VSD • Communicatio n b/t two ventricles
VSD
• Communication b/t two ventricles
VSD
• May occur alone or with other abnormalities
• About one-third of small VSDs close spontaneously
Ventricular Septal Defect
• Commonest acyanotic CHD (~25%)
• Associated with-Down Syndrome
Fetal hydantoin syndrome
Fetal alcohol syndrome
Trisomy 13, 18
Apert syndrome
Anatomy
• Compartments of ventricular septum:
- Membranous septum
- Inlet septum
- Trabecular septum
- Outlet or infundibular septum
• Defects result from a deficiency of growth or failure of alignment or fusion of component parts
Classification-pathology
1.Membranous VSD- (perimembranous, paramembranous , conoventricular, infracristal, subaortic) – Most common (90%)
2.Muscular VSD- (Swiss cheese ,inlet, trabecular, central, apical, marginal ,or outlet types)
3. Supracristal VSD- (subpulmonary, outlet, infundibular, or conoseptal. subarterial defect) Least common
Classification-pathology
Hemodynamics:
• L→R shunt in ventricles occur with high pressure gradient throughout systole – pansystolic murmur
• Blood to normal pulmonary valve – ejection systolic murmur
• Large vol of blood to lungs – pul plethora• Blood to left atrium – Lt. atrial enlrgement• Blood to normal mitral valve – delayed
diastolic murmur at apex
Hemodynamics
• Lt ventricles to outlets – empties relatively early – early A2
• Rt ventricle & pul artery – increased ejection time – delayed P2-S2 widely split &variable
Hemodynamics
Hemodynamics
• Depends on: a) size of the shunt
b) PVR
• Based on size of VSD:
- Restrictive VSD(<0.5 cm2 )
- Moderately restrictive VSD
- Non-restrictive (>1 cm2 )
Restrictive VSD
• Small, hemodynamically insignificant • Size <0.5 cm2
• Between 80% and 85% of all VSDs• All close spontanously 50% by 2 years 90% by 6 years 10% during school years• Muscular close sooner than membranous
A moderately restrictive VSD
• Size -> 0.5 cm2 (>5mm) in diameter
• Moderate shunt (Qp:Qs = 1.5-2.5:1.0)
• May lead to left atrial and LV dilation and dysfunction, as well as a variable increase in pulmonary vascular resistance
Large nonrestrictive VSDs
• Large VSDs with normal PVR
• Usually >1.0 (>10 mm) in diameter
• Usually requires surgery
• Will develop CHF and FTT by age 3-6 months
Clinical Manifestations:
1. Small VSD: asymptomatic, normal growth
2. Moderate to large: repeated chest infections, Effort intolerance ,fatigue , failure to thrive, pulmonary HTN
3. If unoperated: Pulmonary HTN, cyanosis and decreased level of activity
Physical examination
1. Small VSD: well developed, acyanotic
2. Moderate VSD: forceful LV impulse , prominent systolic thrill along the lower left sternal border
Physical examination
Large VSD: tachypneic, repeated chest infections, poor weight gain, CHF dyspnea, feeding difficulties, poor growth, profuse perspiration, recurrent pulmonary infections, and cardiac failure in early infancy.
Reversal of shunt: cyanosis, clubbing, respiratory distress.
Auscultation
• Heart sounds
• S1 : masked by pansystolic murmur
• S2: masked but can be heard at 2nd lt ICS – widely split and variable, with accentuated P2 - single and loud (PAH)
• S3: maybe audible at the apex
Murmurs
• Shunt - loud, harsh, or blowing pansystolic murmur grade 3-5/6 best heard at left 3rd & 4th interspaces is widely transmitted over the precordium at lower LSB
• Flow – • Pulmonary : ejection murmur (drowned)• Mitral : rumbling delayed diastolic murmur
at the cardiac apex, indicates a Qp:Qs of 2:1 or greater
Fairly large perimembranous VSD in
Chest radiography
• Small VSDs -N
• Medium- VSDs -minimal cardiomegaly and a borderline increase in pulmonary vasculature
• Large VSDs – gross cardiomegaly . The pulmonary vascular markings are increased and frank pulmonary edema (Plethoric) if pul arterial HTN
• Oligemic lung fields in reversal of shunt, pul stenosis
Electrocardiography
• Depends on shunt size & degree of pulmonary hypertension
• Small VSDs - N tracing
• Medium VSDs – broad, notched P wave ( left atrial overload), LVH
• Large VSDs – RVH with right-axis deviation. With further progression - biventricular hypertrophy; P waves may be notched or peaked
• RVH in Eisenmenger’s complex
Echocardiography
• Echo - Number, position & size of defect, chamber size
• Two-dimensional echo – site, size of defect ,pul. stenosis or pul HTN
Management:• Large VSDs Medical:
Treatment of chest infection Control of heart failure Infective endocarditis prophylaxis Dental hygiene Frequent feeding of high calorie formula, correction of
anemia Non-surgical closure with umbrella device
Surgical
• Repair of defect under open heart surgery
• Clamshell-type catheter occlusion -closing apical muscular VSDs.
• Transcatheter device closure - trabecular (muscular) and perimembranous VSDs
Indications of surgery:• Large defects- if CHF not responding to
medical management (within first 6 months of life)
• After 1 year of age, significant LR shunt, Qp: Qs ratio at least 2:1 without pul HTN
• Supracristal VSD of any size because of the high risk of aortic valve regurgitation
Contraindication of surgery
1. Severe pulmonary vascular disease
2.Muscular septum VSDs , particularly apical defects and multiple (Swiss cheese–type)
Natural history• Small VSD – Spontaneous closure( 30-
50%) during 1st yr of life (membranous & muscular defects)
• Small muscular VSDs are more likely to close 80% than membranous VSDs 35%
• The vast majority 45% close by age 4 years
• Spontaneous closure has been reported in adults
Mod to Large VSDs
• Less commonly close spontaneously
• CHF develops in large VSDs after 8 weeks of age
• Repeated chest infection ,FTT
• IE –independent of VSD size – rare in < 2yrs .risk is 2% above 2 yrs
Natural History:
• Pulmonary hypertension →pulmonary vascular disease (Eisenmenger syndrome
• Aortic valve regurgitation - the greatest risk supracristal VSD