VSD Flashcards

1
Q

What is the most common congenital cardiac malformation?

A

VSD

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2
Q

In what percentage of patient do VSDs occur?

A

32% of patients, either in isolation or with a range of other malformation

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3
Q

What four components is the ventricular septum made up of?

A

1) Membranous/Perimembranous
2) Trabecular/Muscular
3) Outlet/infundibular septum
4) Inlet/AV Canal/AVSD

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4
Q

What are the most common types of VSDs?

A

Perimembranous (80% of VSDs)

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5
Q

Where can perimembranous VSDs further extend to?

A

Inlet or outlet

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6
Q

How are outlet VSDs subdivided?

A

VSD outlet defect with anterior deviation of the outlet septum (e.g ToF, associated with aortic override) and those with posterior deviation (as seen with aortic arch interruption)

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7
Q

Where can Muscular VSDs be situated?

A
Completely surrounded by muscles; frequently multiple
Inlet
Trabecular
apical
or anterior part of septum
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8
Q

What is a sub arterial VSD = Outlet VSD = infundibular = supra cristal VSD?

A

Located beneath the semilunar valves in the outlet septum. Deficiency of infundibular septum resulting in an area of fibrous continuity between the semilunar valves. Often associated with progressive AR due to prolapse of the aortic cusp, usually right.

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9
Q

What factors affect the pathophysiology of a VSD?

A

Size of VSD

PVR relative to SVR, which determines magnitude and direction of flow through the defect

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10
Q

Effect of small VSD with a high resistance to flow

A

Small left-to-right shunt and minimal haemodynamic disturbance

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11
Q

Effect of large VSD with no pulmonary outflow tract obstruction

A

Large left-to-right shunt
Low PVR
High SVR

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12
Q

What increases a left-to-right shunt in a VSD?

A

Higher SVR (e.g. aortic coarctation)
or
LVOTO (e.g valvular, sub or supravalvular AS)

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13
Q

What causes the direction of the shunt to reverse in VSDs?

A

When PVR becomes higher than SVR

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14
Q

Clinical findings in Very small VSD

A

ESM at LSE

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15
Q

Clinical findings in small VSD

A

Thrill: +
Murmur: PSM loud LSE radiating to apex

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16
Q

Clinical findings in moderate VSD

A
Thrill: + 
Murmur: PSM, LSE to apex with mitral MDM 
Apex: LV+  
S2 obscured by mitral
ECG: LV+, LA+, LAD
CXR: Increased CTR, plethora
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17
Q

Clinical findings in Large VSD

A
Thrill: No 
Murmur: ESM at upper LSE and mitral MDM 
Apex: LV+ , RV+
S2 single with increased P2
ECG: LV+, LA+, RV+
CXR: Increased CTR, plethora, prominent PAs
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18
Q

Clinical findings with pulmonary vascular obstructive disease (Eisenmenger)

A
Thrill: No 
Murmur: None or soft ESM
Apex: RV++, palpable pA
S2: Single loud palpable P2
ECG: RV+, RA++, RAD
CXR: Increased CTR, no plethora, large central PAs
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19
Q

Where is an inlet VSD?

A

Inlet of the ventricular septum, immediately inferior to the AV valve apparatus, typically occurs in Down Syndrome

20
Q

What determines direction and magnitude of VSD shunt?

A

PVR
Size of defect
LV/RV systolic and diastolic function
Presence of RVOTO

21
Q

VSD clinical presentations in adults

A
  • VSD operated in childhood without residual VSD
  • VSD operated in childhood with residual VSD
  • Small VSD with insignificant L-R shunt without LV volume overload or PHTN which was not considered for surgery in childhood
  • VSD with L-R shunt, pHTN, LV volume overload
  • Eisenmenger syndrome
22
Q

Complications of residual VSD

A
  • IE (2/1000 Pt years, 6x higher than normal population)
  • Heart failure due to LV volume overload prolonged L-R shunt
  • Double chamber RV
  • Subaortic stenosis
  • RCC prolapse –> AR
  • arrhythmias inc CHB
23
Q

Treatment Options for VSD

A
  • Surgical closure (mostly pericardial patch) with good long-term results is the treatment of choice
  • Transcatheter closure
24
Q

Which patients should undergo surgical VSD closure?

A

1) Patients with symptoms that can be attributed to L-R shunting through the (residual) VSD and who have no severe Pulmonary Vascular disease
2) Asymptomatic patients with evidence of LV volume overload attributable to VSD

25
Q

Which patients should be considered for surgical VSD closure?

A

1) Patients with history of IE
2) VSD-associated prolapse of AV cusp causing progressive AR
3) Patients with VSD and PAH with net L-R shunt (Qp:Qs >1.5) present and PAP or PVR <2/3 of SVR (baseline or when challenged with NO or after targeted PAH therapy)

26
Q

When should surgery be avoided?

A

Eisenmenger VSD
Exercise-induced desaturation is present
If VSD is small, not outlet VSD, does not lead to LV volume overload of PAH and if there is no history of IE

27
Q

When should trans-catheter VSD closure be considered?

A

1) Increased risk factors for surgery, multiple prev cardiac surgical interventions or VSDs that are poorly accessible for surgery
2) Muscular VSDs that are located centrally in inter ventricular septum
3) Perimembranous VSDs

28
Q

Which patients with VSDs should get annual follow-up?

A

LV dysfunction, residual shunt, PAH, AR, RVOTO, LVOTO

29
Q

What follow-up should patients with a small VSD (native or residual, normal LV, normal PAP and asymptomatic) and no other lesions have?

A

3-5 year intervals

30
Q

What follow-up should VSD device closures have?

A

Regular follow-up during the first 2 years and then depending not he result, every 2-4 years

31
Q

What follow-up should Surgical VSD closures have (without residual abnormality)?

A

5 year intervals

32
Q

Are there exercise/sport restrictions I patients with small VSD (w/o pHTN/Significant arrhythmias or LV dysfunction) or VSD closure?

A

No restrictions.

Patients with PAH must limit themselves to low-intensity recreational activity/sports

33
Q

Is pregnancy contraindicated in patients with VSD?

A

Pregnancy is contraindicated in Eisenmenger syndrome?
Risk is low in asymptomatic patients with normal LV and no PAH.
Recurrence rate of CHD is 6-10%

34
Q

Is IE prophylaxis recommended for patients with VSD?

A

Only for high risk patients.

35
Q

What is Eisenmenger syndrome?

A

Occurs when increased pressure of blood flow in the lung becomes so great that the you develop a cyanotic R-L shunt.
Increased PVR and decreased compliance of Pulmonary vessels –> elevated PASP –> RVH –> RH pressure > LH pressure

36
Q

What is a double chamber RV?

A

Hypertrophied RV muscle bundles divide the RV cavity into high pressure proximal chamber and low pressure distal chamber that can lead to PBF obstruction (RVOTO) and RV cavity obliteration

37
Q

For which type of VSD is TTE least useful?

A

small apical muscular VSD

38
Q

By what age do membranous VSDs partially or completely close?

A

Age 20

39
Q

Outlet VSDs

A

Beneath the pulmonary and aortic valves

Never close spontaneously and risk of AR 2.5 x more common than membranous VSD

40
Q

Inlet VSDs

A

Account got 5-8% of VSDs
Located posteriorly int he inlet septum
Extends from annulus of TV to attachments of the leaflets
Large and do not close spontaneously
Single defect unless in settings of AV septal defects

41
Q

Which VSDs do not spontaneously close?

A

Inlet and Outlet VSDs

42
Q

Membranous VSD

A
Most frequent VSD (75-80%)
Defect inferior to AV
Borders the septal leaflet of the TV
Aneurysm of ventricular septum
Partial or complete closure up to age 20
Extends to inlet or trabecular septum
43
Q

Muscular VSD

A
5-10% of all VSDs
Trabecular portion of septum (from inlet septum to apex)
High rate of spontaneous closure
Difficult to visualise and repair
May be single or multiple 'Swiss cheese'
44
Q

When would you perform cardiac catheterisation in a patient with VSD?

A

1) To assess shunt severity
2) Degree of RVOT obstruction
3) Reversibility of PHTN

45
Q

What is a restrictive VSD?

A

Small defect that allows little or no blood flow from left to right side of the heart