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COM CPR E1 > 9. Heart Development (Brauer) > Flashcards

9. Heart Development (Brauer) Flashcards

1
Q

Vasculogenesis

A

new blood vessel formation from the coalescence and assembly of endothelial cells into functional vessels during embryonic development of the cardiovascular system

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2
Q

Angiogenesis

A

new blood vessels take shape from existing blood vessels by “sprouting” of endothelial cells thus expanding the vascular tree

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3
Q

Intussusceptive angiogenesis

A

By intussusception a new blood vessel is created by splitting of an existing blood vessel in two. In this type of vessel formation, the capillary wall extends into the lumen to split a single vessel in two

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4
Q

Four phases of intussusceptive angiogenesis

A

First, the two opposing First, the two opposing capillary walls establish a zone of contact.

Second, the endothelial cell junctions are reorganized and the vessel bilayer is perforated to allow growth factors and cells to penetrate into the lumen.

Third, a core is formed between the two new vessels at the zone of contact that is filled with pericytes and myofibroblasts. These cells begin laying collagen fibers into the core to provide an extracellular matrix for growth of the vessel lumen.

Finally, the core is fleshed out with no alterations to the basic structure.

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5
Q

Hematopoeisis

A

starts in the yolk sac mesoderm at Day17 and finishes by Day 60

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6
Q

Hemangioblasts

A

Rise from undifferentiated mesoderm and from aggregates (blood islands), from which vasculature will form. They are multipotent precursor cells that can differentiate into both hematopoietic progenitor (form erythrocytes and macrophages) and endothelial precursor cells.

*cannot make lymphocytes

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7
Q

Definitive hematopoietic stems cells

A

Programmed from hemogenic endothelial cells, which found in the AGM (aortic gonadal mesonephric) dorsal aorta region. They appear around Day27, migrate to the liver around Day30, and completely disappear from the AGM region by Day40.

*capable of generating myeloid and lymphoid cell lineages.

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8
Q

vessels assembled “de novo”

A

Presumptive dorsal aortae and aortic arches, the internal carotid arteries, and the anterior and posterior cardinal veins are assembled from individual endothelial cells

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9
Q

Angiomas

A

Benign tumors that result from an overgrowth of capillaries via vasculogenesis. Capillary (capillaries) vs. Cavernous (venous sinuses) hemangiomas. Prevalence is 2.5% of neonates

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10
Q

Formation of early cardiogenic precursors

A
  • Mesoderm cells travel through primitive streak to embryo’s head, form horseshoe-shaped area with two limbs (AKA primary heart field)
  • Vascular endothelial growth factor (VEGF) signals limbs’ cells to organize into two tubes
  • Lateral mesoderm splits into somatic, splanchnic layers. Concurrently, primitive pericardial cavity forms lateral to each tube
  • At inferior end, each endocardial tube connects to vitelline vein stemming from yolk sac
  • Mesoderm cells also form pair of longitudinal vessels (AKA dorsal aortae
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11
Q

Formation of the primitive heart tube

A
  • Embryo folds into cylindrical shape as lateral borders meet at midline –> Two endocardial tubes fuse, forming primitive heart tube
  • Left, right vitelline veins also fuse, forming sinus venosus (AKA inflow tract)
  • Aortae fuse, forming aortic sac (AKA outflow tract)
  • Primitive pericardial cavities fuse around heart tube, forming pericardial cavity
  • Heart tube remains attached to pericardial cavity by sheet of mesoderm called dorsal mesocardium; heart tube now has two layers (endothelial lining, cardiac myoblasts)
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12
Q

Layers of the simple heart tube

A

 Endothelial lining forms endocardium

 Cardiac myoblasts form myocardium – Some myocardial cells in sinus venosus begin to produce rhythmic electrical discharge

 Mesenchymal cells of dorsal mesocardium form proepicardial organ – These cells proliferate, migrate over myocardium, form epicardium

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13
Q

Primary heat field

A

From pharyngeal mesoderm. Gives rise to ventricular myocardium and will develop into left and right atria and the left ventricle

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14
Q

Secondary heart field

A

Second wave of progenitor cells from pharyngeal mesoderm that will become the right ventricle and outflow tract. The secondary hear field also contributes to the lengthening of the heart tube, especially at the arterial end.

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15
Q

Improper cardiac looping

A
  • Heterotaxy: abnormal left-right axis
  • Ventricular inversion is reverse looping (right sided left ventricle)
  • Situs inversus totalis – total reverse
  • Partial situs ambiguous – partial, heart and GI reversed
  • Visceroatrial heterotaxia – reversed (right) heart, but normal GI
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16
Q

Fetal cardiac blood flow

A
  • blood entering from the IVC is shuttled through the foramen ovale into the left atrium
  • LA receives the oxygenated blood that is transferred to the LV and out into fetal systemic arterial side
  • blood entering the RV from the RA includes less oxygenated blood from SVA and coronary sinus but also a portion of the blood from the IVC
  • Blood exiting the RV re-enters the systemic arterial side via the ductus arteriosus with only about 11-13% actually going through the pulmonary arteries to reach the developing lungs
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17
Q

Transverse sinus development

A

The dorsal mesocardium formed by splanchnic mesoderm located beneath the foregut, maintains the positioning of the primitive heart tube within the pericardial cavity. Rupture of the dorsal mesocardium, leaves the transverse sinus behind

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18
Q

Fate of Sinus Venosus

A
  • Sinus venosos opening begins to shift to the right
  • Left vitelline and umbilical veins disappear
  • Left sinus venosus and left horn shift to right common atrium
  • Most of left cardinal vein disappears, what is left is the coronary sinus
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19
Q

Fate of Right Sinus Horn

A
  • As the right atrium enlarges, the sinus venous now only opens into the future right atrium (sinoatrial orifice).
  • Right sinus horn, along with proximal right vitelline and cardinal vein become incorporated into the atrium
  • Right Cardinal vein become the SVC
  • Right Vitelline vein becomes IVC
  • Upon incorporation of the SVC and IVC, a pari of tissue flaps (left and right atrial venous valves) develop on either side
20
Q

Crista terminalis

A

The junction between pectinate/rough part of right atrium and smoothed- walled part (sinus venarum– part of sinus venosus incorporated into atria)

21
Q

Differential growth

A

Makes the muscular interventricular septum and muscular atrial septum. Never fully closes a lumen, needs new tissue for that to happen

22
Q

Endocardial cushion tissue

A

Makes the fibrous (membranous) portions of atrial and ventricular septum and conotruncal ridges of the outflow tract.

23
Q

AV septum

A

Superior (dorsal) and inferior (ventral) endocardial cushions fuse at midline

Subsequent growth up and down from the AV septum contributes to the atrial and ventricular septa as well.

24
Q

Formation of tricuspid and bicuspid valves

A

Appear to form from the ECT during the 5th and 6th weeks with possible contributions from the epicardial-derived cells. Leaflets are freed from the walls by cavitation and remodeling of the ventricular myocardium and remnants help form the chordae tendineae and papillary muscles.

25
Q

Atrial septum

A
  • During 5th and 6th week
  • 2step process
  • septum primum (cardiac outflow to atrium during looping). Also receives contribution from DMP or spina vestibule
  • septum secundum (thicker) grows down, covering up ostium primum. Never reaches AV septa –> Foramen Ovale
  • need leaky divider
  • ostium primum (hole in septum primum near AV septum). Cushion tissue from AV septum and DMP close it
  • ostium secundum forms on top of septum primum as the first foramen closes
26
Q

Blood flow change right after birth

A

Pulmonary circulatory pressure ↓ while systemic circulation ↑

o When umbilical cord cut, low-resistance circuit removed → systemic circulation increases

o Lung fluid replaced by air as neonate takes first breaths/cries

o Oxygen diffuses into blood vessels surrounding alveoli, pulmonary arterioles relax, pulmonary resistance falls, blood flows into lungs

27
Q

Closing of ductus arteriosus

A

o Pressure changes cause decreased blood flow through ductus arteriosus

o Complete closure: 12–24 hours after birth

o Physical remnant: ligamentum arteriosum

28
Q

Closing of foramen ovale

A

o Pressure in right side of heart falls, seals foramen ovale

o Physical remnant: fossa ovalis

29
Q

Ostium II or high atrial septal defect

A

90% of the ASDs
Hole in atrial septum caused by either:
1. Excessive absorption of septum I forms an overly large ostium II.
2. Inadequate development of septum II.

30
Q

Ostium I or low atrial septal defect

A

Failure of up-growth of AV

cushion tissue from AV septum and DMP to fill in ostium primum.

31
Q

Cyanosis

A

deoxygenated blood mixing with oxygenated blood to the point that it lowers the overall oxygen content

Often also manifested visually by clubbing of fingers, bluish fingernail beds and lips.

The individual also fatigues easily.

Can be seen in patients having oxygen saturation below 90%.

32
Q

Partitioning of outflow tract

A

Conus arteriosus, truncus arteriosus, and aortic sac starts with a common lumen and it must be divided into two tubes in such a way that it connects the future aorta to the LV and the pulmonary artery to the RV.

  • Aortic arch VI will connect the RV with the lungs and
  • Aortic arch III & IV connects the LV to rest of body.
33
Q

myocardialization

A

the outer myocardial wall is thinned as some myocardial cells begin to be replaced by cushion cells in specific areas and there is further remodeling through apoptosis.

34
Q

double-outlet right ventricle

A

both aorta and pulmonary artery exit via the right ventricle with an
accompanying ventricular septal defect;

symptoms show within days including cyanosis, breathlessness,
murmur and later, poor weight gain;

1:3000

35
Q

conotruncal ridges

A

New cushion tissue formation in the outflow tract that spiral down toward ventricular
septum and eventually fuse to form the conotruncal
septum that divides the outflow tract.

Cell origin: NCC and endocardial-derived cushion tissue

36
Q

Ventricular septal defects

A

One of the most common defects. 12-15/10,000

Failure of proper closure by abnormal or inadequate fibrous tissue is the cause 95% of the time.

Usually it starts out as acyanotic (left-to-right shunt) but becomes cyanotic sometime after birth (usually months to within a couple of
years depending on size) as the RV hypertrophies due to
increased work load.

Eventually the RV hypertrophies enough so that the RV pressure builds and exceeds the left side, so now a right to left shunt develops (cyanosis).

Eventually die of cardiac failure if not addressed.

37
Q

Persistent truncus arteriosus

A

1/10,000

The pulmonary artery further up (some distance away) the undivided truncus.
–> Causes a VSD because of the ridges contribution to the fibrous portion.

Undivided truncus overrides both right & left ventricle. There is mixing of oxygenated and deoxygenated blood within truncus
so it can present with low degree of cyanosis.

Pulmonary congestion –> RV hypertrophy –> increased right ventricular pressure –> eventual more severe cyanotic condition

38
Q

Tetralogy of Fallot

A

9-10/10,000

Conotruncal ridges form off-center leading to unequal division of pulmonary trunk and aorta

  1. VSD (missing fibrous portion).
  2. Pulmonary infundibular stenosis.
  3. Overriding aorta.
  4. RV hypertrophies in the fetus because of the small pulmonary opening.
39
Q

Transposition of great vessels

A

5/10,000

Conotruncal ridges fail to spiral

pulmonary artery is connected to the LV and the aorta to RV.

Survive only because of existing shunts such as VSD, ASD, patent ductus arteriosus (only way to get blood to and from the
lungs), etc.

Even with shunts, a life expectancy may be only 3 years without surgery. Prognosis: one-third die within first year, most of these within the first month unless treated.

Long-term survival is now possible due to improvements in corrective surgery.

40
Q

Pulmonary valvular atresia

A

Semilunar valves are fused leading to RV hypoplasia

  • Patent Foramen Ovale
  • Ductus arteriosus is always patent and is only route for blood to get to lungs
  • May need transplant
  • Surgically can open the pulmonary valve and if the RV is not too weak, the person can live
  • if VSD, mixing of blood, but can live with a “univentricular” heart
41
Q

Aortic valvular stenosis

A
  • leads to hypertrophy of LV and eventually to cardiac failure and pulmonary hypertension
  • 4:1, male to female ratio
  • can be congenital, d/2 infection, or degenerative
    1-2% of population
42
Q

Bicuspid aortic valve

A 
2 instead of 3
Regurgitation --> later stenosis 
Initially asymptomatic
But leads to LV hypertrophy 
1-2% of population 
Assoiciated with aortic aneurism
43
Q

Aortic valvular atresia

A
  • if valves are completely fused the LV is underdeveloped
  • wide ductus arteriosus forms because it is the only way O2-enriched blood from placenta can get into left side
  • Leads to RV hypertrophy during fetal period
  • After birth, O2-enriched blood must enter right atrium by way of an atrial septal defect and then enter the systemic circulation by passing through a patent ductus arteriosus
  • likely needing transplant
  • surgery has 5yr survival rate in 70% of patients
44
Q

Tricuspid atresia

A
  • obliteration of right AV orifice
  • fusion of tricuspid valves always
    associated with patency (keep open) of foramen ovale
  • fusion of tricuspid valves always
    associated with patency (keep open) of foramen ovale
  • ventricular septal defect
  • underdeveloped right ventricle
  • hypertrophy of left ventricle
  • patent ductus arteriosus
  • can be corrected surgically if RV is not too small
  • may require transplant
45
Q

Hypoplastic left ventricle

A

2-3/10,000

  • LV is underdeveloped with absent or small bicuspid and aortic valves
  • ascending portion of the aorta is underdeveloped
  • -> univentricular heart with the RV doing all the work

surgical intervention can provide 5yr survival rate in 65% of pts.

COM CPR E1 (20 decks)

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