Dr Swati Prashant MD Paediatrics Index Medical College, Indore,MP,India drprahantw@gmail.com. www.paediatrics4all.com The most common L →R Shunts are : 1. VSD : 27% 2. ASD : 13 % 3. PDA : 11 % . It constitutes 13 % of all CHD . There is an abnormal communication between the 2 Atrias . ASD’ s are of 3 types . 1 Ostium Secundum defect : 70% .Defect is at the fossa Ovalis or rarely superior or Posterior to fossa . 2. Ostium Primum defect : 30% . Defect is Defect is an Endocardial Cushion defect lying Inferior to fossa . It may be associated with Mitral Valve defect . 3. Sinus Venosus defect : 10% ,associated with defect at entry of SVC in Rt. Atrium . Haemodynamics 1. Oxygenated blood from Lt Atrium ↓ Right Atrium It receives extra blood , causing Right Atrial enlargement ↓ Large volume of Blood passes through Normal Tricuspid Valve Causing Delayed Diastolic Murmur ( DDM ). ↓ large Volume is received by RV Rt. Ventricle enlarges ( cardiac impulse ↓ Large vol . Thru. Pulmonary Artery causes Ejection Systolic Murmur & delayed closure of P2 , Therefore A2 -P2 WIDE split & loud p2 . As age advances PH OCCURS . Mild effort intolerance Chest infections CCF Rare . Parasternal Impulse A2—P2 Wide split fixed Systolic Thrill & Murmur in P2 area due to flow thru. Pulmonary valve . . Complications are rare After age 20 yrs. PH occurs . ECG---RVH & RBB X-Ray---mild cardiomegaly , RAH ,RVH ,PA prominent , plethora. TREATMENT : 1. T/t of Infections , ccf 2. Surgery Common syndromes asso. With ASD : Down’s Syndrome , Holt Oram syndrome , Lutembachker , Noonans syndrome . It is most common amongst the CHD . Constitutes 27% of all CHD’s . Location : 90% of VSD are in Membranous part of the Septum Others occur in Muscular part & can be multiple . Syndromes: Trisomy 13 - 15 , 17-18. Absent Radius & Ulna , poly & Syndactyly . HAEMODYNAMICS Left → Right shunt . Lt. Ventricle blood →enters Rt. Ventricle through the defect . At the same time Rt. Ventricle is also contracting. So the blood is almost directly going to Pulmonary Artery . Large vol. Thru. PA → CAUSE Ejection Sys. Murmur + delayed P2 , due to delayed empting .Also there is early empting of LV causing early A2 . Therefore there is a wide split A2 P2 . ↑ blood in LA causes LA ENLARGEMENT. ↑ blood flow thru. Mitral valve causes DDM at apex . Shunt itself causes PANSYSTOLIC Murmur as blood is going thru. The shunt in systole ----in Tricuspid area -lt. Sternal border 3,4,5 space . Symptomatic around 6 –10 wks. CCF develops . Palpitation , dyspnea on exertion . Frequent chest infections . Wide pulse pressure . Hyperkinetic precordium with systolic Thrill . Cardiomegaly with Left ventricular Apex . Wide split 2 nd HEART SOUND P2 accentuated Pansystolic Murmur at Lt. Sternal border ( 3 ,4 ,5th IC SPACE . ECG : 1) RVH initially & in newborn . 2) IN small & mod . Size VSD ,RVH comes to normal after ↓ of pulmonary resistance . 3) In large VSD without PAH there is LVH 4) In large VSD + PS /PAH : ECG shows RVH + LVH or purely RVH . X-RAY CHEST 1. LVH—Depends on size of shunt . 2. Plethora 3. Aorta N or small in size . 4. LAH in large shunts . 5. If VSD is small : Heart size normal, pulmonary vasculature is normal . 6. If VSD + PS : Heart size is normal , normal lung fields . 7. If VSD + PAH : Heart size is normal ,but lung fields are Plethoric . Small VSD : PSM + normal P2 , disappearance of murmur + ECG becomes Normal . Large VSD : RV pressure = LV pressure , therefore murmur becomes softer + PAH + accentuated P2 Large VSD + PS : ejection systolic murmur +↑ RV pressure + normal PA pressure + P2 soft Medical : T/t --CCF , Infections , Anemia , Endocarditis . Surgery : Indications 1. CCF in infancy not responding to medical t/t . 2. L→ R shunt is large 3. VSD ( large) + PS / PH or AR . 4. Surgery : contraindicated in PAH + reversal of shunt . Surgery : Closure of VSD WITH A Dacron patch , through Rt. Atrial approach . Surgery is advised if PAH develops , within 2 yrs. Complications of Surgery : Complete Heart Block , residual VSD . It is a communication between the Pulmonary Artery & the Aorta . Aortic attachment is just distal to the Left Subclavian Artery . Ductus arteriosus is normally present in fetal life . It closes normally after birth . It constitutes 11% of all cardiac defects . L→R shunt from Aorta to Pulmonary Artery . Flow is both during systole as well as Diastole , as pressure is always higher in Aorta with normal Pulm . Artery . This L →R shunt causes murmur . Murmur starts in systole after 1st HS & Continues in Diastole but with diminished intensity , therefore Continuous murmur. LA receives large amt. of blood ,therefore LA enlarges In size . ↑ blood flow through Mitral valve -> causes accentuated 1st HS + DDM . LV also receives more blood → overloading → prolongation of lt. Ventricular systole & ↑ in LV size . Prolonged systole → cause delayed closure of Aortic valve ---late A2 . Late A2 causes paradoxical split in large shunts . Large vol. Coming to Aorta causes Aortic dilatation ( ascending ) , this causes Ejection click & Ejection systolic murmur , but this is masked by continuous murmur . Patient becomes symptomatic early in life . Develops CCF around 6-10 wks of life , or even earlier within 7 days of birth with murmur + ccf . In older children there is effort intolerance , palpitation , chest infections . As there IS a leak of blood to PDA from systemic blood there is a wide pulse pressure + collapsing pulse . Prominent CAROTID pulsations + features L → R shunt is s/o PDA . Cardiac impulse & Apex Beat are Hyperkinetic s/o LVH due to ↑ blood Volume . Continuous / systolic murmur + Thrill at Lt. 2nd space . SO IF SHUNT IS LARGE : 1. 1 st HS is accentuated due to ↑ Mitral flow . 2. 2 nd HS is narrow /paradoxically split 3. P2 is louder than normal . Continuous murmur best heard in P2 AREA ECG : LVH--- ‘ Q’ & tall ‘T’ waves are characteristic of Lt . Ventricular vol. Overload . X-Ray chest : cardiomegaly with LV enlargement .( large shunt -- large size, large shunt --narrow split , small shunt --- no split .) LA enlarged , Ascending Aorta ( knuckle) prominent . In Newborn & infants ---PH is +nt at birth causing Ejection syst. Murmur . Later as PH ↓ the murmur becomes continuous . CCF same as in VSD . In PDA ,PH later due to flow develops earlier than VSD . As PH develops later diastolic component ↓ ,so the murmur becomes Ejection syst. Murmur . If PH --P2 is loud + DDM +nt If PS --P2 is soft or N + no DDM If L→ R becomes R→L there is no murmur , but DIFFERENTIAL CYANOSIS is present In PDA + PH causing reversal . For closure of PDA 1. Indomethacin ( prostaglandin synthetase inhibitor ) given orally Dose is 0.1 mg /kg / day 12 hourly in 3 doses. Hepatic / Renal / Bleeding tendency----CI 2. Surgical ligation PDA . 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