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10. Congenital Heart dz > VSD > Flashcards

VSD Flashcards

1
Q

Components/regions of IVS

A

o Inlet portion
 TV orifice → papillary muscles
 Smooth walled
 Separates MV and TV valves
o Apical/trabecular portion
 Heavily trabeculated
 Primarily apical, from attachment of TV leaflets → apex and upward to crista supraventricularis
o Outlet/infundibular/conal portion
 Btw RVOT and LVOT
 Smooth walled, cranial to crista supraventricularis
o Membranous portion
 Below Aov on L side
 Cranial aspect of septal TV leaflet, btw TV and PV on R side
 Separate AoV from TV

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2
Q

What is the crista supraventricularis

A

o Muscular ridge in RV, U shaped
o Part of infundibular/outlet septum → smooth walled
o Btw TV and PV
o At jct of RVFW and IVS

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3
Q

Embryologic development of IVS

A

o IVS develops from apical → basilar
 Inlet and membranous portions are last to form

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4
Q

What is a VSD

A

communication btw ventricles

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5
Q

Prevalence

A

7% dogs, 15% cats with congenital defects

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6
Q

Breeds predispositions

A

WHWT, Lakeland terriers, English Bulldogs, English Springer Spaniel

Most common congenital defect in lamas, cows, horses

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7
Q

What determines the clinical significance of the defect

A

associated w size/ location, concomitant defects

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8
Q

What is the most common type

A
  • Most commonly perimembranous defect (80% of cases)
    o Below base of R or noncoronary cusp when viewed from LV
    o Adjacent to cranial edge of septal TV leaflet, caudoventral to supraventricular crest
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9
Q

Pathophysiology of L to R VSD, small vs large defect

A

o L to R VSD: RV is a conduit → pulmonary overcirculation → LV volume overload
 Normal RV size
* Simultaneous ventricular systole as blood is shunted to R side → enter RVOT and bypass RV
 Small defect: insignificant volume overload
 Large defect: significant L sided volume overload
* Can also cause R sided overload
* Chamber dilation is α to qty of shunting

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10
Q

What determines the amount of shunting in non restrictive defects

A

PVR

 RV = LV systolic pressure
 PAP = SAP

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11
Q

What can happen to PA

A

o MPA enlargement (all length) → ↑ blood flow
 Distinguish from post stenotic dilation where enlargement is distal to valve

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12
Q

Hemodynamics of restrictive defects

A

o Restrictive defect: LV > RV systolic pressure
 Resistance to flow across defect
 Little to no functional importance → restrict magnitude of shunting
 DO NOT ELEVATE PAP

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13
Q

Classification of VSDs

A

Variable

Muscular
Juxtaarterial
Perimembranous

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14
Q

Muscular VSD: location, features

A

Entirely surrounded by muscular septum
 Apical or mid ventricular
* Central: mid muscular
o Multiple channels on RV side
o Coalesce into single defect on LV side
o Posterior to trabecula septomarginalis
* Apical: most frequent
o Often large
o Multiple channels on RV side
o Coalesce into single defect on LV side
* Marginal: small defect along RV septal jct
 Multiple muscular defects → swiss cheese septum
 Rare in dogs/cats

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15
Q

Juxta-arterial VSD: location, features

A

in outlet septum, below PV and AoV
 High incidence of AI as AoV leaflet prolapse into defect
 Fibrous continuity of AoV and PV

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16
Q

Perimembranous VSD: location, features

A

surrounded by membranous septum
 Cranial aspect of septal TV leaflet
 Paramembranous: large, encroaching supraventricular crest and extending toward RVOT
 Fibrous continuity of AoV and TV

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17
Q

Defects can further described based on

A

location: apical, outlet, inlet

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18
Q

Inlet VSD

A

can be part of perimembranous or muscular septum
 Historically directly ventral to septal TV leaflet
 Associated w endocardial cushion defect
 Often with ASD → AVSD

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19
Q

Outlet VSD

A

perimembranous or muscular
 Below AoV on L side
 Below PV on R side

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20
Q

Other classifications

A
  • Older classification according to position of VSD in relation to supraventricular crest
    o Infracristal → perimembranous
    o Supracristal → juxtaarerial
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21
Q

What are malalignement or conotruncal VSDs

A

defect present from ventriculo-arterial a malalignment
o Loss/malposition of supraventricular crest and portion of membranous/muscular outlet septum
o Look for fibrous continuity btw valves to further classify

22
Q

Significance of IVS aneurysm

A

o May represent spontaneously closed defects

23
Q

Un/non-committed VSD

A
  • VSD NOT anatomically related to/close to great vessel
    o Separated by considerable muscle
  • Not an anatomic definition
    o Used to define VSDs in DORV when distant from both arterial valves
24
Q

Committed VSD

A
  • VSD was anatomically related to/close to great vessel
25
Doubly committed VSD
= infundibular VSD can be muscular or rimmed by semilunar valve tissue o Considered doubly committed subarterial when  Little to no muscule btw OT components * Always associated w loss of muscular outlet septum  Absence of Subpulmonary infundibulum  Ao and PV leaflets are in fibrous continuity
26
What is the infundibular septum
separates LVOT and RVOT o Subpulmonary infundibulum:  Sleeve support leaflets of PV  Separates RVOT from surface of heart
27
Other names for infundibular VSD
o Supracristal o Subpulmonary o Subarterial o Doubly committed o Outlet
28
Subaortic VSD
 Most frequent type of DORV  Ao is to R of PA  VSD is more closely related to Ao vs PA  Presence of bilateral conus separates semilunar valves * Ao conus: btw AoV and MV anterior leaflet
29
Subpulmonary VSD
 Dilated PA  VSD is supracristal, subjacent to PV  Pulmonary conus * Separate MV anterior leaflet and PV * No conus btw VSD and PV  Conus septum: separates AoV and PV
30
2D echo findings
* R parasternal LAX LV outflow view o Junction of muscular septum → anterior Ao wall o Cannot see supracristal defect * R parasternal SAX view at level of Ao and LA/PA o High perimembranous defects  Under TV and above Ao o Supracristal defects: proximal to PV * Muscular VSD: anywhere along muscular septum * Avoid 4 chamber views (echo drop out) * Aneurysmal dilation of membranous portion of IVS in RV o If perforated, usually ventral portion of aneurysmal pocket o Can be associated with spontaneous closure of VSD
31
M-Mode echo findings
* TV flutter in systole (38% of dogs w VSD)
32
Spectral color Doppler findings
* AI: often seen, especially with supracristal VSD o AoV prolapse * Restrictive VSD: PG should >80mmHg (or 5m/s) * Lower PG indicative of larger defects, ↑ RVP * Flow profile across VSD: plateau shape o Represent PG from R to L ventricle * Qp:Qs>2 → significant shunting
33
Describe inlet VSD
* IVS btw MV and TV: extend from valve to trabeculae * Muscular or perimembranous o Aligned IAS and IVS o Malalignment of septums w/ straddling TV
34
Inlet VSD other names
AVSD canal type VSD perimembranous VSD w/ inlet extension
35
Describe muscular VSD
* Apical portion of IVS : midseptal, apical, anterior, inferior * Muscular borders * Spontaneous closure if small (Hu) * Multiple defects: swiss cheese IVS
36
Describe outlet VSD
* Smooth wall outlet portion btw RVOT and LVOT * Absence/hypoplasia of conal septum = under PV o Fibrous continuity Ao → PV
37
Outlet VSD other names
o If absent conal septum: conal septal, infundibular, doubly committed juxtaarterial, supracristal, subpulmonic/subarterial o If conal septal malalignment: conoventricular, perimembranous w/ outlet extension
38
Describe perimembranous VSD
* Base of heart: separate TV from AoV o Behind septal TV leaflet o Below R coronary Ao cusp * Fibrous continuity TV → AoV * Most common o Spontaneous closure can occur → aneurysm * Restrictive flow → behind TV tissue * AI: AoV cusps prolapse from venturi effect
39
Perimembranous VSD other names
infracristal, subaortic
40
What is Gerbode defect
* Membranous IVS at Mv and TV offset o AV node penetrating bundle * Shunt LV → RA
41
Pathophys VSD
* L → R shunting: L sided enlargement o LV volume overload from shunt + AI o Leads to CHF * Pulmonary overcirculation → ↑ PVR → Eisenmenger
42
Hemodynamic significance depend on:
o Size of defect: small restrictive vs large (LVP = RVP) o PVR and SVR
43
PE VSD
o Systolic murmur: inversely proportional to defect size o Diastolic murmur: AI  To and fro possible
44
ECG VSD
* LAE: wide P waves * LVE: ↑ R wave amplitude
45
CTX VSD
* Left sided cardiomegaly * Pulmonary overcirculation
46
Natural history depending on size
* Small VSD: usually well tolerated o No treatment needed o Can close spontaneously: reported in dogs * Moderate VSD: variable px * Large VSD: will likely develop CHF
47
How to reduce shunt flow
o Arteriolar vasodilation → ↓ SVR o PA banding → ↑ PVR and RVP
48
Cardiac KT oximetry
O2 step up in RV and PA
49
Cardiac KT pressure study
o Large defect: RVP = LVP o Pulmonary vascular disease 2nd to pulmonary overcirculation → ↑ PVR and PCWP
50
Angio cardiac KT
LV to RV shunting o AI can be identified w/ aortic angio

10. Congenital Heart dz (28 decks)

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