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
Q

Doubly committed VSD

A

= 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
Q

What is the infundibular septum

A

separates LVOT and RVOT
o Subpulmonary infundibulum:
 Sleeve support leaflets of PV
 Separates RVOT from surface of heart

27
Q

Other names for infundibular VSD

A

o Supracristal
o Subpulmonary
o Subarterial
o Doubly committed
o Outlet

28
Q

Subaortic VSD

A

 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
Q

Subpulmonary VSD

A

 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
Q

2D echo findings

A
  • 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
Q

M-Mode echo findings

A
  • TV flutter in systole (38% of dogs w VSD)
32
Q

Spectral color Doppler findings

A
  • 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
Q

Describe inlet VSD

A
  • 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
Q

Inlet VSD other names

A

AVSD canal type VSD
perimembranous VSD w/ inlet extension

35
Q

Describe muscular VSD

A
  • Apical portion of IVS : midseptal, apical, anterior, inferior
  • Muscular borders
  • Spontaneous closure if small (Hu)
  • Multiple defects: swiss cheese IVS
36
Q

Describe outlet VSD

A
  • Smooth wall outlet portion btw RVOT and LVOT
  • Absence/hypoplasia of conal septum = under PV
    o Fibrous continuity Ao → PV
37
Q

Outlet VSD other names

A

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
Q

Describe perimembranous VSD

A
  • 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
Q

Perimembranous VSD other names

A

infracristal, subaortic

40
Q

What is Gerbode defect

A
  • Membranous IVS at Mv and TV offset
    o AV node penetrating bundle
  • Shunt LV → RA
41
Q

Pathophys VSD

A
  • L → R shunting: L sided enlargement
    o LV volume overload from shunt + AI
    o Leads to CHF
  • Pulmonary overcirculation → ↑ PVR → Eisenmenger
42
Q

Hemodynamic significance depend on:

A

o Size of defect: small restrictive vs large (LVP = RVP)
o PVR and SVR

43
Q

PE VSD

A

o Systolic murmur: inversely proportional to defect size
o Diastolic murmur: AI
 To and fro possible

44
Q

ECG VSD

A
  • LAE: wide P waves
  • LVE: ↑ R wave amplitude
45
Q

CTX VSD

A
  • Left sided cardiomegaly
  • Pulmonary overcirculation
46
Q

Natural history depending on size

A
  • 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
Q

How to reduce shunt flow

A

o Arteriolar vasodilation → ↓ SVR
o PA banding → ↑ PVR and RVP

48
Q

Cardiac KT oximetry

A

O2 step up in RV and PA

49
Q

Cardiac KT pressure study

A

o Large defect: RVP = LVP
o Pulmonary vascular disease 2nd to pulmonary overcirculation → ↑ PVR and PCWP

50
Q

Angio cardiac KT

A

LV to RV shunting
o AI can be identified w/ aortic angio