101514 dev of heart Flashcards
cardiac precursors are from?
splanchnic mesoderm
cardiogenic crescent
primary heart field-the U shaped region of splanchinic mesoderm that heart develops from
folding in the cranial caudal plane results in a
ventral heart
what can incomplete formation of the ventral wall of the thorax cause in heart dev?
ectopic cordia (anterior thoracic wall fails to close properly
what is the INITIAL primitive heart tube?
primitive L ventricle (at this time, has arterial and venous poles). arterial pole is superior
what allows for elongation of the primitive heart tube?
secondary heart field
cardiac jelly
expanse of ECM in primitive heart tube–it’s in btwn the myocardium and endocardium. it’s a good scaffold for later things to migrate to.
what does epicardium of primitive heart tube derive from?
proepicardial organ, a derivative of the coelomic epithelium that overlies inflow region
cardiogenic mesoderm forms what?
endocardial endothelial cell
atrial myocyte
ventricular myocyte, PUrkinje fiber
proepicardium forms what?
coronary sm musc
endothelial cell of coronary vessel
fibroblast (for visceral pericardium)
venous inflow enters what in the simple tubular heart?
sinus venosus
arterial outflow is originally from what?
primitive RV
looping usually going in what direction?
right
heart begins to beat when?
21 days
what tissues are used for partitioning of heart
cardiac muscle
cardiac mesenchyme (encocardial cushion tissue)
extracardiac mesenchyme (mesoderm origin)
neural crest mesenchyme
by what day does the sinus venosus (right and left horn) connect with the primitive heart tube primordial atrium?
22
what happens with regards to the sinus venosus during wks 5-8?
left sinus venosus becomes a tributary of the right sinus venosus
so all venous return enters the right side of heart
where does smooth area of right atrium come from?
absorption of sinus venosus (primarily the right horn)
where does the appendage (auricle) come from?
primordial atrium
where does endocardial cushion tissue form?
AV canal and outflow region (involves epithelium to mesenchyme transformationation–endocardial cells turn into cardiac mesenchyme cells which move into the cardiac jelly)
what subdivides the AV canal?
septum intermedium
cardiac mesenchyme contributes also to formation of what?
valve leaflets and chordae tendinae
fibrous skeleton of the heart
does the interventricular septum close?
no, it never does.
a secondary interventricular communication is closed by formation of membranous interventricular septum
what is present in the proximal and distal portions of the outflow region?
endocardial cushion tissue
aortic sac is divided by what?
neural crest derived mesenchyme that forms the aorticopulmonary septum
endocardial cushion tissue can be present in
division of common AV canal
proxima and distal portions of outflow region
membranous interventricular septum
how is o2 rich blood shunted around liver?
ductus venosus
what explains the inactivity of the pulmonary circulation?
high vascular resistance in lungs (fluid in lungs)
congenital heart disease problems can present when?
stillbirth
at birth
or remain undetected until later life
types of L to R shunt
ASD
VSD
AVSD
PDA
have D’s in their names
are late cyanotic
obstruction types of congenital heart disease
pulmonary stenosis
aortic stenosis
coarctation
they are acyanotic
types of R to L shunt
tetralogy transposition truncus TV atresia TAPVR
all start with T’s
valvular regurgitation types of congenital heart disease
Ebstein
plexogenic pulmonary HTN
medial hypertrophy intimal proliferation plexiform lesions (irreversible damage)
more severe in VSD than PDA, which are both more severe than in ASD
majority of atrial septal defects are at what location
secundum
why do less than 10% of ASD lead to pulmonary HTN?
b/c of the low pressure and volume of the atrium
where is the location of 90% of VSD?
septum-membranous VSD
what is the most common congenital heart anomaly
VSD
VSDs are usually associated with
other anomalies (only 30% of them occur in isolation)
what to do for VSD?
surgical closure, usually around year 1
can ASD be asymptomatic?
yes, can be until adulthood
perimembranous VSD
defect is usually large
muscular VSD
defect is usually small
spontaneous closure by fibrous adhesions occurs in more than 60% of cases by year 1
most don’t need surgery
what is PDA closure delayed by?
prostaglandin E
when should PDA close structurally?
by 3 months
classic PE finding for PDA
harsh, continuous, machinery like murmur
is PDA usually seen with other anomalies or in isolation?
in isolation
atrioventricular septal defect
deficient AV septum, associated with mitral v and tricuspid v anomalies
what is associated with complete AVSD?
Down syndrome
complete AVSD is characterized by
common AV valve (five leaflets)
what causes early cyanosis
R to L shunts
what can you get with R to L shunts?
paradoxical emboli, decompression sickness
symptoms of R to L shunts
cyanosis
digital clubbing
polycythemia (too many RBCs)
what is the most common form of cyanotic congenitcal heart dis
tetralogy of fallot
tetralogy of fallot
anteriosuperior displacement of infundibular septum leads to-ventricular septal defect, subpulmonary stenosis, overriding aorta, R ventricular hypertrophy
clinical outcome of tetralogy of fallot depends on
severity of subpulmonary stenosis–will determine how much damage lungs will incur (the more stenosis, the more protected the lungs will be)
findings for tetralogy of fallot
boot shaped heart on XR due to R ventri hypertrophy
transposition of great arteries
aorta arises from RV
pulmonary artery arises from LV
sequalae of transposition of great arteries
separate pulmonary and systemic circulations (two separate loops)
R ventr hypertrophy
pulmonary HTN
two types of transposition of great arteries
intact ventricular septum
or
with VSD
truncus arteriosus
origin of aorta and pulmonary artery from truncal artery
most have large VSD
sequalae of truncus arteriosus
mixing of blood
increased pulmonary blood and pulm HTN
tricuspid atresia
complete occulsion of tricuspid valve orifice
results from unequal division of AV canal (mitral valve is enlarged)
needs coexisting ASD/PFO and VSD
causes R ventricular hypoplasia
symptomatic, high mortality
total anomalous pulmonary venous return
pulmonary veins don’t directly drain into L atrium (L atrial hypoplasia)
connect via left innominate vein or coronary sinus
ASD/PFO allows oxygenated blood to enter systemic circulation
aortic coarctation
constriction of aorta
what are the two types of aortic coarctation
preductal or infantile (with PDA)
postductal or adult (w/o PDA)
clinical presentation of aortic coarctation
bicuspid AV (in 50%)
preductal:
lower body cyanosis
requires surgery
postductal:
depends on degree of narrowing
upper extremity HTN
rib notching on CXR
aortic stenosis can present with what finding
systolic murmur
LV hypertrophy and LA dilatation
hypoplastic left heart syndrome
aortic valve atresia with intact ventricular septum
Ebstein anomaly
inferiorly displace and adherent septal and posterior leaflets
reduent anterior leaflet
dilated annulus with tricuspid regurg
primary and secondary heart fields are derived from
splanchnic mesoderm
what contributres to septation of the AV canal and outflow region?
cardiac mesenchyme (cushion tissue)
what is the least worrisome congenital heart defect
ASD
