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10. Congenital Heart dz > ASD > Flashcards

ASD Flashcards

1
Q

Embryology: describe atrial septation

A
  • 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
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2
Q

What becomes the L horn of sinus venosus

A

Coronary sinus

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3
Q

What becomes the R horn of sinus venosus

A

Part of RA

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4
Q

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

A
  • 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
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5
Q

Types/classification ASD

A

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

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6
Q

Ostium primum defect: etiology, localization

A

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

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7
Q

Ostium secundum defect: etiology, localization

A

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

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8
Q

Sinus venosus defect: etiology, localization

A

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

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9
Q

Coronary sinus defect: etiology, localization

A

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

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10
Q

Distinguish an ASD from a PFO.

A
  • 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
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11
Q

Prevalence

A

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

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12
Q

Most common cause of PFO

A

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

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13
Q

Breeds predispositions

A

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

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14
Q

Pathophys: on what depend shunting

A
  • 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)
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15
Q

Pathophys: consequences and hemodynamics

A
  • ↑ 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
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16
Q

Consequences of large shunting

A
  • Large shunt can ↑ PVR → PH → Eisenmenger physiology
  • No to limited LAE: ↑ pulmonary venous return shunts back into RA
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17
Q

DDX for ASDs

A

anomalous pulmonary venous return into RA → similar pathophysiology

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18
Q

Clinical findings: c/s

A

asymptomatic to R/L CHF

19
Q

Clinical findings: PE

A

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

20
Q

Clinical findings: CTX

A

RAE, RVE, RVH, MPA dilation, pulmonary overcirculation

21
Q

Clinical findings: ECG

A

R axis deviation

22
Q

Clinical findings: echo

A

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

23
Q

Natural history

A

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

24
Q

Types of coronary sinus defect Hu

A

 I: completely unroofed + L CrVC
 II: completely unroofed, no L CrVC
 III: partially unroofed mid portion
 IV: partially unroofed terminal portion

25
Q

Shunting depend on

A

Size of defect
Relative resistance of systemic and pulmonary circulations

26
Q

Hemodynamics of large ASD

A

o Large ASD: should be considered as single atrium
 Blood flows preferentially across AV pathway of least diastolic resistance
 RV: thinner walls, more distemsible
 Secondary RA, RV and pulmonary circulation volume overload
* If significant: endocardial cushion defect + RCM possible

27
Q

Signalment

A

o Suspected to be more common in cats
o ↑ prevalence in Boxer

28
Q

Pathophys L to R shunt

A

higher RV compliance
o R sided volume overload: RAE and RVE
o ↑ pulmonary blood flow → pulmonary overcirculation
 Eisenmenger syndrome: PH development from pulmonary vascular dz → shunt reversal

29
Q

When does R to L shunt occurs

A

w/ concurrent defects : PS, PH → RVH → ↓ RV compliance compared to LV

30
Q

Hemodynamic consequence depends on

A

magnitude and duration of shunt
o Most shunt occurs in diastole
o Inspiration: ↓L to R shunting from ↓ LA filling + ↑RA filling

31
Q

C/s

A

asymptomatic if small, uncomplicated, restrictive lesions

32
Q

PE

A

o Usually no murmur from ASD itself: low velocity shunting across defect
o Soft L basilar ejection type murmur OR mid diastolic soft murmur
 Relative pulmonic/tricuspid stenosis
 ↑ transvalvular flow
o Diastolic murmur: PI
o Fixed split S2: delayed PV closure from ↑ flow
 No variation in respiration due to shunting
o Systolic murmur over L apex: MR
 Suspect endocardial cushion defect w cleft MV

33
Q

DDX

A

anomalous pulmonary venous return to RA
o Similar functional circulatory disturbances

34
Q

ECG changes

A
  • R axis deviation/RBBB: RVE
    o Deep S wave in lead II, III, aVF
    o P wave enlargement
    o Prominent T wave
  • Signs of RVE: ↑ QRS duration
35
Q

CTX changes

A
  • R sided enlargement from volume overload: RAE, RVE, RVH
  • MPA dilation
  • Pulmonary overcirculation + prominent vasculature
36
Q

2D echo changes

A

o RVA/RVE: degree of enlargement reflect severity of shunting
o Smaller LV
o Defect visualized in IAS
 Area of abnormal sonolucency in region of defect
 Careful with echo dropout in the region of fossa ovale
 Secondum defect vs PFO: flap valve present

37
Q

M-Mode echo

A

o Paradoxical septal motion → R sided volume overload

38
Q

Color flow doppler echo

A

o Visualize defect and flow across atria
 Starts mid to late diastole → ↓ through mid diastole
 ↑ with atrial contraction
 Reversal in early systole: transient R to L shunt
o Relative pulmonic stenosis

39
Q

Contrast echo: bubble study

A

o Can clarify type and degree of shunting
o LA → RA shunting: negative contrast in RA, no bubbles in LA
o RA → LA shunting: bubbles visualized in LA

40
Q

Cardiac KT: oximetry findings

A

o L to R shunting: ↑O2 saturation in RA, RV, PA
o DDX:
 LV → RA shunt (Gerbode defect)
 VSD + TR
 AVSD
 Systemic AV fistula
 Abnormal PV return

41
Q

Cardiac KT: pressure study

A

o If CHF: ↑ RA/RV diastolic P and central venous P
o Relative PS: ↑ PG

42
Q

Cardiac KT: angio

A

inferior to echo for dx
o Shunt quantification via contrast material

43
Q

Natural history

A
  • Secondum ASD often well tolerated
  • Primum or endocardial cushion defects more likely to lead to
    o CHF or PH
    o Px is guarded to poor

10. Congenital Heart dz (28 decks)

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