Embryology Flashcards
cardiogenic mesoderm
gives rise to endo, epi, and myocardium
- does not form fibrous skeletal elements or valves
Cardiac looping
induced by rapid growth of ventricles
caudal end folds up and posterior –>puts venous and atrial things posterior
Sinus venosus
most caudal structure in heart tube (receives all blood form embryo)
Becomes RA
L sinus horn–>coronary sinus
R sinus horn–> sinus venarum
Primitive atrium
will become the pectinate regions of the LA and RA (i.e. auricle regions)
Primitive ventricle
will form the trabeculated portions of the LV
bulbus cordis
becomes the trabeculated portion of RV, root of ascending aorta an pulmonary trunks, outflow parts of both RV and LV
conus cordis
part of bulbous cordis that becomes smooth walled outflow of both LV and RV
Truncus arteriosus
part of bulbous cordis that becomes ascending aorta and pulmonary trunk
Septum Primum
forms first in atrial partitioning
has a small opening in inferior part called ostium primum (very short lived)
Osteium secundum
second step in atrial partitioning
forms in septum primum
allows blood to flow from RA to LA and bypass the lungs
Septum secundum
3rd step
forms laterally to primum, thicker and more muscular, will become interatrial septum
contains foramen ovale which is the definitive blood shunt (sealed at birth)
septum primum is the valve for foramen ovale
Patent foramen ovale
common, lack of fusion of foramen ovale and primum
usually asymptomatic, unless there is a pathology that increases pressure in RA, when it can open up
example of ASD (10% of all defects)
Neural crest cells
migrate into heart and form a ring of tissue around the IV septum called endocardial cushions, creating a right and left atrioventricular canal
will form the heart valves and membranous portion of ventricle wall
VSD (ventricular septal defect )
30% of all congenital defects
- holes in either muscular or membranous (more common) septa
severity depends on size
L–>R shunting of blood
sx= pulmonary hypertension, decreased systemic blood flow, LV hypertrophy
endocardial cushion (neural crest) disorders
cause persistent AV canal
ASD (ostium primum defect)
Membranous VSD
Aortic stenosis
narrowing of great vessel lumen due to stenosis of heart valve (usually semilunar)
Tetralogy of fallot
caused by unequal division of truncus arteriosus
1) narrowing of pulmonary trunk
2) overriding aorta (very large)
3) Membranous VSD
4) RV hypertrophy
due to pulmonary stenosis
** common cause of cyanosis of newborn
Transposition of great vessels
Aorta exits from RV, PT comes from LV
due to conotruncal ridges failing to spiral
Persistent truncus arteriosus
1 artery that leaves from both RV and LV–> mix of oxygenated and deoxygenated blood to systemic circulation
from conotruncal ridges failing to form
another cause of cyanosis in the newborn
dextrocardia
looping disorder that causes a right sided heart
ectopic cordis
body wall defect in which there is no fusion of the thoracic wall–> heart forms externally
DiGeorge syndrome
neural crest disorder--> cardiac valve defects, CATCH-22 Chromosome 22 deletion abnormal face thymic aplasia (immunocompromised), cleft palate hypocalcemia (PTH defect)
3rd Aortic arch
R= Common Carotid a. L= Common Carotid a.
4th Aortic arch
R= R Subclavian . L= Arch of aorta
6th Aortic arch
R= Pulmonary a. L= Pulmonary a. and ductus arteriosus
7th aortic arch
R= Subclavian a. L= Subclavian a.
Patent ductus arteriosus
ductus arteriosus does not close L--> R blood shunt pulmonary overflow R side hypertrophy decreases systemic flow
Preductal coarctation of aorta
Infantile, presents immediately
bypass the constriction via ductus arteriosus prenatally, but at birth there is no diversion
–> tachycardia, cyanosis of LOWER LIMBS, low femoral pulse
Postductal coarctation of aorta
adolescent, present later,
during development there is no way to divert the block unless collateral circulation is developed via posterior and anterior intercostals which brings blood to descending aorta
presents as individual becomes more active
Sx= fatigue, HA, HT upper limg, weak femoral pulse, hypotension in lower limbs
Retroesophageal R subclavian a.
R subclavian passes behind esophagus
can compress the esophagus–> dysphagia lucoria
double aortic arch
aortic arch persists on both sides compressing the esophagus and causing dysphagia
Tracheoesophageal Fistula
development of an abnormal fistula (opening) b/w trachea and esophagus due to lack of septum formation
proximal esophageal atresia
sx: infant that can’t eat (vomits immediately)
stomach become distended with air
Fetal survivability based on lung development
6-16 weeks= non-survivable due to lack of lungs and surfactant
surfactant production begins at week 21, becomes survivable
preemies suffer from respiratory distress syndrome due to lack of surfactant
