the urinary system (renal agenesis/polycystic kidney)  urine not added to amnionic fluid

              • Bilateral renal agenesissevere oligohydraminos

            • Results in: compression of mat. abdomen & thoraxnot enough room for lungs to expandpulmonary hypoplasia

      • Esophageal atresia (EA) and/or Tracheoesophageal Fistula (TEF): abnormality in partitioning of the esophagus & trachea by the tracheoesophageal septum

        • Most common variation=upper part of esophagus ends in blind pouch (EA) & lower part opens into the trachea (TEF)

        • TEFs are most common abnormality in dvlpmt of lower resp. tract

        • EAs & TEFs commonly accompanied by polyhydraminos b/c amnionic fluid does not enter GI tract for absorption (if poly.  suspect GI anomaly)

        • Clinical Findings for EA & TEF

          • Polyhydraminos prenatally

          • Copious frothy bubbles of mucus in the mouth

          • Coughing & choking when fed

          • Difficulty breathing, cyanosis or pneumonia may develop if there is a connection to the trachea

          • If there is a fistula, air builds up in abdomen

          • Often associated w/ other abnormalities (Down’s syndrome, duodenal atresia, CV defects)

        • Treatment=surgery (other defects corrected 1st), ~100% survival w/o other defects

  • Bronchial Tree and Lungs

    • Derivation

      • Bronchi & lungs develop from resp. diverticulum of foregut

    • Development

      • Factors affecting development:

        • Interaction btwn endoderm & mesoderm: epi. (endo) produces shh which acts on meso, meso produces growth factors  endo to develop airways & air sacs

        • Establish adequate vasculature & surfactant

        • Chemical factors

          • Shh: separation of trachea & esophagus

          • Corticosteroids: differentiation of Type II cells

          • Thyroid hormones: normal development of lungs

          • Many growth factors

        • Mechanical factors: fetal breathing movements, patency of fetal airways, adequate thoracic space, adequate amniotic fluid volume

      • Stage of Lung Development:

        • Embryonic (26 days-6wks): lung bud develops, branches into main, lobar, & segmental bronchi (bronchopulmonary segments are established)

          • Pulm. artery, vein, & capillary bed present

          • Primitive pleural cavities develop

        • Pseudoglandular (5-16 wks): formation of terminal bronchioles, survival still impossible (no resp. bronchioles, alveoli, or contact w/ BVs)

          • Cartilage, glands, & bronchial smooth muscle developing

          • Diaphragm forming

          • Pulm. vessels are branching

        • Canalicular period (16-26 wks): gas exchange portion begins to develop, terminal bronchioles divide into several resp. bronchioles

          • Terminal sacs appear toward end

          • Type II cells present

          • Surfactant formed at low levels wk 20-26 &  w/ time

          • Vasculature develops close to resp. bronchioles (survival is possible at end)

        • Terminal Sac (26wks-birth): terminal sacs  in #, capillaries bulge into developing alveoli, well developed Type I and II cells

          • Type I cells thin & rudimentary blood-air barrier is formed (gas exchange)

          • Significant rise in surfactant levels at wk 30

        • Alveolar period (30wks-8yrs): alveoli mature &  in # during first 2yrs

          • Most mature alveoli form after birth through age 8

    • Clinical Correlations

      • Forensic med. (determine stillbirth vs. death after birth): at birth lungs=1/2 full of fluid so

        • Stillborn  lungs have fluid  sink in water

        • Died after birth  lungs filled w/ air  float in water

        • Better test=lungs, larynx, trachea, & bronchi in water

        • Newborn lungs have dilated alveoli, open bronchi, & open capillaries full of RBCs

      • Surfactant=complex of lipids & proteins including phosphotidyl choline & surfactant proteins A, B, C, D; lines alveoli, reduces surface tension, & prevents collapse of alveoli

        • Excreted by fetus into amniotic fluid

        • Adequate levels=essential for survival

      • Assessment of fetal lung maturity (using amniotic fluid via amniocentesis)

        • Early test: L/S ratio (L=lecithin-phospholipid in surfactant, S=sphingomyelin-phospholipid in cell mem.)

          • 2.0 L/S – mature

          • 1.5< L/S < 2.0 – borderline

            • 50% of these babies develop RDS (test doesn’t tell you which)

          • L/S 1.5 – immature

          • Time consuming, expensive, & only can be used before water breaks

        • Other tests: look at surfactant in amniotic fluid to determine maturity

          • Some less expensive & some can be used after water breaks

      • Respiratory Distress Syndrome (RDS): alveoli partially collapsed & covered by amorphous material containing fibrin, cellular debris & macrophages preventing gas exchange

        • Due to insufficient surfactant

        • Leading cause of death in premature babies

        • Material represents hyaline membrane (old name=hyaline membrane disease)

        • Treatment: corticosteroids (aids development of surfactant), assisted ventilation, administration of artificial surfactant

          • Ideally delay labor & treat w/ corticosteroid until surfactant produced

      • Pulmonary hypoplasia=underdevelopment of lungs w/  # of alveoli & airways; due to:

        • Thoracic compression – due to bilateral renal agenesis/urinary outflow obstruction  oligohydraminos  pressure on fetal thorax

        • Decreased intrathoracic space – due to congenital diaphragmatic hernia (most common cause of pulmonary hypoplasia)

        • Decreased fetal breathing – due to CNS damage

  • Formation of Pleural and Pericardial Cavities

    • Derivation

      • Lateral mesoderm splits into 2 layers & embryo undergoes cephalocaudal & lateral folding

      • In intraaembryonic cavity:

        • Somatic mesodermparietal layer of serous membranes

        • Splanchnic mesodermvisceral layer of serous membranes

        • Layers=continuous at dorsal mesentery

      • 4wks – intraembryonic cavity = horseshoe-shaped cavity, curving around cranial end of embryo; septum transversum incompletely separated the cranial primitive pericardial cavity from peritoneal cavity  3 distinguishable regions

        • pericardial cavity around the heart

        • 2 pericardioperitoneal canals

        • Peritoneal cavity

    • Development

      • Division of pericardial cavity from the pleural cavities

        • Pleuropericardial folds aris from lateral wall, extend medially & extensions (enclose phrenic nerve) are known as pleuropericardial membranes

        • They fuse & separate the pleural cavities from the pericardial cavities

        • In Adult they are the fibrous pericardium

        • Phrenic nerves become located btwn fibrous pericardium & pleura

      • Formation of the diaphragm

        • Septum transversum = mesoderm btwn thoracic cavity & stalk of yolk sac

          • partially separates thoracic & abdominal cavities

        • Pleuropericardial membranes separate pericardial from pleural caivites

          • Pleural cav. communicate w/ peritoneal cav. via pericardioperitoneal canals

        • Pleuroperitoneal folds grow from posterolateral wall of pericardioperitoneal canals & fuse w/ septum transversum & mesentery of esophogaus to separate pleural from peritoneal by wk 7

        • Summary:

          • Septum transversumcentral tendon of the diaphragm

          • Pleuroperitoneal membranes extend from posterolateral walls across pericardioperitoneal canals & fuse w/ septum transversum  posterolateral portion of diaphragm

          • Body wall added to outer margins of pleuroperitoneal membranes

          • Myoblasts in dorsal mesentery of esophaguscrura of diaphragm

            Part of Gut

            Blood supply



            Pharyngeal arch sources
            Pulmonary & bronchial arteries, esophageal arteries
            Celiac artery

            Part of floor of mouth

            Pharynx & derivatives

            Respiratory system




            Liver, gallbladder, biliary duct system

            Duodenum proximal to bile duct


            Has connection w/ yolk sac & umbilical region

            Superior Mesenteric Artery

            Duodenum distal to bile duct

            Jejunum & ileum

            Cecum & vermiform appendix

            Ascending Colon

            R ½ to 2/3 of transverse colon


            Inferior mesenteric artery, except for bladder & urethra

            L 1/3 to ½ of transverse colon

            Descending colon

            Sigmoid Colon


            Superior portion of anal canal

            Derivates of UG sinus
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