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Flashcards in Development and Congenital Anomalies Deck (24)

Heart Development Timeline

Weeks 3-8
Day 22: heart starts to beat
Week 3: embyo cannot obtain nutrients via diffusion because CV system functions

Progenitor heart cells migrate (gastrulation) to cardiogenic area at cranial end of the embryo (day 16-18)


Formation of Initial Heart Tubes

Endoderm induces vasculogenesis and myoblast formation = primordial vessels
2 endocardial tubes form in cardiogenic area (R and L) in splanchnic layer of lateral plate mesoderm

Folding brings R and L tubes together (days 21-22) and fuse, elongate, form dilations and constrictions

Dilations and Constrictions are future heart chambers


4 Layers of the Heart

Day 22: pericardial cavity and heart tube with 4 layers epicardium, cardiac jelly, and endocardium

Epicardium = outer epithelial layer of heart tube
Myocardium = forms muscular walls
Cardiac Jelly = forms AV cushions
Endocardium = endothelial layer of heart


Dilations and Development of Heart Tube

1. Truncus Arteriosus: divides into aorta and pulmonary trunk
2. Bulbus Cordis: smooth part of R and L ventricles (R= conus arteriosus, L= aortic vestibule)
3. Primitive Ventricle: trabeculated part of R and L ventricles
4. Sinus Venosus: smooth part of R atrium, coronary sinus, oblique vein of L atrium

*Junction of trabeculated and smooth parts of R atrium = crista terminalis


Heart Tube Lengths and Folds

Cranial portion: bends caudally (towards tail), ventrally, and to the R, but still a single tube


Septation of the Heart: Partitioning of AV Canal

Weeks 4-7
Partitioning of AV Canal: mesenchyme and neural crest cells enter cardiac jelly for endocardial cushions = separate atria and ventricles

Superior and inferior cushions form AV septum, separating single AV canals into R and L AV canals


Septation of the Heart: Partitioning of the Primordial Atrium

Weeks 4-7
Partitioning of Primordial Atrium: septum primum grows from atrial roof towards cushions = large foramen primum

Forms then disappears once septum primum fuses with cushions = forms R and L atria

Apoptosis occurs in septum: forms primum secondum so blood shunts from R to L; Septum secondum grows from R atrial roof towards fusing cusions to form the foramen ovale via septum and covers foramen secondum and septum primum and acts as a valve so blood only goes from R to L atrium


Septation of the Heart: Partitioning of the Primordial Ventricles

Weeks 4-7
Partitioning of the Primordial Ventricles
A muscular interventricular septum forms but interventricular foramen remains
A membranous interventricular septum forms to close the foramen during division of outflow tract
This is formed by conotruncal ridges and endocardial cushions


Septation of the Heart: Partitioning the Ventricular Outflow Tract

Weeks 4-7
Partitioning the Ventricular Outflow Tract
Neural crest cells migrate to outflow tract to form conotruncal ridges (spiraling) = forms aorticopulmonary septum that divides the tract into aortic and pulmonary channels

NS develops as infolding of ectoderm and edges of neural crest delaminate and travel through body

Neural crest cells migrate along aortic arches to proximal great vessels and outflow tract


Neural Crest Cells Structure Formation

Neural crest cells form part of conotruncal ridges of outflow tract, membranous interventricular setpum, and lower cusps of aortic and pulmonary semilunar valves


Fetal Circulation: Prenatal

1. Gas and nutrient exhange via placenta
2. O2 rich blood bypasses liver via ductus venosus
3. Higher pressure in R side of heart
4. Low pulmonary blood flow due to constricted vessels
5. R to L shunts via ductus arteriosus and foramen ovale


Fetal Circulation: Postnatal

1. Umbilical vein obliterates to form ligamentum teres and umblicial arteries obliterate foriming the medial umbilical ligaments
2. Ductus venosus closes forming the ligamentum venosum
3. Lower pressure in R side of heart
4. Increased pulmonary blood flow as vessels vasodilate
5. R to L shunts close to ligamentum arteriosus and fossa ovale


Acyanotic Congenital Heart Defects

adequate blood O2, L to R shunt, atrial or ventricular wall defect

1. Ventricular Septal Defect
2. Atrial Septal Defect
3. Patent Ductus Arteriosus
4. Coarctation of the Aorta
5. Pulmonary Stenosis
6. Aortic Stenosis


Cyanotic Congenital Heart Defects

R to L shunt, low blood O2 caused by abnormal flow to lungs ot total mixing of systemic and pulmonary blood flow in heart = improper partitioning of ventricular outflow tract

1. Transposition of the Great Arteries
2. Truncus Arteriosus
3. Tricuspid Atresia
4. Tetralogy of Fallot
5. Total Anomalous Pulmonary Venous Return
6. Pulmonary Atresia
7. Ebstein’s Anomaly


Acyanotic Defects: Volume Load vs. Pressure Load

Volume Load: L to R shunt
1. Ventricular Septal Defect
2. Atrial Septal Defect
3. Patent Ductus Arteriosus

Pressure Load: obstructed ventricular outflow
1. Coarctation of the Aorta
2. Pulmonary Stenosis
3. Aortic Stenosis


Cyanotic Defects: High Pulmonary Flow vs. Low Pulmonary Flow

Hgh Pulmonary Flow:
1. Transposition of the Great Arteries
2. Truncus Arteriosus

Low Pulmonary Flow:
1. Tetrology of Fallot


Ventricular Septal Defect

Perimembranous: 70% endocardial cushions and conotruncal ridges fail to fuse with septum via neurocristopathy or endocardial cushion defect

Muscular: 30%; excessive remodeling of ventricular wall; large defect or several smaller defects

Effect: high volume of blood is shunted to R ventricle causing hypertrophy of L atrium and ventricle and pulmonary HTN


Atrial Septal Defect

Patent foramen ovale resulting from perforations in septum primum or secondum defect via excessive reabsorption of ostium secondum

If septum secundum defect, it can either be a large foramen ovale with normal septum primum or large foramen ovale with very short septum primum

Septum primum fails to fuse with endocardial cushions = ostium primum defect

Effect: high volume of blood is shunted to R atrium causing hypertrophy of R atrium and ventricle and pulmonary HTN


Patent Ductus Arteriosus

Remains open after birth
Effect: high volume of blood from aorta is shunted into pulmonary trunk causing hypertrophy of L atrium and ventricle


Coarctation of the Aorta

Construction of aorta distal to subclavian artery
Can be pre or post ductal - location relative to ductus/ligamentum arteriosus; post more common
Aorta constricts similar to ductus arteriosus

Effect: high pressure and blood flow to limbs, hypertrophy of L ventricle, vessels remodel to develop collateral circulation (bypass coarctation) resulting in large and tortuous arteries


Pulmonary Stenosis

asymmetrical septation of outflow tract and adnormal valve
High pressure in R ventricle causes hypertrophy and valves to calcify with age, further reducing blood flow


Tetralogy of Fallot

most common cyanotic defect; won't show up until child is more active

4 co-occurring heart abnormalities:
1. Pulmonary stenosis
2. R ventricle hypertrophy
3. Ventricular septal defect
4. Overriding aorta

Caused by asymmetrial fusion of conotruncal ridges resulting in misalignment of ventricular outflow tract and the aortic and pulmonary valves
Patent ductus arteriosus allows blood to flow into lungs and be oxygenated


Transposition of Great Arteries

Most common cyanotic defect in newborns

Conotruncal ridges fail to spiral during formation of aorticopulmonary septum leaving the aorta and pulmonary trunk connected to the wrong ventricles = 2 parallel circulations occur

Fatal without other heart defects that allow blood to shunt around the heart


Persistent Truncus Arteriosus

Failure of conotruncal ridges to partition the outflow tract and form aorticopulmonary septum

Single truncus arteriosus leaves ventricles

Membranous interventricular septum can be absent as it is partly formed by conotruncal ridges