Heart Flashcards
primative ventricle folds to the R and outflow tract ends up on L –> R sided LV
ventricular inversion
abnormal L-R development of some or all organs; seen in immobile cilia syndrome and Kartagener syndrome
heterotaxia
defect in dyenin
complete reverse symmetry of the heart and GI organs, not fatal but may be symptomatic
situs inversus
situs ambiguous- reversal of some organs
heart and GI tract are asymmetrically arranged from one another (R sided heart, left sided GI), causing problems with inflow and outflow; life threatening
visceroatrial heterotaxia
chromosome 22q11 deletion, thymic aplasia, hypocalcemia
ToF
associated with downs syndrome
persistent AV canal; ASD/VSD
failure of contruncal ridge formation and fusion, abnormal migration of NCC
sx: pulmonary congestion, RV hypertrophy, increased R ventricular pressure
persistent truncus arteriosus (blood from RV and LV flow into same vessel b/c no separation occurred)
usually accompanied by VSD
conotruncal ridges fail to spiral; abnormal migration of NCC
prognosis: 1/3 die within first year, many within first few months
transposition of great vessels (aorta and pulmonary a connected to wrong ventricles); complete separtion of pulmonary and systemic circulation
not compatible with life unless shunt (PDA, PTA, or VSD) is present
not enough AV cushion to form valve; complete agenesis of valve; no communication between RA and RV
accompanied by patent foramen ovale, IV septal defects, hypoplastic RV, hyperplastic LV, PDA
tricuspid atresia
needs ASD/VSD or transplant
- conotruncal ridges form off center causing unequal division of pulmonary trunk and aorta; abnormal migration of NCC skews development of AV septum
- pulmonary trunk is small, aorta is large
VSD; pulmonary infundibular stenosis; overriding aorta; RV hypertrophy; cyanosis caused by crying, fever, exercise
tetralogy of fallot
associated with digeorge syndrome; most common cause of early childhood cyanosis
PROVe it
failure of AV septum fusion
pulmonary HTN, exercise intolerance, SOB, cardiac congestion, increased risk of endocarditis
persistent AV canal
initial L –> R shunting d/t increased blood flow from lungs and decreased pulmonary resistance
pulmonary congestion –> RV hypertrophy –> CHF
ASD
RV hypertrophy causes switch to R –> L shunting, thats when cyanosis starts
2:1 prevalence in females vs males
foramen secundum defect most common
excessive absorption of septum I or inadequate development of septum II
vs
failure of AV cushion from AV septum and DMP to fill in ostium
ostium II (high atrial septal defect)
ostium I (low atrial septal defect)
faulty fusion of R/L bulbar ridges and AV cushion –> free flow of blood between R and L ventricles
starts out L –> R shunt (acyanotic) and pulmonary HTN
when pulm pressure > systemic pressure switches to R –> L shunt and cyanosis
VSD
most common congenital heart defects
SL valves fuse –> RV hypoplasia
univentricular heart
pulmonary valvular atresia
patent foramen ovale forms as only way blood gets from R –> L
ductus arterious remains patent as only way for blood to get to lungs
better if there is VSD so blood can get over there
hypertrophy of LV –> cardiac failure and pulmonary HTN
can be congenital, d/t infection (rheumatic fever), or degenerative with age
aortic valve stenosis
atrial septum, membranous IV septum, AV and SL valves
endocardial cushion
coronary sinus
L horn of sinus venosus
IVC
SVC
IVC: posterior, subcardinal and supracardinal veins
SVC: R common and anterior cardinal veins
trabeculated parts of atria
trabeculated parts of ventricles
a: primitive atrium
v: primitive ventricle
smooth part of LA
smooth part of RA
L: primitive pulmonary vein
R: R horn of sinus venosus
ascending aorta and pulmonary trunk
truncus arteriousus
- 1/3 to 1/2 of blood traveling to aorta enters pulmonary a causing blood to be circulated through the lungs 2-3 x for every 1x it enters systemic circulation –> LV hypertrophy, increased pulmonary resistance and pulmonary congestion –> CHF
- blowing type of murmur
- maternal rubella
PDA
low O2 content stimulates prostaglandin release, which relaxes smooth muscle and keeps it open
narrowing or aortic lumen distal to L subclavian a
sx: increased blood pressure in the upper extremities, lack of pulse in femoral artery, high risk of both cerebral hemorrhage and bacterial endocarditis,
Turner syndrome
coarctation of aorta
postductal: nbd d/t collateral circulation through intercostal and internal thoracic a
preductal: no collaterals, little to no blood gets to lower body or legs
vascular ring around trachea and esophagus, may lead to esophageal dysfunction and strangulation of trachea
double aortic arch
- L AA IV and L dorsal aorta completely obliterated and replaced by corresponding R sided vessels
sx: dysphagia and dyspnea (if L subclavian a passes behind the esophagus and ligamentum arteriosum passes in front of trachea on R)
R aortic arch
- R subclavian is formed by distal portion of R dorsal aorta and 7th intersegmental a.
- R AA IV and proximal R dorsal aorta obliterated
sx: dysphagia and dyspnea d/t R dorsal arch crossing esophagus
aberrant origin of R subclavian
interrupted aortic arch- similar + disappearance of L AA IV; digeorge syndrome
aortic arches:
3
4
6
3: R/L carotids
4: R subclavian, aortic arch
6: R/L pulmonary arteries, ductus arteriosus
R/L coronary arteries from hepatic progenitor stem cells
