HE 24 & 25 Great Vessels and Heart Flashcards
(38 cards)
draw embryological heart and arches, include all labels and blood flow
Aortic arches/aortic sac
truncus arteriosus
dorsal aorta
heart tube
sinus venosus
sinus horns
development of arches:
associated with paired pharyngeal arches located on future neck
five arches (six originally) but number 5 is transient so we refer to 1,2,3,4,6
arches not all present at the same time, form cranial to caudal, cranial gone or rearranged before caudal develope.
Rearrangement of arches to great arteries
draw new orientation of aortic arch
Recurrent Laryngeal positioning
Number 6 right branch is re-routed allowing right recurrent laryngeal to slip up to subclavian vein.
left stays by ligamentum arteriusum and aortic arch, curves posteriorly towards arch.
Coarctation of Heart
stenosin or constriction of the aortic arch
cause: unknown, possibly genetic with downs or turners
associated with cardiac valve defects and can go undagnosed until adult.
varies in severity
preductal coractation
not as common less than 5%
- just before ductus arteriosis
- blood to head and neck normal, ductus arteriosis must supply blood to lower half before birth
BIRTH-FO closes and so should ductus arteriousus
-andministered prostoglandin E2 to keep duct open until repair and be made
- differential cyanosis: blue tint on legs and lower half but not the head.
- all blood to lower half mixed, and more venus blood than o2 blood
postductual coarctation
less common, just after ductus arteriosus
- blood to h&E are fine
- EXTENSIVE collateral circulation is developed prior to birth.
Typically enlargement of internal thoracic and intercostal arteries to re-route blood supply.
Draw early sinus horns to the sinus venarum
include three main veins draining in
draw reconfiguration
left UV and VV and right Umbilical V all removed
left to right shift
R cardinal inlets become superior and inferior vena cava
left sinus horn becomes coronary sinus out of left cardinal inlet
cardinal vein adult derivatives
inlets (come from A/P and YS) to heart to become internal jugular vv
subclavian vv
brachiocephalic vv
most of IVC
overview of heart histology (3 layers)
Tunica Intima-endocardium
- endothelium: simple squamous
- subendothelial: CT layer
Tunica Media-myocardium
-cardiac muscle
Tunica Adventitia-epicardium
-loose CT and adipose tissue (CA’s)
Cardiac valves
specialization of endocardium (TI)
- extensions of fibroelastic tissue deep to endothelium, covered on lumen surface by endothelium
- stains blue in Trichrom….collagen?
purkinje fibers
like islands withing the subendocardial layer
-layer order: lumen-subendothelial-subendocardial-myocardium
large pale moth eaten cells, modified cardiac muscle fibers
-few myofilaments, not contractile, for heart conduction
timeline overview of heart development
week 3:heart and embryonic BV’s forming
- embryonic circulation established
- heart begins to beat
- cardiac loop complete - partitioning of heat to four chambers
- aortic arches undergo primary changes
8 formulation of heart valves completed
Formation of heart
Primary heart field: horse shoe shaped cells around cephalic end of embryo
-cells migrated out of the cephalic end of the primary streak (progenitor heart cells) as epiblast left and right sides (invaginated through streak into visceral mesoderm.
creation of PHF interaction of factors
Interaction between endoderm and visceral mesoderm @ cranial end
BOTH endoderm and VM secrete BMP2,4 (bmp4 increases FGF8 production-important for expression of cardiac genes)
endoderm secretes Crescent and Cerberus (blocking WNT proteins)
-as a result of BMP & C & C visceral mesoderm driven to NKX2.5 expression which is required for cardiac primary heart field
DRAW
PHF established (whats next before folding)
PHF: cardiogenic region
cells induced to form
- cardiac myoblasts
- angioblasts
new blood vessels coalesce into Heart Tube with R&L portions surrounded by cardiac myoblasts
Cephalocaudal Body Folding
week 3-4
- due to differential growth mainly from the neural tube
- moves heart into position, head end, to cervical end, to thoracic end
- pericardial cavity flipped to bottom, and gut tube begins forming over top. up to oropharyngeal membrane (look up)
lateral body folding
weeks 3-4
-due to differential growth mainly from SOMITES
-thoracic region: R&L sides come to gether each with their own portion of pericardial vacity
=fuse tubes of dorsal aorta and make one pericardial vacity
Hear forming from two heart tubes
result of lateral folding, lumen fuse together (fused EC) and lined by endothelium
cells micrate from the tissues on the surface of the septum transversum and sinus horns to make the epicardium
heart begins to BEAT
Secondary Heart field
after primary heart field forms, SHF forms more medially, reverse horseshoe.
-made from additional cardiogenic cells of the visceral mesoderm
cephalocaudal folding results in SHF around the PHF
-will become the outflow and inflow structures
associated with pharyngeal arches and developing neck region, and dorsal surface of fused heart
-neural crest associated
- cushion tissue formation
- SLV formation
- control of SHF contributions to card looping
cardiac looping beginning
Ends week 4
- creates adult orientation
- differentiates heart tube regions, heart parts
begins with tube with slight constrictions and slight dilations with just inflow and outflow
Conotruncal Region
- Truncus arteriosus
- conus cordis
Bulbous Cordis
Primative Ventricle
Primitive Atria
Sinus venosus
sinus horns
Cardiac looping in process
rapid growth of outflow end causes lengthening and twisting of the tube around central axis
cells where give rise to this? still unclear
CT and BC grow inferiorly
PV moves to the left
PA moves posterior and superior back to midline (SV follows)
molecular basis for looping and dysfunction
PITX2
same gene driven by FGF8 making cilia nodal swept left, nodal induces lat plate mesoderm to form left side structures by promoting PITX2
dextrocardia
- apex to the right
- can occur alone or with situs inversus (all visceral organs)
