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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