Ventricular Septal Defect

Seoul National University Hospital

Department of Thoracic & Cardiovascular Surgery

Primary Ventricular Septal Defect

1. Definition
A hole or multiple holes in the interventricular septum.
A VSD may be part of another major cardiovascular
anomaly and may be acquired, and primary VSD may have
minor coexisting morphologic abnormalities

2. History
Roger
Eisenmenger
Lillehei, Varco

: 1st description in 1879

: Autopsy finding in 1897
: Repair using controlled cross
circulation in 1954
DuShane et al in Mayo Clinic
: Intracardiac repair
with pump oxygenator in 1955~1956
Lillehei
: Atrial approach to VSD in 1957

Ventricular Septal Defect

1. Embryology
VSD occurs at 1st. 8 weeks of fetal life through interaction
between interventricular muscular partition, endocardial
cushions, and bulbar ridges that separate great vessels.

2. Etiology
Chromosomal
Familial
Geographic
Environmental

Ventricular Septal Defect

Pathophysiology
Defect in the interventricular septum permits
left-to-right shunting of blood
RV volume overload & pulmonary overcirculation
can produce congestive heart failure in infancy &
irreversible pulmonary hypertension later in life
Shunt reversal (right-to-left) due to elevated
pulmonary vascular resistances leads to systemic
hypoxemia (Eisenmenger syndrome)

Morphology of VSD
1. Size
1) Large
: approximately the size of aortic orifice
2) Moderate : still restrictive, but sufficient size to raise
RV pressure to of LV and Qp/Os>2.0
3) Small
: insufficient size to raise RV pressure &
Qp/Qs < 1.75

2. Location
1) Perimembranous VSD :
80%
2) VSD in RV outlet
: 5-10%
3) Inlet septal VSD
:
5%
4) Muscular VSD
:
5%
5) Confluent VSD
6) VSD with straddling or overriding TV

Morphologic Classification of VSD

Classification
Perimembranous
(junctional)

Extension

Inlet
Anterior
Outlet
Muscular
Outlet (conal)
Trabecular
Inlet
Anterior
Apical
Doubly committed subarterial (RV outlet)
Inlet septal
Atrioventricular septal type
Malalignment
Anterior (TOF)
Posterior (COA, IAA)
Rotational (Taussig-Bing)

Morphologic Types of VSD

VSD MO type

VSD MO type

VSD PMOE type

VSD PMIE type

VSD PMIE Type

Associated Lesions with VSD

1. PDA
6% of all ages, 25% of infants in heart failure
2. COA ; 5%
3. Congenital aortic stenosis
2% requiring operation for VSD (sub AS> valv AS)
4. Infundibular pulmonary stenosis
5. Congenital mitral valve disease ; 2%
6. Absent pulmonary arteries, peripheral PS
7. Positional anomalies

Pulmonary Vascular Disease

Grade

I : Medial hypertrophy without intimal proliferation.

II : Medial hypertrophy with cellular intimal reaction.
III : Intimal fibrosis, as well as medial hypertrophy,
early vascular dilation.
IV : Generalized vascular dilation, areas of vascular
occlusion by intimal fibrosis & plexiform lesion.
V : Other dilation lesion such as cavernous and
angiomatoid lesions.
VI : Necrotizig arteritis in addition to grade V changes

Clinical Features & Diagnosis

1. Prevalence
2 per 1,000 live births
20% of CHD
Associated & isolated VSD : 50% of CHD
Higher incidence in premature

2. Clinical features
Symptoms and signs of heart failure
Cardiomegaly & large pulmonary blood flow
Pansystolic or systolic murmur
Biventricular or left ventricular hypertrophy

3. Two-dimensional echocardiography
4. Cardiac catheterization & angiocardiography

Natural History of VSD

1.
2.
3.
4.
5.
6.
7.

Spontaneous closure
Pulmonary vascular disease
Bacterial endocarditis ; rarely recently
Premature death
Clinical course
Development of aortic incompetence
Development of infundibular PS

Spontaneous Closure of VSD

1. Mechanism of narrowing or closure
1) Adherence of TV leaflet or chordae tissue
2) Aneurysm of membranous septum erroneously related
-- rare in conoventricular, juxtaarterial, AV canal,
muscular defect

2. Rate
About 80% of VSD at 1 month eventually narrow or close
About 60% of VSD at 3 months eventually narrow or close
About 50% of VSD at 6 months eventually narrow or close
About 25% of VSD at 12 months eventually narrow or close
Becomes rare after 12 ~ 18 months of age

VSD Spontaneous Closure

Probability

Pulmonary Vascular Resistance

Resistance

Description

< unit/BSA <

<4

4 ~
5 ~
8>

5
8

Normal
Mild elevated
Moderately elevated
Severely elevated

PA Banding in VSD of PVD ?

This increases right-left shunt, the saturation in the aorta
will fall, and so does the venous blood returning to the RA
(maximally desaturated).
For the lungs, shock means low oxygen and pressure in
the PA and shock is the most potent vasodilator in the
body, mainly in the PA.
To reverse completely lung lesions "extracting oxygen
from the PA .
Once you extract it, the lung lesions reverse completely
What causes hyperresistant PA hypertension is the
quantity of oxygen in the PA. If the PA would have had
hyperflow with low oxygen, it would not have developed
hyperresistant pulmonary hypertension

Indications for Operation

1. Severe and intractable heart failure or respiratory
symptoms during the 1st 3months of life.
2. Severe symptoms, growth failure, rising PVR
older than 3 months of age.
3. VSD with PVR more than 4 unit during 6-12 months.
4. VSD with elevated PVR first seen after infancy.
5. Moderate VSD with no size change in childhood.
6. Juxtaarterial , juxtaaortic VSD is a special situation.

Techniques of Operation
1. Route
1) Right atrium
2) Right ventricle, or left ventricle
3) Pulmonary artery

2. Repair of VSD
1) Conoventricular VSD
2) Juxtaarterial VSD
3) Inlet VSD
4) Muscular VSD

3. Closure of associated PDA

4. Pulmonary artery banding & debanding

VSD. Surgical Anatomy

VSD Operation

VSD AV
Canal type

VSD - PM Operative View

VSD PM Patch Closure (1)

VSD PM Patch Closure (2)

VSD. PMIE Patch Closure (1)

VSD. PMIE Patch Closure (2)

VSD. PMOE Patch Closure

VSD closure through anterior leaflet of TV detachment

RV Anatomy for Apical VSD

Apical Muscular VSD

Patch Closure via RVtomy

Apical Muscular VSD

Patch Closure via RVtomy

(A) Trabeculations overlying the VSD are taken down. (B) Interrupted
pledgetted sutures are placed full thickness at the superior margin of the
defect, maintaining the pledgets on the left ventricular side (C) Closure of
the VSD with a Dacron patch

Flap Valve Double Patch Closure

Flap valve double patch closure of Ventricular Septal Defects

in children with Increased Pulmonary Vascular Resistance

Closure of Trabecular VSD

Sandwich Technique

Sutures & patch can be passed through

the other VSD or mitral valve

Results of Operation for VSD

1. Hospital mortality

5. Physical development

2. Modes of early death

3. Incremental risk factors
for hospital death
1) Early date of op.
2) Multiple VSD
3) Associated anomalies
4. Survival
Pulmonary vascular D.

6. Conduction disturbance
7. Cardiac function
8. Residual shunting
9. Pulmonary hyperinflation
10. Iatrogenic aortic or
tricuspid incompetence
11. Pulmonary hypertension

Special Situation & Controversies

1.
2.
3.
4.
5.
6.

VSD and patent ductus arteriosus

VSD and coarctation of aorta
Pulmonary artery banding
Approach for conoventricular VSD
Percutaneous closure of VSD
Closure of VSD when PVR is high