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VENTRICULAR SEPTAL DEFECT
(VSD)
It is a hole on interventricular septum
Congenital or acquired
VENTRİKÜLER SEPTAL DEFEKT (VSD)
Congenital
• Isolated VSD can be seen in
nearly 2 per 1000 live
births.
• It is the most frequent
congenital cardiac anomaly.
• can be associated with
other anomalies.
Acquired
• It is mostly seen as a
complication of acute
myocardial infaction.
• Rarely trauma is a cause .
VSD
MORPHOLOGICAL CLASSIFICATION
Yerleşim
Perimembraneous
%80
Neighbourhood
• Tricuspid valve , conduction
system (posteroinferior)
Subarterial
%5-10
( Juxta- arterial, conal,
infundibular)
• Both semilunar valves (
Right coronary cusp)
Muscular
%5
• It is surrounded by muscle
Inlet septal
(AV kanal , AV septal)
<%5
• Conduction system
(posteriorinferior)
VSD
MORFOLOJİK SINIFLAMA
VSD
MORFOLOJİK SINIFLAMA
CLASS ACCORDING TO SIZE
• VSD büyüklükleri; aort
orifis çapına göre
değerlendirilebildiği gibi
• VSD rezistans indekslerine
(Rİ) göre de
değerlendirilebilir.
• VSD Rİ = LVP - RVP x m2
•
Qp-Qs
• LVP= Sol ventrikül basıncı;
• RVP= Sağ ventrikül
basıncı;
• Qp= Pulmoner kan akımı;
• Qs= Sistemik kan akımı;
• m2= Vücut alanı
VSD
Large VSD
• VSD diameter ≥ Aortic
diameter
Moderate VSD
• VSD diameter < Aort
diameter
• VSD Rİ < 20 Ü/m2
• Resistance to flow is small
• RVP = LVP
• Qp/Qs ratio depends on
degree of pulmonary vascular
resistance (PVR).
• RVP=1/2 LVP
• Qp/Qs≥2
VSD
Small VSD
• VSD has not enough space
to increase the right
ventricular sistolic pressure.
• VSD Rİ>20Ü/m²
• Qp/Qs<1.75
Symptoms and signs
• Patients with large VSD and increased Qp/Qs
• Weak peripheral pulses
• Tachypnea, subcostal drawings, profuse
sweating
• Hepatomegaly, high jugular venous pressure,
• Difficulty in feeding, growth retardation
•
Large VSD and light PVR
• There is a strong pansystolic (holosystolic)
murmur or thrill on the left parasternal region
over the 3th ,4th intercostal space (
subarterial VSD on 2nd, 3th ICS),
• Apical diastolic murmur because of increased
blood flow passing throughout th mitral valve.
• S2 is strong and splitted due to increased
pulmonary flow.
Large VSD and high PVR
• Left to right shunt decreases and becomes
bidirectional.
• Hyperactivity of the heart and cardiomegaly
decrease.
• Pansytolic murmur change in character, becomes
short and soft.
• Apical diastolic murmur is no more heard.
• S2 is forcefull.
• The patient becomes cyanotic If PVR>SVR.
(Eisenmenger sendrome)
CHEST X-RAY
Large VSD and light PVR
Large VSD and high PVR
Patients with Moderate size VSD
• Pansystolic murmur
• Light – moderate left and right ventricular
enlargement.
small VSD
• There is harsh pansystolic murmur due to
small VSD and shunt.
• EKG ve Chest X ray are normal.
Echocardiography:
• 2 Dimensional, colour Doppler ECHO
• Give us incredible information about the
situation and size of the VSD
• QP/QS can be calculated.
• Associated anomalies like Aortic coarctation
and PDA .
HEART CATHETERIZATION
• To measure Pulmonary artery pressure,
• Left to right shunt and PVR
• To define the place, number and size of the
VSD
• To show definitely the associatied anomalies.
SPONTANOUS CLOSURE
•
•
•
•
•
Large VSD ;
1 month %80
3 month %60
6 month %50
12 month %25 spontaneous closure chance.
SPONTANOUS CLOSURE
Less chance to close
• Perimembranous
• Juxta aortic
• Inlet septal
More chance to close
• Juxta-tricuspid
• Muscular (outlet)
COMPLICATIONS
• Pulmonary Vascular disease
• Large VSD can have serious pulmonary
resistance (Rp) in first 2 years of life
Pulmonary Vascular disease
(Heath Edwards Classification)
• Grade 1: Medial hyperthrophy.
• Grade 2: Medial hyperthrophy and intimal cellular
proliferation
• ---------------------------------------------------------------------• Grade 3: Medial hyperthrophy and intimal fibrosis
early generalized vascular dilatation
• Grade 4: Generalized vascular dilatation, vascular
oclusions due to intimal fibrosis, plexiform lesions.
• Grade 5: Cavernous ve angiomatoid lesions.
• Grade 6: Necrotizing arteritis.
Infective Endocarditis
•
•
•
•
It is seen 0.15-0.3% of patient per year
More often small and moderate VSDs
Right sided vegetations (Tricuspid kapak)
Lung infections
• Aortic insufficiency
• In the first decade 35-80 % .
• Especially subarterial VSD
Early Death
• 9 % of the patient with large VSD die within the
1st year.
• PDA, Coarctation, large ASD
• Recurrent lung infections (Viral).
• Pulmonary edema (heart failure).
• After the first decade Eisenmenger complications
(Hemoptisis, polycytemia, cerebral emboli,
abscesses, right heart failure)
• 50% of patients die before 35 years of age.
Pulmonary Vascular Resistance
•
•
•
•
•
Resistance
< 4 ünite m2
< 5 ünite m2
< 8 ünite m2
> 8 ünite m2
Normal
mildly elevated
moderately elevated
severely elevated
INDICATIONS FOR OPERATION
• Large VSD
• Every patient with intractable heart failure under
medical treatment can be operated before 12 months.
• (Swiss cheese – Pulmonary banding)
• If there is growth failure or Rp >8ü m2 at 6 month, the
operation should be performed.( If Rp < 4ü m2 , the
operation can be deferred untill 12 month.)
• After infancy Rp is truely and precisely measured. If Rp
< 8ü m2 patient can be operated,
If Rp >8ü m2 ,
after isoproteronol perfusion remeasurement should
be made
If Rp ≤ 7ü m2 patient can be operated,
INDICATIONS FOR OPERATION
• Moderate VSD
• If Ppa 40-50 mmHg and Qp/Qs is about 3 Rp
is rarely elevates and we can wait for
operation untill 5 years of age.
• Small VSD
• İnfective endocarditis, ventrikül dysfunction is
rarely seen (After 10 years of age)
SURGICAL TREATMENT
• Pulmonary banding
• 1-Swiss cheese septum with intractable heart
failure
• Complications
• Hospital mortality is high
• Pulmonary stenosis, migration
PATCH CLOSURE
• Perikardial, Dacron and PTFE patches can be
used for closure.
• Interrupted suture (Teflon pledgeted single) or
continuous suture can be used.
• From the right atrium------ Perimembranous.
• From the right ventricle----- subarterial
• (Ventricular scar can cause RBBB, Arythmia
yüksek)
Rigth Atrium
Continuous suture
Right Ventriculotomy
Interrupted suture