Lecture 31: Heart Development and Abnormalities Flashcards
Describe the structure of the embryological heart at 3 weeks:
Cranial - Bulbus cordis (flow to aortic arches) - Primitive ventricle - Primitve atrium - Sinus venosus (receives venous blood) Caudal
Pericardium from BC to PA
What happens just after 3 weeks?
Cardiac looping, heart begins to grow but pericardium cant keep up and cause looping to occur
Describe the structure of the heart at 3 weeks 1 day
Cardiac looping
- PV moves right, caudal, ventral
- PA moves left, cranial, dorsal
Forms an S
SV forms two entrances
Describe the embryological heart at 3 .5 weeks
PA starts to move dorsal to BC
SV carried with PA (this will eventually be folded behind into coronary sinus
Describe the heart just prior to four weeks
[Growth quicker in regions compared to junctions]
= Bulging is more pronounced
SV hidden from view, Right and left horns present.
Describe the heart at four weeks
Cardiac looping stops
- Ineratrial septum starts to develop in the BC
- LV forms apex
- IV septum starts to form at the BC/PV junction forming RV/LV (note formed from different parts of primitive heart)
Whats found prior to four weeks on the RSV and LSV?
Common cardinal vein
Umbilical vein
Vitelline vein
Whats found prior to four weeks on the RSV and LSV?
Common cardinal vein
Umbilical vein
Vitelline vein
Describe the heart at six weeks:
- Left Pul Veins sprouting from LA
- IVC and SVC establish on RA
- PA forms auricles whilst veins enlarge to form part of atrium (smooth part)
- Pair of ridges from inside truncus arteriosus and conus cordis in a spiral and fuse forming a septum (must occur in specific direction or else)
Describe the heart at 7-8 weeks:
- In the truncus arteriosus cell death causes the spiral septum to split = aorta and pulm. trunk
- Deep inside heart this doesnt split, helping form IV septum and conus arteriosus
Describe the heart in a full term fetus:
Similar to adult except:
- Pulmonary trunk also has ductus arteriosus so redirects blood from pul to aorta
- Interatrial septum incomplete permits RA to LA passage
Describe the formation of the interatrial septum:
1) - Downgrowth of septum primum
- L,R,Inf, Sup endocaridal cushions form primitive AV divide
2) Sup and Inf endocardial cushions fuse to form septum intermedium dividing AV canal
3) Cell death in septum primum forming ostium secondum
4) Downgrowth of thicker septum secondum, whilst ostium primum completely sealed with septum intermdium
i.e downgrowth from top of atria heads towards the developing AV mass and then partially dies off whilst a second downgrowth occurs creating a one way valve as blood can only enter other atrium by bending thinner first septum.
Describe blood flow in the fetal circuit:
- Deoxygenated blood travels from cap. -> SVC -> RA -> RV -> Pulmonary -> Ductus arteriosus-> aorta -> Cap of placenta and viscera of legs -> IVC
- Oxygenated blood in placenta -> IVC -> RA -> LA -> LV -> Aorta -> Cap of head and arms AND/ OR down aorta to Placenta, legs
- Note in IVC oxygenated blood and deoxygenated blood do not mix and IVC blood is directed across RA to LA.
- Blood going to placenta and legs is a mixture
- No blood around high resistance pulm. circuit
= Insurance that head and heart getting oxygenated blood
Describe the changes at birth to the fetal circuit:
- Lungs get rid of fluid on first breath
- Lung resistance decreases
- Blood leaving RV goes low R PT instead of Ductus arteriosus (high resis)
- Increased blood to LA for first time (i.e large volume) and reduced pressure of return to RA thus LA pressure exceeds RA and foramen ovale flap closes
- Ductus arteriosus responds to oxygen and closes (SM contracts).
Whats the impact of untreated atrial spetal defect?
1) - During diastole LA blood is shunted into RA (less resistance, more compliant) (During diastole)
- EDV rises in RV and increased blood flow to pulm. circuit
2) After years or decades; Pulm. art thicken in response to large blood flow and in turn RV hypertrophies because increased resistance.
= Right side HF
or
RA->LA shunt develops -> Eisenmengers syndrome, cyanosis and death