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
•Gr 1 Lt to Rt shunts
•Gr 2 Rt to Lt shunts
•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
*TGA,singlventricle,
TA,total anomalous
pulm. Return w/o
obstruction
 decreased pulm.blood
flow
* mod. to severe cyanosis
* ESM, delayed and
diminished P2 (PS)
* in PH ,accentuated &
palpable P2,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
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
or more
• diastolic murmur
• cyanosis
• ccf
one major &two
minor are essential
MINOR
• systolic murmur less
than gr III
• abnormal S2
• abnormal ECG
• abnormal X-ray
• abnormal BP
VENTRICULAR SEPTAL
DEFECT
• most common ACHD
• 2nd 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=1.52.5:1.0) &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 3rd,4th&5th Lt
interspace.Also well heard at the 2nd space but not
conducted beyond apex
• Lt. 2nd 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


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


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
 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.
 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.
 Alternate approach is through the rt.atrium,
particularly when PVR is increased .
 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?