ASD

Question 1

Embryology: describe atrial septation

Answer 1

• Septum primum: 1st to develop
  o Ridge of crescent shaped growing superior to inferior toward AV canal
   Ostium primum
  o Becomes lined by tissue from endocardial cushions
  o Proliferation of septal tissue and endocardial cushion tissue → combine to close ostium primum
  o Before closure: tissue resorption in dorsal portion
   Programmed  death creates small cribriform perforations → coalesces to form large interatrial communication → maintain blood flow
   Ostium secondum
• Septum secondum: 2nd to develop
  o Expands on the R of septum primum from atrial roof to ¾ of atrial septum
  o Thick wall muscular ridge forming limbus of fossa ovalis
   Channel for interatrial blood flow through ostium secondum
• Foramen ovale

Question 2

What becomes the L horn of sinus venosus

Answer 2

Coronary sinus

Question 3

What becomes the R horn of sinus venosus

Answer 3

Part of RA

Question 4

What is the sinoatrial jct during embryologic development and what does it become

Answer 4

• Sinoatrial junction: form R and L venous valves
  o R valve → eustachian valve on CaVC and thebesian valve on CS
  o L valve → fuse to margin of fossa ovalis

Question 5

Types/classification ASD

Answer 5

Ostium primum defect
Ostium secundum defect
Sinus venosus defect
Coronary sinus defect

Question 6

Ostium primum defect: etiology, localization

Answer 6

o From incomplete ostium primum fusion to endocardial cushion
 Lower/ventral atrial septum
 Directly above AV valves
o Often associated w cleft of anterior MV leaflet +/- TV atresia/dysplasia
 Recognized as a form of AVSD
 Often very large

Question 7

Ostium secundum defect: etiology, localization

Answer 7

most common
o Shorter septum secondum OR excessive absorption of septum primum
o Central atrial septum w/i fossa ovalis, caudal to intervenous tubercle
 Insufficiency of tissue at the fossa ovalis

Question 8

Sinus venosus defect: etiology, localization

Answer 8

o PVs shunting into RA/Cr or CaVC
o Dorsal interatrial septum, posterior and superior to fossa ovalis
o Usually in conjunction with anomalous connection of R PV

Question 9

Coronary sinus defect: etiology, localization

Answer 9

o Normally, CS travels across LA to empty into RA
o Associated with unroofed CS, at site of coronary sinus ostium
o Reported w persistent L CrVC

Question 10

Distinguish an ASD from a PFO.

Answer 10

• Normal interatrial connection during fetal life
  o Should close postnatally when LAP > RAP → valve of fossa ovalis pressed against limbus
   = Functional seal
   Anatomic seal during 1st years of life from fibrous adhesions
• Persistent foramen ovale can occur if
  o Failure to close from persistent ↑ RAP after birth
   Less clinically important if normal RAP since no shunting will occur
   Probe can be passed in foramen ovale of 30% of Hu, but defect is functionally closed
  o LAE or RAE → stretch limbus → ostium secondum no longer covered

Question 11

Prevalence

Answer 11

cats 9%, dogs 0.7% of cardiac defects
o Ostium primum ASD more common in cats vs dogs
o Small ASD most likely undetected

Question 12

Most common cause of PFO

Answer 12

most likely only recognized with PS
 Small R to L shunt

Question 13

Breeds predispositions

Answer 13

o Boxers → most common congenital defect
o Old English sheep dogs
o Samoyeds

Question 14

Pathophys: on what depend shunting

Answer 14

• Shunting depend on size of defect + SVR/PVR (not related to PG btw atria, which is small)
  o Restrictive: small defect that maintain differential pressures btw chambers
  o Large defects: no resistance to flow
   Shunt direction determine by compliance of ventricles
   RV more compliant = L → R shunt
  o Normally L to R shunt (↑P → ↓P)
   R to L shunt w conditions that ↑RA/RV pressures (PS, PH, TVD)

Question 15

Pathophys: consequences and hemodynamics

Answer 15

• ↑ flow from LA → RA
  o R sided volume overload → may lead to myocardial failure
   Also affect LA
  o Relative pulmonic/tricuspid stenosis
  o Delayed PV closure

Question 16

Consequences of large shunting

Answer 16

• Large shunt can ↑ PVR → PH → Eisenmenger physiology
• No to limited LAE: ↑ pulmonary venous return shunts back into RA

Question 17

DDX for ASDs

Answer 17

anomalous pulmonary venous return into RA → similar pathophysiology

Question 18

Clinical findings: c/s

Answer 18

asymptomatic to R/L CHF

Question 19

Clinical findings: PE

Answer 19

o Soft to moderate intensity systolic murmur at L base
 Relative PS
o Split S2

Question 20

Clinical findings: CTX

Answer 20

RAE, RVE, RVH, MPA dilation, pulmonary overcirculation

Question 21

Clinical findings: ECG

Answer 21

R axis deviation

Question 22

Clinical findings: echo

Answer 22

o 2D/M-Mode evaluation
 Defect visualized: echo dropout
 RA/RV dilation
* MR/TR from annular dilation
 Paradoxical septal motion → when RV diastolic P > LVP

o Spectral and color Doppler: often sufficient for dx
 Relative PS → ↑ flow through PV
 Small PG: velocity of shunting blood may not > Nyquist limit
* More restrictive ASD: aliased flow
* Mean PG should be obtained by tracing shunt flow profile → helps differentiate hemodynamically significant defects

o Contrast enhanced echo can help clarify type/degree of shunting
 Shunting starts mid to late systole → decrescendo
* ↑ with atrial contraction
* Reversal in early systole: transient R to L shunt
o ↑ with inspiration, ↓ with expiration

o PFO is difficult to differentiate from ostium secondum defect since in the same region
 If membrane of fossa ovalis is seen, can confirm PFO

Question 23

Natural history

Answer 23

o Secondum defect seem well tolerated depending on size
o Primum defects more likely to cause biventricular failure