10/31 Cardiovascular Embryology and Anatomy - Wondisford Flashcards Preview

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Flashcards in 10/31 Cardiovascular Embryology and Anatomy - Wondisford Deck (24):

importance of yolk sac in human devpt

allantois and yolk sac both don't have as significant a role as they do in other organisms' devpt (ex. chicken) bc the PLACENTA serves as the clearinghouse for nutrients and waste


importance of yolk sac: critical for blood cell development (devpt of vitelline system)

  • umbilical vessels establish connections with chorion
  • vitelline vessels establish connections to umbilical vesicle, serve as source of blood cells
  • dorsal aorta and cardinal vessels (paired) → body
  • venous drainage to primordial heart goes through sinus venosus


fetal erythropoiesis


site shifts throughout embrynoic devpt

"young liver synthesizes blood"

  1. yolk sac (3-8wk)
  2. liver (6wk-birth)
  3. spleen (birth→10-18wk)
  4. bone marrow (18wk-adulthood)


hemoglobin devpt


diff bw fetal and adult Hb

HbF (alpha2gamma2) → HbA (alpha2beta2)

"alpha always, gamma goes, becomes beta"


  • HbF binds 2,3BPG less avidly → higher affinity for oxygen than HbA
  • important diff: allows HbF to extract oxygen from HbA across placenta
    • seen in leftward shift of HbF oxygen dissociation curve


heart morphogenesis

(horseshoe model)

1. heart tubes (horseshoe) start off...

  • superior to the mouth
  • ventral to intra-embryonic coelom (develops into pericardial, pleural, peritoneal cavities)
    • distal part of each limb of intraembryonic coelom is continuous with extraembryonic coelom at the lateral edges

as head grows, heart tubes fold ventrally → trap foregut on either side by paired dorsal aorti

  • pericardial cavity is now anterior
  • head and mouth are now superior

heart tubes approach each other in midline → venous drainage develops

septum transversum (primordium of central tendon of diaphragm) will separate heart and lungs from peritoneal cavity!


embryologic derivatives

1. truncus arteriosus segment

  • aortic sac → pharyngeal arches
  • truncus arteriosus (b/w sac and bulbus cordis) → ascending aorta and pulmonary trunk

2. bulbus cordis segment

  • bulbus cordis → outflow tract (smooth part) of LV and RV

3. ventricle segment

  • primitive ventricles → trabeculated part of both ventricles
  • primitive atria → trabeculated part of both atria

4. atrium segment

  • left horn of sinus venosus → coronary sinus
  • right horn of sinus venosus → smooth part of RA
  • right cardinal veins → SVC
  • primitive pulmo veins → smooth part of LA



embryologic derivatives of key veins


  • R vitelline v
  • L vitelline v
  • R umbilical v
  • L umbilical v
  • anterior cardinal v
  • posterior cardinal vv

  • R vitelline v → hepatic vein
  • L vitelline v degrades
  • R umbilical v degrades
  • L umbilical v → remains
  • anterior cardinal v → SVC, jugular, sublavian
  • posterior cardinal vv → IVC, azygos system


heart morphogenesis


basic development timeline

division of heart

  • heart is the first functional organ in vertebrate embryos
    • beats spontaneously by week4
  • primary heart tube loops to establish L/R polarity beginning in week 3.5 of gestation
  • cilia appear to be important in normal heart rotation

division of heart

  • AV endocardial cusions (invaded by NC cells) approach each other and fuse in ventral-dorsal direction
  • AV canal is split into L and R canals, where AV valves will eventualy form


neural crest cell derivatives

  1. PNS (dorsal root ganglia, CNs, autonomic ganglia, Schwann cells)
  2. melanocytes
  3. chromaffin cells of adrenal medulla
  4. parafollicular (C) cells of thyroid
  5. pia and arachnoid
  6. bones of skull
  7. odontoblasts
  8. aorticopulmonary septum
  9. endocardial cushions


Kartagener's syndrome

rare autosomal recessive disorder

type of primary ciliary dyskinesia

  • defects in dynein (involved in L/R asymmetry) cause ciliary dysfx
  • defective movement of cilia → recurrent chest, ear, sinus infections and infertility


1. situs inversus

2. chronic sinusitis

3. brinchiectasis


most common positional defect of heart: DEXTROCARDIA


atrial septal devpt


key players: septum primum, septum secundum, foramen primum, foramen secundum

Q: why have holes in the heart?

typical fate of foramen ovale

1. septum primum grows toward endocardial cushions → foramen primum narrows

2. foramen secundum forms as small hole within septum primum

3. foramen primum disappears afer fusion of septum primum with endocardial cushion

foramen secundum maintains a R→L shunt!!! so heart grows another septum to take care of it

4. septum secundum develops and expands to cover most of foramen secundum

  • residual foramen is called foramen ovale
  • remaining portion of septum primum → valve of foramen ovale!

Q: what's the point of having holes in the heart?

  • A: during devpt, want to be able to bypass the lungs!


*foramen ovale usually closes and fuses soon after birth bc of increased LA pressure as blood flows from lungs to LA

  • doesn't happen in 25% of population → patent foramen ovale


atrial septal defects


3 types

common consequence of all three & correlation with age

1. ostium secundum type (90%)

  • caused by abnormal/insufficient growth of septum primum or secundum

2. ostium primum type (5%)

  • when septum primum doesnt fuse with endocardial cushion
  • seen in Down syndrome, assoc with AV valve defects

3. patent foramen ovale (common: 25% of adults)

  • caused by faulre of septum primum and secundum to fuse after birth
  • not considered a true ASD and tx (closure) is controversial


both ASD and PFO can lead to paradoxical emboli (venous thromboemboli entering systemic arterial circ)

  • pathway: embolus from leg/pelvis → through ASD → into LV → CNS → stroke
    • unlikely in patients without ASD bc clots would typically just go to lungs → pulmonary embolism
  • likelihood increases with age bc L→R shunt in atrium overloads the lung, leading to pulmo HTN (due to vasoconst) and reversal of atrial shunt
    • Eisenmenger's syndrome!


ventricular septation

most common congenital heart defect (25% of all defects)

most commonly occurs in membranous septum



  • muscular ventricular septum forms first; opening = interventricular foramen
  • aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen
    • requires neural crest cells


conotruncal abnormalities

due to failure of neural crest cells to migrate to heart


1. transposition of great vessels (aorta off of RV, pulmonary trunk off of LV)

2. Tetralogy of Fallot

  • LVH
  • ventricular septal defect
  • aorta that overrides LV and RV
  • infundibular stenosis (R→L shunt)

3. persistent truncus arteriosus (deoxy blood going into blood)





early vs late

  • direction of shunt
  • pathophys
  • examples

early cyanosis

  • "blue babies" due to RL shunts : deoxy blood reaches systemic circulation
    • transposition of great vessels
    • Tetralogy of Fallot
    • persistent truncus arteriosus

late cyanosis

  • "blue kids" due to LR shunts : eventually overwhelm lungs → incr PVR → reverse shunt to R→L (Eisenmenger's Syndrome)
    • ASD
    • VSD
    • patent ductus arteriosus


valve development

aortic/pulmonary : derived from endocardial cushions of outflow tract

mitral/tricuspic : derived from fused endocardial cushions of AV canal

*valvular anomalies may be...

  • atretric/stenotic/regurgitant (ex. tricuspic atresia)
  • displaced (ex. Ebstein anomaly)
    • Ebstein anomaly: portion of RV is atrialized bc tricuspid valve is too low → functional RV is small.
    • assoc with lithium tx for bipolar disorder in moms)


Ebstein anomaly

portion of RV is atrialized bc tricuspid valve is too low → functional RV is small.

assoc with lithium tx for bipolar disorder in moms)


Tetralogy of Fallot


why squat?

characterized by 4 findings:

  • large VSD (vent septal defect)
  • overriding aorta
  • obstruction of RV outflow tract
  • RV hypertrophy

due to obstruction of RV outflow tract, blood is shunted through the VSD from R→L


long periods of squatting can help kids become less cyanotic. why?

  • squatting increases systemic vascular resistance → harder to unload LV → harder for R to L shunt to push blood to left side


summary 2


CORRECTION: late cyanosis is L to R shunt


evolution of pharyngeal arch arteries

in humans, aortic arch arteries arise in cranio-caudal sequence and form a basket of arteries around the pharynx


aortic arch derivatives

1st arch : maxillary a

2nd arch : stapedial and hyoid aa

3rd arch : common carotid a and proximal part of internal carotid a

4th arch : left? aortic arch. right? prox part of R subclavian a

6th arch : prox part of pulmonary a and (L side only...) ductus arteriosus


coarctation of aorta

postductal coarctation : constriction distal to ductus arteriosus

  • permits devpt of collateral circ during fetal period → assists with passage of blood to lower body
  • presents later in life with weak lower extremity pulses, upper extremity HTN, rib notching from collateral circ


preductal coarctation : Turner Syndrome : constriction proximal to DA

  • before birth, blood flows through DA to desc aorta for distribution to lower body
  • collateral do not develop in utero → can be life-threatening condition in neonate


juxtaductal coarctation : constriction at DA

  • most common
  • behaves most like a postductal coarctation if unrecog'd at birth


preductal vs postductal coarctation of aorta


which one has collateral formation? why?

preductal coarctation of aorta DOES NOT result in formation of collaterals

  • since blood can flow through DA in utero, lower limbs stay perfused
  • after birth, when DA closes, lower limbs experience significant sudden drop in perfusion → potentially life-threatening

postductal coarctation of aorta DOES result in formation of collaterals

  • DA is not useful in providing lower limbs with blood supply → lower limbs signal for angiogenesis → collaterals form
  • after birth, when DA closes, collateral system is able to continue taking on task of perfusion, so no sudden drop in flow


umbilical veins


  • chars of blood
  • 3 imp shunts

blood in umb vv has PO2 of 30mmHg

80% saturated with )2


three shunts:

  1. blood entering fetus: via ductus venosus into IVC
  2. most O2-rich blood reaching heart: via IVC, diverted into foramen ovale
  3. deoxy blood entering RA: from SVC→RA→RV→main PA→patent ductus arteriosus→descending aorta


how does ductus arteriosus close at birth?


what do you give to close it?

what do you give to keep it open?

at birth, infant takes a breath

  • low resistance in pulmonary vasculature → incr LA pressure
  • foramen ovale closes
  • increase in 02 (from respiration) and decrease in prostaglandins → closure of ductus arteriosus
    • remnant of DA = ligamentum arteriosum



PGE1 and E2 : keep PDA open