2) VSD & PDA - Dr. Aso

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1 2) VSD & PDA - Dr. Aso Ventricular Septal Defect (VSD) Most common cardiac malformation % Types of VSD: According to position perimembranous, inlet, muscular. According to size small, medium, large. Membranous: Most common, are usually single,( called peri membranous ) May extend into adjacent muscle Muscular: Inlet: Mid portion of septum to the apex. Single or multiple (Swiss cheese septum ) At level of both Av valves Size of defect: Small (restrictive): Trivial L R shunt. (LV pressure > RV ) Normal pulmonary arterial &RV pressure. Normal cardiac chambers. Large (nonrestrictive): aortic annulus RV, LV pressure equalizes. Direction & magnitude of shunt determined by ratio of pulmonary to systemic vascular resistance. RV, pulmonary arterial hypertension. Main pulmonary artery, LA, LV are enlarged Medium will be in between Pathophysiology 1

2 Clinical features: Varies according to: size of defect, pulmonary blood flow & pressure. Most often asymptomatic. Loud, harsh, blowing, holosystolic murmur heard best over LLSB frequently accompanied by thrill. Large VSD: Dyspnea, feeding difficulties, poor growth, profuse perspiration, recurrent chest infection & cardiac failure in early infancy. Cyanosis usually absent, duskiness noted during crying or infection. Physical signs: Prominent L precordium, palpable para sternal lift. Lateral displacement of apex beet, apical thrust. Holosystolic murmur (less harsh, more blowing). Pulmonary component of S2 may be increased pulmonary hypertension Investigations: CXR: ECG: normal or minimal cardiomegaly. Borderline increase in pul. Vasculature. Large VSD: gross cardiomegaly (RV, LV, LA, PA). Prominent pulmonary vascularity. normal or may suggest LV hypertrophy Large VSD: biventricular hypertrophy. P- wave notched or peaked. Echocardiography Cardiac catheterization Treatment: Reassurance & encourage to live normal life with no restriction of activities. Protection against infective endocarditis. Regular follow up Large VSD: Aim of treatment: o Control the symptoms of H.F. o Prevent the development of pulmonary vascular disease. Surgical closure of defect: Indications: o Patient at any age with large defect in whom clinical symptoms, FTT can t be controlled medically. o Supracristal VSD. o VSD complicated with AR or subvalvular PS Complication of surgery: o Residual defect. o Heart block. 2

3 Prognosis & complications: Spontaneous closure: % most often during first 2 years of live (small muscular are > likely to close (up to 80 %) than membranous (up to 35 %). Most often asymptomatic. Moderate Large VSD: Early & successful therapy may become smaller & up to 8 % may close completely. Repeated episodes of chest infection. H.F & FTT. Pulmonary HT & evidence of pulmonary vascular disease. Eisen menger complex. Aortic valve regurgitation Acquired infundibular pulmonary stenos is. Patent Ductus Arteriosus (PDA) 6 8 % of CHD, F:M 2 : 1 Ass. With maternal rubella infection in early pregnancy. Common problem in premature infants. Ductus Arteriosus: Fetal life, patency of Ductus is maintained by : Relaxant effect of low O2 tension. Prostaglandines (E2). In full term neonates, once PO2 passing through Ductus reaches 50 mmhg Ductal wall constricts. Functional closure of Ductus hrs. in normal neonate, anatomical occlusion 4 m of age Ligamentum arteriosum Pathophysiology 3

4 Types &clinical manifestations: Small PDA: Usually asymptomatic. Normal cardiac size. Pressure within PA, RA & RV are normal. Large PDA: PA pressure may be elevated to a systemic pressure. Risk of pulmonary vascular disease. Often symptomatic (HF & growth retardation). Bounding peripheral pulsations. Wide pulse pressure. Moderate gross cardiomegaly. Heaving apical impulse. Thrill (systolic) max. in 2 nd L ICS +/_ radiation. Machinery continuous murmur max. in 2 nd L ICS. Investigations: CXR: Small PDA: normal. Large PDA: moderate gross cardiomegaly (LV, LA). Prominent intra pul. Vascular marking. Normal or prominent aortic knob. ECG: Small normal, large LV or biventricular hypertrophy. Echocardiography Cardiac Catheterization Prognosis & complications Small PDA: May live a normal span with a few or no symptoms. Spontaneous closure after infancy is extremely rare. Large PDA: HF in early infancy, FTT. Pulmonary or systemic emboli. Treatment: Surgery: Ligation & division of Ductus, preferably before 1 st year of live. Trans-catheter closure of defect. 4

5 Summary Acynotic CHD Classification Left to right shunts Obstructive lesions Regurgitant lesions Frequent resp. infections Forcible heaving precordium Generally uncommon & Precordial buldge Hyperkinetic precordium Tendency for sweating & CCF Shunt & flow murmurs Plethoric lung fields on CXR E.g. ASD, VSD, PDA, AP Window Systolic thrill No cardiomegaly Delayed corresponding component second heart sound Ejection systolic murmur Ventricular hypertrophy on ECG E.g. PS, AS, COA asymptomatic E.g. MR, AR, TR, PR Acynotic CHD: L R shunts Atrial Septal Defect Ventricular Septal Defect Patent Ductus Arteriosus Left parasternal impulse Left ventricular type apial Wide pulse pressure Wide, fixed split S2 Pulmonary ejection systolic impulse Systolic thrill LV type impulse Systolic or continuous thrill murmur Pansystolic murmur Continuous murmur Tricuspid diastolic flow murmur rsr in V1 in ECG Mitral diastolic flow murmur LV dominance in ECG Mitral diastolic flow murmur 5