1. VENTRICULAR SEPTAL DEFECT (VSD)
It is a hole on interventricular septum Congenital or acquired

2. VENTRİKÜLER SEPTAL DEFEKT (VSD)
Congenital
Acquired
Isolated VSD can be seen in nearly 2 per live births.
It is the most frequent congenital cardiac anomaly.
can be associated with other anomalies.
It is mostly seen as a complication of acute myocardial infaction.
Rarely trauma is a cause .

4. VSD MORPHOLOGICAL CLASSIFICATION
Yerleşim
Neighbourhood
Perimembraneous %80 Subarterial %5-10 ( Juxta- arterial, conal, infundibular) Muscular %5 Inlet septal <%5 (AV kanal , AV septal)
Tricuspid valve , conduction system (posteroinferior)
Both semilunar valves ( Right coronary cusp)
It is surrounded by muscle
Conduction system (posteriorinferior)

5. VSD MORFOLOJİK SINIFLAMA

7. VSD MORFOLOJİK SINIFLAMA

10. 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

11. VSD Large VSD Moderate VSD VSD diameter < Aort diameter RVP=1/2 LVP
VSD diameter ≥ Aortic diameter
VSD Rİ < 20 Ü/m2
Resistance to flow is small
RVP = LVP
Qp/Qs ratio depends on degree of pulmonary vascular resistance (PVR).
VSD diameter < Aort diameter
RVP=1/2 LVP
Qp/Qs≥2

12. VSD
Small VSD
VSD has not enough space to increase the right ventricular sistolic pressure.
VSD Rİ>20Ü/m²
Qp/Qs<1.75

13. Patients with large VSD and increased Qp/Qs Weak peripheral pulses
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

14. 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.

15. 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)

16. CHEST X-RAY
Large VSD and light PVR
Large VSD and high PVR

17. Patients with Moderate size VSD
Pansystolic murmur
Light – moderate left and right ventricular enlargement.

18. small VSD
There is harsh pansystolic murmur due to small VSD and shunt.
EKG ve Chest X ray are normal.

19. 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 .

20. 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.

21. SPONTANOUS CLOSURE
Large VSD ;
1 month %80
3 month %60
6 month %50
12 month %25 spontaneous closure chance.

22. SPONTANOUS CLOSURE Less chance to close More chance to close
Perimembranous
Juxta aortic
Inlet septal
Juxta-tricuspid
Muscular (outlet)

23. COMPLICATIONS Pulmonary Vascular disease
Large VSD can have serious pulmonary resistance (Rp) in first 2 years of life

24. 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.

25. Infective Endocarditis
It is seen % of patient per year
More often small and moderate VSDs
Right sided vegetations (Tricuspid kapak)
Lung infections
Aortic insufficiency
In the first decade % .
Especially subarterial VSD

26. 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.

27. Pulmonary Vascular Resistance
< 4 ünite m2 Normal
< 5 ünite m mildly elevated
< 8 ünite m moderately elevated
> 8 ünite m severely elevated

28. 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 m patient can be operated, If Rp >8ü m2 , after isoproteronol perfusion remeasurement should be made If Rp ≤ 7ü m2 patient can be operated,

29. INDICATIONS FOR OPERATION
Moderate VSD
If Ppa 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)

30. SURGICAL TREATMENT Pulmonary banding
1-Swiss cheese septum with intractable heart failure
Complications
Hospital mortality is high
Pulmonary stenosis, migration

31. 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)

32. Rigth Atrium

34. Continuous suture

35. Right Ventriculotomy

36. Interrupted suture