1. Ventricular septal defects (VSDs) are the most common congenital heart defect, accounting for up to 40% of cases. They can be classified based on their location as perimembranous, muscular, inlet, or outlet.
2. The natural history and clinical presentation depends on the size of the defect. Small restrictive VSDs may close spontaneously, while larger defects can lead to pulmonary hypertension.
3. Intervention is recommended for symptomatic patients or those with evidence of pulmonary hypertension, left heart volume overload, or aortic regurgitation in the case of an outlet VSD.
Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle.
Some babies with tricuspid atresia have other conditions, such as pulmonary stenosis or transposition of the great arteries, that also affect blood flow through their heart. These conditions require treatment, too.
Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle.
Some babies with tricuspid atresia have other conditions, such as pulmonary stenosis or transposition of the great arteries, that also affect blood flow through their heart. These conditions require treatment, too.
ACYANOTIC DISEASE- Non cyanotic heart diseasesNelsonNgulube
ETIOLOGY AND EPIDEMIOLOGY
Congenital heart disease occurs in 8 per 1,000 births. The spectrum of lesions ranges from asymptomatic to fatal. Although most cases of congenital heart disease are multifactorial, some lesions are associated with chromosomal disorders, single gene defects, teratogens, or maternal metabolic disease (see Table139-2).
Congenital heart defects can be divided into three pathophysiological groups (Table 143.1).
1. Left-to-right shunts
2. Right-to-left shunts
3. Obstructive, stenotic lesions
Acyanotic congenital heart disease includes left-to-right shunts resulting in an increase in pulmonary blood flow (patent ductus arteriosus [PDA], ventricular septal defect [VSD], atrial septal defect [ASD]) and obstructive lesions (aortic stenosis, pulmonary stenosis, coarctation of the aorta), which usually have normal pulmonary blood flow.
VENTRICULAR SEPTAL DEFECTEtiology and Epidemiology
The ventricular septum is a complex structure that can be divided
into four components. The largest component is the muscular
septum. The inlet or posterior septum comprises endocardial
cushion tissue. The subarterial or supracristal septum com
prises conotruncal tissue. The membranous septum is below
the aortic valve and is relatively small. VSDs occur when any of these components fail to develop normally (Fig. 143.1). VSD,
the most common congenital heart defect, accounts for 25% of all congenital heart disease. Perimembranous VSD
The lecture is for medical student. It is from Dr RUSINGIZA Emmanuel, MD, senior lecture at UR( UNIVERSITY OF RWANDA) .
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2. A: STRAIGHT HEART TUBE
B:BULGING
C: C- LOOP
a
b c d e
RV
LV
O
RV
LV
A
O
RV LV
A
O
RV LV
A
3. WHICH ONE IS INCORRECT
1. Prevalence of VSD s is not race dependent
2. A restrictive VSD may close spontaneously during adult life
3. Late development of subaortic stenosis are well described
4. A moderately restrictive VSD leads to left atrial and ventricular dilation and dysfunction as well
as a variable increase in pulmonary vascular resistance
4. PREVALENCE, ETIOLOGY
Most common congenital heart defect. accounting for up to 40 % of cardiac anomalies .
Chromosomal disorders associated with an increased incidence of VSD , (Down syndrome),
(Di George syndrome), (Turner syndrome).
Familial forms , TBX5, GATA4, and NKX2.5 mutations .
Children from an adult with a VSD that is not associated with a genetic disorder may have a
risk of VSD as high as 3 % if the father is affected and a 6 % risk if the mother is affected
5.
6. TYPES OF VENTRICULAR SEPTAL DEFECTS
TYPE 1 :( 1 ) subarterial valve; defect: in the left
ventricular outflow tract just below the aortic valve
(conal,subpul, infundibular, supracristal, doubly
commited) ( 4 ) outlet
TYPE 2 :( 2 ) perimembranous defect, membranous
septum ( yellow , white , and blue dashed
circumference for outlet, trabecular and inlet subtype,
)
TYPE3 :( 3 ) inlet or atrioventricular defect, which lies
inferior to the septal leaflet of the tricuspid valve; and (
5 ) inlet and apical
TYPE 4 : ( 6 ) muscular defects, which are entirely
bounded by the muscular septum and are often
multiple
6
5
2
1
3
4
7. TYPE 1
Conal,subpul, infundibular, supracristal, doubly commited ( 4 ) outlet
Aortic regurgitation (87% IN 20Y)
Prolapse of the anterior aortic valve leaflet. ( LCC,RCC
6 % of defects 30% in Asian
Spontaneous closure of this type of defect is uncommon
Doubly committed subarterial :
More common in Asian patients,
In the outlet septum,
Bordered by fibrous continuity of the aortic and pulmonary valves.
8. TYPE 2
Synonyms: perimembranous, paramembranous,conoventricular
SUBTYPES : Inlet, trabecular, outlet, and confluent. (multiple areas of the septum)
Most common VSD, (80 % of defects)
Bordered by fibrous continuity between the leaflets of an AV valve and
an arterial valve.
AI (Prolapse of,RCC,NCC)
9. TYPE 3
Synonyms: inlet, AV canal type, endocardial cushion
May be associated with AV canal defect.
Trisomy 21 syndrome.
5–8 % of VSDs .
10. TYPE 4(MUSCULAR)
Rim totally composed of septal muscle
Subclassified as inlet, trabecular outlet, or confluent .
20 % of VSDs in infants
Spontaneous closure is common,.
Frequently multiple.
“Swiss-cheese” septum
12. OTHER ANOMALIES
Ven septum psudoaneurysm
BAV
Sub AO stenosis
Caoarctation
Pulmonary Valve stenosis
DCRV
AV valve malformations
13. CASE 1
22 y/o male
DOE FCII
Harsh systolic murmur ,LSB
Load P2
Diastolic rumble on apex
14. PATHOPHYSIOLOGY
A restrictive VSD
1. Produces a significant pressure gradient between the left ventricle and the right ventricle
2. Pulmonary-to-aortic systolic pressure ratio < 0.3
3. Small (≤1.4 : 1) shunt.
4. Less than 5mm, or defect size <=25% of annulus diameter
5. Normal PA and branches
6. Normal LV, LA size
15. PATHOPHYSIOLOGY
A moderately restrictive VSD
1. Qp/Qs of 1.4 to 2.2 :
2. pulmonary-to-aortic systolic pressure ratio less than 0.66.
3. Diameter of defect >25% <75% of annulus size or 5-10 mm
4. RVP,PAP normal or near normal
5. Mild to moderate PA,LA,LV dilation
16. PATHOPHYSIOLOGY
A large or non-restrictive VSD
1. Qp/Qs > 2.2
2. pulmonary-to-aortic systolic pressure ratio greater than 0.66.
3. Defect diameter >75% of aortic diameter
4. PH in less than 2years
18. NATURAL HISTORY
1. A restrictive VSD may close spontaneously during childhood and sometimes in adult life.
2. A perimembranous defect ,doubly committed VSD,
1. Progressive AR.
2. Subaortic and subpulmonary stenosis
3. Left ventricular to right atrial shunt
3. A moderately restrictive VSD
1. Left atrial and ventricular dilation and dysfunction
2. Variable increase in pulmonary vascular resistance.
4. A large or nonrestrictive VSD
1. Ventricular volume overload early in life
2. Progressive rise in pulmonary artery pressure
3. A fall in left-to-right shunting.
19. WHICH ONE IS INCORRECT?
1. Infants with large nonrestrictive defects tend to present later than restrictive ones
2. Diastolic murmur of MV in neonates with large VSD may occur without any other anatomical
disorder
3. Cyanosis is rare in early childhood,
4. Medical management of the symptomatic infant is directed at improving symptoms before
surgery
5. Most adult patients with a small restrictive VSD are asymptomatic
20. CLINICAL FEATURE IN NEONATE
Restrictive defect, the murmur becomes apparent only as the pulmonary vascular resistance
falls.
Large nonrestrictive defects tend to present later. breathlessness, congestive heart failure, and
failure to thrive in the second and third months a pulmonary ejection murmur and a mitral
rumble
Cyanosis is rare in early childhood, and if it is present, other causes of a raised pulmonary
vascular resistance should be excluded (e.g., mitral stenosis or coexisting lung disease).
Medical management of the symptomatic infant : diuretics , ACE inhibition
22. CLINICAL FEATURE IN ADULT
Small restrictive VSD :
Asymptomatic.
Harsh or high-frequency pansystolic murmur, usually grade 3 to 4/6, maximal intensity at the left sternal border
in the third or fourth intercostal space.
Moderately restrictive VSD
Dyspnea in adult life, perhaps triggered by atrial fibrillation
Displaced cardiac apex with a similar pansystolic murmur as well
An apical diastolic rumble
Third heart sound at the apex from the increased flow through the mitral valve.
Large nonrestrictive Eisenmenger VSDs
Central cyanosis and clubbing of the nailbeds
Right ventricular heave, a palpable and loud P2, and a right-sided S4. A
Pulmonary ejection click, a soft and scratchy systolic ejection murmur,
High-pitched decrescendo diastolic murmur of pulmonary regurgitation (Graham Steell).
Peripheral edema usually reflects right-sided heart failure.
24. ECG
Mirrors the size of the shunt and the degree of pulmonary hypertension.
Small, restrictive VSDs: normal tracing.
Moderate-sized VSDs :left atrial overload ,left ventricular volume overload, deep Q and tall R
waves with tall T waves in leads V5 and V6 and perhaps eventually atrial fibrillation.
After repair, : usually normal with right bundle branch block.
55. INDICATIONS FOR INTERVENTION
1. The presence of a significantVSD
1. The symptomatic patient shows a Qp/Qs > 1.5 : 1,
2. Pulmonary artery systolic pressure > 50 mm Hg,
3. Increased left ventricular and left atrial size, or deteriorating left ventricular function
in the absence of irreversible pulmonary hypertension.
2. Presence of a perimembranous or outlet VSD with more than mild aortic regurgitation
3. History of recurrent endocarditis.
4. In children, a nonrestrictive VSD and a smaller VSD with significant symptoms failing to respond
to medication.
56. Elective surgery is usually performed between 3 and 9 months of age.
PVR< 7 Wood units, closure :safely undertaken if there is a net left-to-right shunt of at least 1.5 :
1 or
strong evidence of pulmonary reactivity on challenge with a pulmonary vasodilator (oxygen,
nitric oxide).
57. REPRODUCTIVE ISSUES
• well tolerated :small or moderate VSDs and in women with repaired
VSDs.
• Pregnancy is contraindicated in Eisenmenger syndrome ,high
maternal (!50%) and fetal (!60%) mortality.
58. FOLLOW-UP
• Good to excellent functional class and good left ventricular function before surgical closure,
life expectancy after surgical correction is close to normal.
• The risk of progressive aortic regurgitation is reduced after surgery,
as is the risk of endocarditis, unless a residual VSD persists.
• Yearly cardiac evaluation :
• with right ventricular outflow tract obstruction,
• left ventricular outflow tract obstruction,
• aortic regurgitation not undergoing surgical repair;
• patients with Eisenmenger syndrome
• adults with significant atrial or ventricular arrhythmias.
• late repair of moderate or large defects, which are often associated with left ventricular
impairment and elevated pulmonary artery pressure at the time of surgery.