26. Development of the Heart Flashcards Preview

Year 1 - Term 2: Carriage of Oxygen > 26. Development of the Heart > Flashcards

Flashcards in 26. Development of the Heart Deck (27):
1

Most prevalent heart abnormalities produce what 3 basic kinds of disorders?

What does the heart develop from?

1. mix O2 poor systemic blood with O2 rich pulmonary blood e.g. septal defects, patent ductus arteriosus

2. narrowed valves or vessels that greatly increase workload of heart e.g. coarctation of aorta

3. Tetralogy of Fallow (both types)

 

Cardiogenic mesodem (origionally lying above cranial end of developing neural tube), angiogenic cell clusters coalesce forming L and R endocardial tubes (each has dorsal aorta, outflow tract etc.)

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2

By how many days is fusion of endocardial tubes complete in heart development?

What forms the primitive myocardium?

What day does the heart start to beat?

21 days = primitive heart tube

Mesoderm from foregut. NB: endocardium also forms

22

3

Label A-C in the developing heart.

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A: Sinus venosus (inflow)

B: Primitive atria

C: Primitive ventricle (become L vent)

Interventriclar sulcus divides primitive ventricle from bulbus cordis

4

Describe heart looping during heart development.

What is dextrocardia?

As heart develops it lengthens. The ends are fixed so it's forced to bulge and twist within the pericardial sac. 

Anomaly where primitive heart tube folds to left in mirror image of normal looping - usually occurs when all organ systems are reversed - situs inversus

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5

Explain septum formation in the atrio-ventricular canal

 

End of 4th week: 2 swellings of mesenchymal tissue arise: atrio-ventricular endocardial cushions -> grow and fuse -> (nb still no direct atria-vent communication) -> blood flows from common atrium into L vent and then into R vent.

Merging of the cushions creates a R and L atrioventricular canal

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6

What contributes to many cardiac malfomatins e.g. atrial septal and ventricular septal?

When does atrial partitioning start?

The endocardial cushions b/c of their key location abnormalities

With appearance of septum primum at around day 28.

7

What is the septum primum?

What is the ostium primum?

What is the ostium secundum?

What grows after the ostium secundum?

What is the foramen ovale?

Crescent of tissue the grows from dorsal wall of atrium towards endocardial cushions. 

The ostium (opening) formed by free edge of septum primum is the ostium primum.

Programmed apoptosis  in upper portion of septium primum before it fuses with the endocardial cushions forms ostium secundum

Septum secundum but it doesn't fuse with endocardial cushions

Free edges of the septum secundum forms the FO

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8

What is the job of the foramen ovale?

The foetus doesn't use its lungs, so most blood diverted to systemic circulation by a R->L shunting between the 2 atriva via foramen ovale.

9

Label A-C in the developing heart.

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A: ostium secundum

B: septum secundum

C: foramen ovale

10

How is the septum primum linked to the foramen ovale?

What happens eventually to the septum primum and secundum and why?

What is the remnant of the foramen ovale called in the adult?

Acts as a valve over it

Pressure increases in L atrium, forces primum against secundum -> both septa fuse forming a common atrial septum. 

Fossa ovale

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11

When do the ventricles start to form?

How do they form?

By end of 4th week, ventricles begin to expand. New cardiac muscle (myocardium) is added on outside of ventricles.

Ventricular septum develops from base of heart (trabeculated muscle) and endocardial cushion grows down to it.

12

Describe the partitioning of the outflow tract - aorta and pulmonary trunk.

Septum forms 2 pairs of swellings (mesoderm) which grow from the inner walls of the outflow tract (truncus arteriosus and bubulbus: R and L bulbar ridges. They twist around each other to form spiral aortico-pulmonary septum. They fuse in the midline and with the top of the muscular ventricular septum.

Thus aorta connects with L ventricle and pulmonary trunk with R ventricle

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13

Give a breif summary of heart development.

Heart tube -> loops -> primitive ventricle -> septum formation (A/V canal) -> atrial partitioning -> ventricle formation -> great vessels partition

14

List 3 ways that the foetus differs from the neonate.

 

Foetal Hb, Placenta, Foetal circulation

15

Describe placental input and output.

Baby -> placenta: umbilical arteries (internal iliac), deO2, high pressure

Placenta -> baby: umbilical vein (becomes ductus venosus), O2, high pressure.

16

Describe the 3 main features of foetal circulation.

1. Ductus arteriosus: protects lungs against circulatory overload, allows R ventricle to strengthen, high pulm vascular resistance and low pulm blood flow, carries moderately saturated blood

2. Ductus venosus: connects umbilical vein to IVC, flow regulated via sphincter, conducts highly oxygenated blood

3. Foramen ovale: shunts highly oxygenated blood from R. atrium to L atrium

 

Reduced pulm blood flow. RV pumps 2/3 C.O.

17

Label A-C in foetal circulation.

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A: ductus arteriosus

B: Foramen ovale

C: Ductus venosus (closes at birth to become ligametum teres)

18

Describe 5 adaptions that occur at birth.

1. Umbilical vein becomes ligamentum teres (umbilicus to liver) and mesentry becomes falciform ligament

2. Ductus venosus constricts so all blood passes through hepatic sinusoids

3. Foramen ovale: decreased flow from placenta and IVC causes lower P in RA, decreased pulmonary vascular resistance 20 to lung expansion, increase in pulmonary blood flow raising LA pressure to higher than IVC, so FO closes due to increased pressure in LA compared to RA

4. Ductus arteriosus: closed by increased paO2 -> ligamentum arteriosum, due to decreased pulm vascular resistance, PA pressure falls below systemic pressure and blood flow through DA deminishes -> closure mediated by bradykinin. Prostaglandin E2 may reopen DA.

5. Umbilical arteries: constricts but some parts remain patent and supply bladder.

19

What is the difference between cyanotic and acyanotic heart lesions?

List 3 cyanotic heart lesions.

List 3 acyanotic heart lesions.

Cyanotic: deoxygenated and oxygenated blood mixing, R -> L shunt. Acyanotic: L -> R shunt or left heart abnormality. 1/3 of congeital heart disease.

Tetralogy of Fallow, persistent truncus arteriosus, transposition of the great vessels

Atrial septal defects, ventricular septal defects, patent ductus arteriosus, and coarctation of aorta

20

What are the 4 features of the tetralogy of fallot?

What is cyanosis caused by?

What does cyanosis vary with?

What is ToF characterised by?

All due to shifting of endocardial cushion to R side. 4 lesions:

1) ventricular septal defect because when intraventricular septum grows up, it doesn't meet with endocardial cushions.

2) Narrow R ventricule outflow (pulm. trunk)

3) R. ventricular hypertrophy due to high R vent. pressure

4. Overriding aorta arising directly above septal defect 

 

R -> L shunting through the VSD

 

The degree of outflow tract obstruction and size of VSD

 

Hypercyanotic episodes - tet spells

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21

What causes a persistent truncus arteriosus?

What is the prognosis?

Single artery (truncus) arises from heart (does not divide), supplying both aorta and pulmonary artery. A large VSD below the truncal valve allows mixing of R and L ventricular blood. Variable degree of cyanosis.

Presents with progressive heart failure. Can be operated on.

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22

What happens in the transposition of the great vessels?

What is the prognosis?

Aorticopulmonary septum fails to follow spiral course - runs straight down. Usually accompanied by open ductus arteriosus.

Blue baby - immediate surgical intervention. Fossa ovalis catheterised.

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23

What are arterial septal defects?

What is a probe patent foramen ovale?

What are the symptoms of ASD?

What is the prognosis?

Can be septum primum (not closing off ostium primum) or septum secundum (not covering foramen ovale properly) defect. 2:1 female to male. 

In up to 25%, a probe can be passed from one atrium to the other. Defect not usually sig. and can be caused from other cardiac defects.

Exercise intolerence, dyspnoea on exertion, fatigue from R heart failure and pulm. hypertension

Generally asymptomatic for first 3 decades, decision to close based on shunt size and symptoms. Can close small defects using transcatheter techniques, thus avoiding sternotomy and bypass.

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24

What is a ventricular septal defect?

What is the prognosis?

25% of congenital heart defects, most common. Ventricular septum failed to grow up to endocardial cushions. 90% of VSD are in the membraneous septum (cushions) and 10% in muscular septum (trabeculated muscle at bottom). 

Symptoms depend on defect size. Many small VSDs close spontaneously.

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25

What is a patent ductus arteriosus?

What is the prognosis?

DA connects the desending aorta to the main pulmonary trunk near the origin of the L subclavian. Normal postnatal closure results in fibrosis -> ligamentum arteriosum. PDA = DA fails to close. Higher pressure blood in aorta goes through DA to pulmonary trunk.

Small PDA doesn't increase risk for heart failure, but does carry risk for bacterial endocarditis. Large ones can be closed with clip but normally done with prostaglandin inhibitor like ibuprofen.

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26

Describe coarctation of the aorta.

What is the diagnosis?

What is the treatment?

Narrowing/stenosis of aorta. Constriction may be above or below ductus arteriosus. Pre-ductal: DA persists allowing blood flow. Post-ductal: collateral circulations must be established for proper perfusion of body and legs.

Young adults may be asymptomatic apart from hypertension and decreased lower extremity pulses. Causes systemic hypertension and secondary LVH (b/c huge afterload on L  side of heart) with heart failure. 

Balloon angioplasty if gradients >30mmHg on cardiac cath.

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27

What can you see in these angiographies?

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Coarctation of the aorta.

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