ASD Flashcards
Embryology: describe atrial septation
- 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
What becomes the L horn of sinus venosus
Coronary sinus
What becomes the R horn of sinus venosus
Part of RA
What is the sinoatrial jct during embryologic development and what does it become
- 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
Types/classification ASD
Ostium primum defect
Ostium secundum defect
Sinus venosus defect
Coronary sinus defect
Ostium primum defect: etiology, localization
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
Ostium secundum defect: etiology, localization
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
Sinus venosus defect: etiology, localization
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
Coronary sinus defect: etiology, localization
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
Distinguish an ASD from a PFO.
- 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
Prevalence
cats 9%, dogs 0.7% of cardiac defects
o Ostium primum ASD more common in cats vs dogs
o Small ASD most likely undetected
Most common cause of PFO
most likely only recognized with PS
Small R to L shunt
Breeds predispositions
o Boxers → most common congenital defect
o Old English sheep dogs
o Samoyeds
Pathophys: on what depend shunting
- 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)
Pathophys: consequences and hemodynamics
- ↑ 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
Consequences of large shunting
- Large shunt can ↑ PVR → PH → Eisenmenger physiology
- No to limited LAE: ↑ pulmonary venous return shunts back into RA
DDX for ASDs
anomalous pulmonary venous return into RA → similar pathophysiology
Clinical findings: c/s
asymptomatic to R/L CHF
Clinical findings: PE
o Soft to moderate intensity systolic murmur at L base
Relative PS
o Split S2
Clinical findings: CTX
RAE, RVE, RVH, MPA dilation, pulmonary overcirculation
Clinical findings: ECG
R axis deviation
Clinical findings: echo
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
Natural history
o Secondum defect seem well tolerated depending on size
o Primum defects more likely to cause biventricular failure
Types of coronary sinus defect Hu
I: completely unroofed + L CrVC
II: completely unroofed, no L CrVC
III: partially unroofed mid portion
IV: partially unroofed terminal portion
Shunting depend on
Size of defect
Relative resistance of systemic and pulmonary circulations
Hemodynamics of large ASD
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
Signalment
o Suspected to be more common in cats
o ↑ prevalence in Boxer
Pathophys L to R shunt
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
When does R to L shunt occurs
w/ concurrent defects : PS, PH → RVH → ↓ RV compliance compared to LV
Hemodynamic consequence depends on
magnitude and duration of shunt
o Most shunt occurs in diastole
o Inspiration: ↓L to R shunting from ↓ LA filling + ↑RA filling
C/s
asymptomatic if small, uncomplicated, restrictive lesions
PE
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
DDX
anomalous pulmonary venous return to RA
o Similar functional circulatory disturbances
ECG changes
- 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
CTX changes
- R sided enlargement from volume overload: RAE, RVE, RVH
- MPA dilation
- Pulmonary overcirculation + prominent vasculature
2D echo changes
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
M-Mode echo
o Paradoxical septal motion → R sided volume overload
Color flow doppler echo
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
Contrast echo: bubble study
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
Cardiac KT: oximetry findings
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
Cardiac KT: pressure study
o If CHF: ↑ RA/RV diastolic P and central venous P
o Relative PS: ↑ PG
Cardiac KT: angio
inferior to echo for dx
o Shunt quantification via contrast material
Natural history
- 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
