VENTRICULAR SEPTAL DEFECT by Dr Amarnath BR BMC
VENTRICULAR SEPTAL DEFECT by Dr. Amarnath BR BMC
CONGENITAL HEART DISEASE (con-together, genitus-born) The majority of congenital anomalies of the heart are present 6 wks after conception & most anomalies compatible with 6 mths of intrauterine life permit live offspring at term.
TYPES OF CHD • Gr 1 Lt to Rt shunts • Gr 2 Rt to Lt shunts • Gr 3 Obsructive lesions
LEFT to RIGHT shunts (acyanotic heart disease) w Frequent chest infections (6 -8 attacks first year of life) w Tendency for increased sweating with related their tendency for developing CCF w Precordial bulge w Hyperkinetic precordium w Tricuspid /mitral DDM w X-ray plethoric +cardiomegaly w VSD, ASD, PDA, AVcanal
RIGHT to LEFT shunts (cyanotic heart disease) w increased pulm. blood flow * mildly cyanotic * increased sweating * CCF * FTT * plethoric lung fields * cardiomegaly *TGA, singlventricle, TA, total anomalous pulm. Return w/o obstruction w decreased pulm. blood flow * mod. to severe cyanosis * ESM, delayed and diminished P 2 (PS) * in PH , accentuated & palpable P 2, ESM * oligemic lung fields * TOF, PA, TA, total anomalous pulm. return w/ obstruction
Obstructive lesions • absence of frequent chest infections • absense of cyanosis • absence of precordial bulge • • presence of forcible &heaving cardiac impulse • systolic thrill +ESM & delayed corresponding S 2 • ECG shows obstructive lesions • X-ray normal sized heart & pulm. Vasculature • pulm. stenosis(rt side) & aortic stenosis, coarctation of aorta(lt side)
NADA’S CRITERIA MAJOR • systolic murmur gr III or more • diastolic murmur • cyanosis • ccf one major &two minor are essential MINOR • systolic murmur less than gr III • abnormal S 2 • abnormal ECG • abnormal X-ray • abnormal BP
VENTRICULAR SEPTAL DEFECT • most common ACHD • 2 nd most common CHD(32%) • SYNONYMS * Roger’s disease * Interventricular septal defect * congenital cardiac anomaly
PATHOPHYSIOLOGY w primarily depends on size&status of pulm. vascular bed rather than location w Small communication (less than 0. 5 cm`) VSD is restrictive & rt. ventricular pressure is normal – does not cause significant hemodynamic derangement(Qp: Qs=1. 75: 1. 0) w Moderately restrictive VSD with a moderate shunt(Qp: Qs=1. 52. 5: 1. 0) &poses hemodynamic burden on LV w Large nonrestrictive VSDs(more than 1. 0 cm`) Rt&Lt ventricular pressure are equalised(Qp: Qs is more than 2: 1) w Large VSDs at birth , PVR may remain higher than normal and Lt to Rt shunt may intially limited – involution of media of small pulm. arterioles, PVR decreases—large Lt to Rt shunt ensues w In some infants large VSDs , pulm. arteriolar thickness never decreases –pulm. obstructive disease develops. when Qp: Qs=1: 1 shunt becomes bidirectional, signs of heart failure abate &pt. becomes cyanotic. (Eisenmenger syndrome)
ANATOMICAL CLASSIFICATION type. I-MEMBRANOUS SEPTUM paramembranous/perimembranous defect (or infracristal, subaortic, conoventricular) type. II-MUSCULAR SEPTUM inlet, trabecular, central, apical, marginal or swiss-cheese type. III-OUTLET SEPTUM deficient supracristal, subpulmonary, infundibular or conoseptal SEPTAL DEFICIFNCY –AVseptal defect (AVcanal)
CLINICAL FEATURES w Race : no particular racial predilection w Sex : no particular sex preference w Age : infants– infants difficult in postnatal period, although ccf during first 6 mths is frequent, X-ray&ECG are normal. children—after first year variable clinical children picture emerges. small VSD – asymptomatic large VSD – common symptoms -palpitation, dyspnoea on exertion, feeding difficulties , poor growth -frequent chest infections
PHYSICAL FINDINGS • Pulse pressure is relatively wide • Precordium is hyperkinetic with a systolic thrill at LSB • S 1&S 2 are masked by a PSM at Lt. sternal border , max. intensity of the murmur is best heard at 3 rd, 4 th&5 th Lt interspace. Also well heard at the 2 nd space but not conducted beyond apex • Lt. 2 nd space –widely split &variable accentuated P 2 • Delayed diastolic murmur at the apex &S 3 • Presence of mid-diastolic , low pitched rumble at the apex is caused by increased flow across the mitral valve &indicates Qp: Qs=2: 1/greater • Maladie de Roger –small VSD presenting in older children as a loud PSM w/o other significant hemodynamic changes
INVESTIGATIONS w ECHOCARDIOGRAPHY two-dimensional &doppler colour flow • CHEST RADIOGRAPHY - normal - biventricular hypertrophy - pulmonary plethora • ELECTROCARDIOGRAPHY -small. VSD ~ normal tracing -mod. VSD ~ broad, notched P wave characteristic of Lt. Atrial overload as well as LV overload, namely, deep Q waves & tall R waves in leads V 5 and V 6 and often AF -large VSD ~RVH with rt. axis deviation. With further progression biventricular hypertrophy; P waves may be notched/peaked.
Other investigations w CAT SCAN (Computed Axial Tomography) • MRI • ULTRASOUND • ANGIOGRAPHY (cardiac catheterization and angiography)
COMPLICATIONS w w w Congestive cardiac failure Infective endocarditis on rt. ventricular side Aortic insufficiency Complete heart block Delayed growth & development (FTT) in infancy Damage to electrical conduction system during surgery(causing arrythmias) w Pulmonary hypertension
INTERVENTION w 3 MAJOR TYPES w SMALL (less than 3 mm diameter) - hemodynamically insignificant - b/w 80 -85% of all VSDs - all close spontaneously * 50% by 2 yrs * 90% by 6 yrs * 10% during school yrs - muscular close sooner than membranous
w MODERATE VSDs * 3 -5 mm diameter * least common group of children(3 -5%) * w/o evidence of ccf/ pulm. htn can be followed until spontaneous closure occurs. • LARGE VSDs WITH NORMAL PVR * 6 -10 mm in diameter * usually requires surgery otherwise… develop CCF & FTT by age of 3 -6 mths. Conservative treatment - treat CCF & prevent development of pulm. vascular disease - prevention & treatment of infective endocarditis
INDICATIONS for SURGERY w VSDs at any age where clinical symptoms and FTT cannot be controlled medically. w Infants b/w 6 -12 mths of age with large defects ass. with PH , even if symptoms are controlled by medication. w Pt. s older than 24 mths of age with Qp: Qs is greater than 2: 1. w Pt. s with supracristal VSD of any size, because of high risk of development of AI. CONTRAINDICATION –severe pulmonary vascular disease.
Surgical correction has to be done before irreversible damage to pulmonary vasculature occurs.
Operative procedure w Usually performed in second year. If symptoms are not disabling , procedure may be deffered to 46 yrs. w Through a median sternotomy with the help of extracorporeal circulation, a longitudinal ventriculotomy is performed usually in the infundibular part of the rt. ventricle & near the ant. descending coronary artery. w Alternate approach is through the rt. atrium, particularly when PVR is increased. w Defect is usually closed with an oval patch of knitted dacron by mattress suture posteriorly and continous suture anteriorly using prolene.
Much more to come Are we all still awake?
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