Anatomy/Embryology of the Heart Flashcards

1
Q

Coronary Sulcus

A

(aka: AV Sulcus)

Contains:

  • Arteries:
    • RCA,
    • Circumflex Branch of Left Coronary Artery;
  • VENOUS:
    • Coronary Sinus;
    • Great Cardiac Vein
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2
Q

Anterior Interventricular Sulcus

A

1) LAD (anterior interventricular artery): branch of L coronary atery
2) Great cardiac vein

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3
Q

Posterior Interventricular Sulcus

A

1) right posterior descending artery (posterior interventricular artery): branch of RCA;
2) middle cardiac vein

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4
Q

Formation of Atrial Septum

A
  1. Stepum Primum: (thin, flexible) - begins to form at the end of the 4th week
    1. Grows from wall of atria toward endocardial cushions
    2. Gap between growing septum primum and endocardial cushion: Ostium (Foramen) Primum
  2. Ostium (Foramen) Secundum forms: perforation (apoptosis) in ostium primum to maintain communiation between L and R atria
  3. Ostium primum closes.
  4. Septum Secundum: (thicker; rigid) - forms on R side of septum primum
    1. incomplete septum which covers ostium secundum, then stops
    2. Free edge of septum becomes: limbus of the fossa ovalis
    3. Portion of setpum primum not covered by septum secundum becomes Fossa ovalis
      1. bc septum primum is flexible, blood can pass from RA to LA (pressure gradient) through the Foramen Ovale
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5
Q

Ventricular septum

A

Two Parts:

  1. Muscular septum: develops with cardiac wall from cardiac muscle; partially separates L and R ventricles, with area of communication called the interventricular foramen
    1. forms during 5th week
  2. Membranous septum: formed from the aorticopulmonary septum and endocardial cushions
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6
Q

Atrial Septum Defect: Primum Type

A
  • ACYANOTIC - left to right shunt
  • Septum Primum doesn’t fuse with endocardial cushion​
  • leaves patent ostium primum
  • usually bc not enough NC cells migrated into endocardial cushion (thus, seen in association with NC defects)
  • endocardial cushion contributes to valves
  • second most common of the heart defects (ventricular is most common)
  • most common defect of the acyanotic type
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7
Q

Atrial Septal Defect: Secundum

A
  • ACYANOTIC - left to right shunt
  • More common than primum ASD
  • ostium secundum not being covered over completely by septum secundum
  • preventing complete closure of foramen ovale
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8
Q

Ventricular Septum Defects

A
  • usually ACYANOTIC
    • However a large L to R shunt may eventually result in overload of the pulm circuit, changes in pulm vasculatire and development of pulmonary HTN
      • if Pressure in pulm circuit eventually rise > pressure in system circuit, the previous L to R shutn through VSD will reverse to
      • R to L shunt = LATE CYANOSIS (Eisenmenger complex)
  • in muscular or membranous septum
  • Muscular VSD
    • result of excessive resorption of the embryonic ventricular septum during growth of the ventricle
  • Membranous VSD
    • ​result of defective formation of aotricopulmonary septum; failure of this septum to fuse with embryonic ventricular septum
    • more common
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9
Q

Patent Ductus Arteriosis

A
  • Failure of the ductus arteriosus to close = postnatal aorta to pulmonary (L to R) shunt
  • ACYANOTIC
  • more common in preterm babies: neonatal hypoxia and elevated prostaglandin levels contribute to this finding
  • Tx: inhibition of prostaglandin synthesis with indomethicin + O2 therapy
    • ​gets PDA to close
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10
Q

Tetrology of Fallot

A

most common heart defect

  • CYANOSIS typically appears some time after birth
  • caused by malpositioning of AORTICOPULMONARY SEPTUM
    • formed displaced to the side of the truncus arteriosus and conus cordis (dextropositioning)
  • Results in:
  1. pulmonary stenosis
  2. overriding aorta
  3. ventricular septal defect (bc aotricopulmonary septum does not fuse with the embryonic ventricular septum)
  4. right ventricular hypertrophy (develops secondarily)

*Pressure in RV is elevated, causeing RV blood to shunt through VSD into overriding aorta.

*R to L shunt –> CYANOSIS

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11
Q

Persistant Truncus Arteriosus

A
  • CYANOTIC
  • aorticopulmonary septum does not form: truncus arteriosus persists rather than becoming ascending aorta and pulmonary trunk
  • both ventricles empty their blood into this common artery
    • deoxy and oxygenated blood is mixed –> CYANOSIS
  • bc the absent aorticopulmonary septum would have contributed to the membranous ventricular septum, VSD coexists with persistent truncus arteriosus
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12
Q

Transposition of the Great Arteries

A
  • CYANOTIC
  • most common cause of cyanosis presenting immediately after birth
  • aorticopulmonary septum, which normally forms in a spiral shape, is not spiraled
  • thus, aorta and pulmonary trunk are reversed from their normal positions
  • RV flows into the aorta
  • LV flows into the pulmonary trunk
  • babies who remain alive after birth must have other defects that allow mixing of blood between the pulmonary and aortic circuit
  • septal defects are common and PDA is typically seen in infants with transposition
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13
Q

Prenatal IVC Flow

A
  • more oxygenated IVC –> foramen ovale –> LA –> LV –> out LV to AA
  • Kept separate from SVC to that the 3 branches of the aortic arch (below) can only be filled with IVC (more oxygenated blood to brain)
    1. brachiocephalic trunk
    2. left common carotid
    3. left subclavian
    • this happens bc ductus arteriosus comes into the aorta just after the subclavian leaves the aorta
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14
Q

Prenatal SVC

A
  • deoxygenated SCV: RA –> very litte through foramen ovale (would have to make a U-turn to get through foramen ovale, so doesn’t) –> tricuspid –> RV –> out pulm trunk (vascular resistance is high in pulm cuircut bc not exapnded so very little in lungs) –> almost all shunts out of pulm circuit into aorta thorugh ductus arteriosus (R to L gradient) –> enters aorta and mixes with IVC in Ascending Aorta –> descending AA to umbilicles and to supply lower limbs
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15
Q

Changes at Birth

A
  • Ductus arteriosus –> ligamentum arteriosum
  • Ductus venosus (liver) –> ligamentum venosum
  • Umbilical vein –> ligamentum teres
  • Right and left umbilical arteries –> medial umbilical ligaments
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16
Q

Ductus Ateriosus After Birth

A

increased O2 and decreased prostaglandin –> closure of ductus arteriosus

  • so once you can breathe, ductal smooth muscle contracts
  • prostiglandin levels inhibit ductal smooth muscle from closing
    • timed event: prostiglandin levels drop at birth
    • thus, preterm babies have higher level of patent ductus arteriosus bc prostiglandin levels have not timed out
      • Tx: give the baby O2 and inhibit synthesis of prostiglandin so ductus closes in preterm baby
      • full term baby needs strucutal intervention
      • Patent ductus arteriosus can sometimes be the reason for survival for a baby with transposition: so admin O2 AND give exogenous prostinglandin to keep baby alive until structural intervention