Transcript VENTRICULAR SEPTAL DEFECT
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 6wks after conception & most anomalies compatible with 6mths of intrauterine life permit live offspring at term.
TYPES OF CHD
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Gr 1 Lt to Rt shunts
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Gr 2 Rt to Lt shunts
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Gr 3 Obsructive lesions
LEFT to RIGHT shunts
(acyanotic heart disease)
Frequent chest infections (6-8 attacks first year of life) Tendency for increased sweating with related their tendency for developing CCF Precordial bulge Hyperkinetic precordium Tricuspid /mitral DDM X-ray plethoric +cardiomegaly VSD,ASD, PDA,AVcanal
RIGHT to LEFT shunts
(cyanotic heart disease)
increased pulm. blood flow * mildly cyanotic * increased sweating * CCF * FTT * plethoric lung fields * cardiomegaly decreased pulm.blood flow * mod. to severe cyanosis * ESM, delayed and diminished P2 (PS) * in PH ,accentuated & palpable P2,ESM * oligemic lung fields *TGA,singlventricle, anomalous pulm. return TA,total anomalous w/ obstruction pulm. Return w/o obstruction
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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 S2 •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 •
MINOR
systolic murmur less or more than gr III diastolic murmur cyanosis • • • abnormal S2 abnormal ECG ccf abnormal X-ray one major &two minor are essential • 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
primarily depends on size&status of pulm. vascular bed rather than location Small communication (less than 0.5cm`) VSD is restrictive & rt.ventricular pressure is normal – does not cause significant hemodynamic derangement(Qp:Qs=1.75:1.0) Moderately restrictive VSD with a moderate shunt(Qp:Qs=1.5 2.5:1.0) &poses hemodynamic burden on LV Large nonrestrictive VSDs(more than 1.0cm`) Rt&Lt ventricular pressure are equalised(Qp:Qs is more than 2:1) 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 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
typeI-MEMBRANOUS SEPTUM paramembranous/perimembranous defect (or infracristal,subaortic,conoventricular) typeII-MUSCULAR SEPTUM inlet,trabecular,central,apical,marginal or swiss-cheese typeIII-OUTLET SEPTUM deficient supracristal,subpulmonary,infundibular or conoseptal SEPTAL DEFICIFNCY –AVseptal defect (AVcanal)
CLINICAL FEATURES
Race : no particular racial predilection Sex :no particular sex preference Age :
infants
– difficult in postnatal period,although ccf during first 6mths is frequent,X-ray&ECG are normal.
children
—after first year variable clinical 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 S1&S2 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 P2 Delayed diastolic murmur at the apex &S3 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
ECHOCARDIOGRAPHY
• two-dimensional &doppler colour flow
CHEST RADIOGRAPHY
- normal - biventricular hypertrophy - pulmonary plethora •
ELECTROCARDIOGRAPHY
smallVSD ~ 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 V5 and V6 and often AF -large VSD ~RVH with rt. axis deviation. With further progression biventricular hypertrophy;P waves may be notched/peaked.
Other investigations
CAT SCAN (Computed Axial Tomography ) • • • MRI ULTRASOUND ANGIOGRAPHY (cardiac catheterization and angiography )
COMPLICATIONS
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) Pulmonary hypertension
INTERVENTION
3 MAJOR TYPES
SMALL (less than 3mm diameter)
- hemodynamically insignificant - b/w 80-85% of all VSDs - all close spontaneously * 50% by 2yrs * 90% by 6yrs * 10% during school yrs - muscular close sooner than membranous
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MODERATE VSDs
* 3-5mm 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
* 6-10mm in diameter * usually requires surgery otherwise… develop CCF & FTT by age of 3-6mths.
Conservative treatment - treat CCF & prevent development of pulm.vascular disease - prevention & treatment of infective endocarditis
INDICATIONS for SURGERY
VSDs at any age where clinical symptoms and FTT cannot be controlled medically.
Infants b/w 6-12mths of age with large defects ass. with PH ,even if symptoms are controlled by medication.
Pt.s older than 24mths of age with Qp:Qs is greater than 2:1.
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
Usually performed in second year.If symptoms are not disabling ,procedure may be deffered to 4-6yrs.
Alternate approach is through the rt.atrium, particularly when PVR is increased .
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.
Defect is usually closed with an oval patch of knitted dacron by mattress suture posteriorly and continous suture anteriorly using prolene.