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Cardiac Embryology
| Question | Answer |
|---|---|
| HEART TUBE: Divisions | 1. Truncus arteriosus 2. Bulbus cordis 3. Primitive ventricle 4. Primitive atria 5. Sinus venosus |
| TRUNCUS ARTERIOSUS | Gives rise to: 1. Aorta 2. Pulmonary trunk |
| BULBUS CORDIS | Gives rise to: 1. Smooth part of RV ("conus arteriosus) 2. Smooth part of LV ("aortic vestibule) |
| PRIMITIVE VENTRICLE | Gives rise to: 1. Trabeculated part of RV 2. Trabeculated part of LV |
| PRIMITIVE ATRIUM | Gives rise to: 1. Trabeculated part of RA 2. Trabeculated part of LA |
| SINUS VENOSUS | Gives rise to: 1. Smooth part of RA ("sinus venarum") 2. Coronary sinus 3. Oblique vein of LA *** Junction of trabeculated andsmooth parts of RA is "Crista terminalis" |
| SMOOTH PART OF LEFT ATRIUM | Formed by incorporation of common pulmonary vein into the atrial wall |
| AORTICOPULMONARY SEPTUM FORMATION | - Neural crest cells migrate through pharyngeal arches 3,4, & 6 - Invade truncal/bulbar ridges causing their growth, twisting together, & eventual fusion to form AP septum. - Divides truncus arteriosus & bulbus cordis into aorta & pulm trunk |
| PERSISTENT TRUNCUS ARTERIOSUS (PTA) | - Abnml neural crest cell migration with only partial development of AP septum. - Single arterial vessel with single semilunar valve, receiving blood from both R & L ventricles - Usually assoc. w/ membranous VSD - Cyanosis (R->L shunt) |
| TYPE I PTA | - Short pulm trunk arises from truncus arteriosus and gives rise to R & L pulmonary arteries |
| TYPE II PTA | - R & L pulmonary arteries arise close to one another directly from truncus arteriosus |
| TYPE III PTA | - R & L pulmonary arteries arise at some distance from one another directly from truncus arteriosus |
| D-TRANSPOSITION OF GREAT ARTERIES (COMPLETE) | - RA connected to morphological RV by tricuspid valve which is discordantly connected to transposed aorta. LA connected to LV by MV, which is connected to pulm trunk. Complete separation of pulm. & syst. circ. - Incompatible w life unless VSD/PFO/PDA. |
| L-TRANSPOSITION OF GREAT VESSELS (CORRECTED) | - RA connected to LV by MV which is connected to transposed pulmonary trunk. - LA connected to RV by tricuspid valve which is connected to transposed aorta. - Blood flow pattern is normal |
| DOUBLE-OUTLET RV (DORV/INCOMPLETE TRANSPOSITION) | - Aorta & Pulm. trunk both arise primarily from RV. Usually associated with a VSD that provides only outlet for blood in the LV. - When VSD is located beneath pulm. semilunar valve, called 'Taussig-Bing' complex. - R->L Shunt, Cyanosis |
| TETRALOGY OF FALLOT (TF) | - Abnml neural crest cell migration so skewed development of AP septum. Results in 1. Pulmonary stenosis 2. RVH 3. Overriding aorta 4. VSD Pulm blood flow depends on PDA so neonate treated with PGE1 - Most common cyanotic malformation |
| MODIFIED BLALOCK-TAUSSIG SHUNT | - Gore-tex shunt placed between the subclavian artery and the pulmonary artery. - Surgical procedure done in Tetraology of Fallot |
| VALVULAR AORTIC STENOSIS | - Caused by thickening and increased rigidity of valve tissue with varying degrees of commisural separation. - MC AV is bicuspid with eccentrically placed orifice leading to LV outflow restriction. - A component of Hypoplastic Left Heart Syndrome |
| ATRIAL SEPTUM: DEVELOPMENT (Part 1) | - Septum primum develops in roof of primitive atrium and grows toward the AV cushions in the AV canal. - Foramen primum forms between free edge of septum primum and AV cushions. It's closed when tissue from AV septum fuses with septum primum. |
| ATRIAL SEPTUM: DEVELOPMENT (Part 2) | - The Foramen secundum forms in the center of the septum primum. - Septum secundum develops to the R of the septum primum - Foramen ovale is the opening b/w upper & lower limbs of the septum secundum |
| ATRIAL SEPTUM: DEVELOPMENT (Part 3) | - During embryonic life, blood is shunted from the RA to the LA via the foramen ovale. - Immediately after birth, fxnl closure of the foramen ovale is facilitated by 1) decrease in RA pressure & 2) increase in LA pressure due to incr pulm venous return |
| FORAMEN SECUNDUM DEFECT: PHYSIOLOGY | - Caused be excessive resorption of septum primum, septum secundum, or both. Results in opening b/w R & L atria. - Can often be tolerated for many years, manifesting as late as age 30. -MC clinically significant ASD. |
| FORAMEN SECUNDUM DEFECT: CLINICAL FINDINGS | - Typically asymptomatic - @ 6-8 wks, soft systolic murmur w/ fixed and widely split S2 - ASDs are associated with a L->R shunting of blood, fatigue, & dyspnea |
| COMMON ATRIUM (COR TRILOCULARE BIVENTRICULARE) | - Caused by complete failure of septum primum & septum secundum to develop. Results in formation of only one atrium |
| PROBE PATENCY OF FORAMEN OVALE | - Caused by incomplete anatomic fusion of septum primum & septum secundum. - Usually of no clinical importance |
| PREMATURE CLOSURE OF FORAMEN OVALE | - Closure of foramen ovale during prenatal life. - Results in hypertrophy of the R side of heart and underdevelopment of the L side of the heart |
| ATRIOVENTRICULAR SEPTUM: FORMATION | - The Dorsal AV Cushion & Ventral AV Cushion approach each other and fuse to form the AV septum. - The AV septum partitions the AV canal into the R AV canal and L AV canal |
Created by:
dsilver2
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