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Ventricular Septal Defect

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Ventricular Septal Defect Deena Abdel_Hadi Embryology At the 2nd intra-uterine week , when the embryo is only 1.5 mm long the heart begins to take shape , a ... – PowerPoint PPT presentation

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Title: Ventricular Septal Defect


1
Ventricular Septal Defect
  • Deena Abdel_Hadi

2
Embryology
  • At the 2nd intra-uterine week , when the embryo
    is only 1.5 mm long the heart begins to take
    shape , a functional circulatory system has been
    established by the 4th week the ventricular
    septum is fully developed by the 8th week.
  • Consequently any radical alteration of the
    architecture of the heart must occur between the
    2nd 8th weeks of intra-uterine life.
  • By about 6 weeks all the principal components
    of the human heart are clearly discernible.

3
Embryology
  • The common ventricular canal is divided by an
    intra-ventricular septum (septum inferius) which
    start at the 3rd or the beginning of the 4th week
    , grows upward backward toward the common
    atrio-ventricular orifice which it divides into
    the mitral tricuspid valves.

4
Embryology
  • This septum is muscular is an outgrowth of the
    ventricular wall itself.
  • It doesnt reach the floor of the bulbus cordis ,
    an opening in the ventricular septum is left in
    the center high up with a downward convex
    partly from the bulbus cordis.(as mentioned is
    usually completely closed by the 7th or 8th
    intra-uterine week).

5
Embryology
  • In order for the ventricular septum to divide
    the common atrio-ventricular orifice evenly ,
    this must shift toward the right , failure of
    this orifice to shift result in tricuspid atresia
    an excessive shift gives rise to mitral
    atresia .

6
Embryology
  • Failure of the bulbar ridges to form the
    membranous part of the septum result in the most
    common forms of V.S.D. .
  • Defects of the muscular septum are usually
    ventral high near the aortic orifice only
    rarely do they occur in the neighborhood of the
    apex

7
Pathophysiology
  • The physical size of the defect is a major, but
    not the only , determinant of the size of the
    left-to-right shunt .
  • The shunt magnetite is also determined by the
    level of pulmonary vascular resistance compared
    with systemic vascular resistance.

8
Pathophysiology
  • When a small communication is present (usually lt
    0.5 cm 2), the defect is called restrictive
    right ventricular pressure is normal .
  • The higher pressure in the left ventricle drives
    the shunt left-to right.
  • In large non-restrictive defects (usually gt 1.0
    cm2), right left ventricular pressures are
    equalized.

9
Pathophysiology
  • In these defects, the direction of shunting the
    shunt magnitude are determined by the ratio of
    pulmonary to systemic vascular resistances.
  • After birth, in the presence of a large
    V.S.D.,the pulmonary vascular resistance may
    remain higher than normal thus the size of the
    left-to-right shunt maybe limited .
  • As pulmonary vascular resistance falls in the 1st
    few weeks after birth because of the normal
    involution of the media of the small pulmonary
    Arteries arterioles,the size of the
    left-to-right shunt increases clinical symptoms
    become apparent.

10
Pathophysiology
  • When the ratio of pulmonary to systemic
    resistance approaches 11, the shunt becomes
    bi-directional, signs of heart failure abate
    (diminished), the patient becomes cyanotic
    (Eisenmenger physiology).
  • Prolonged pulmonary hypertension is prevented by
    early surgical intervention in patients with
    large V.S.D.s

11
Pathophysiology
  • The magnitude of intracardiac shunts is usually
    described by the ratio of pulmonary to systemic
    blood flow.
  • If the left-to-right shunt is small (pulm. to
    syst. flow ratio lt1.751), the cardiac chambers
    will not be appreciably enlarged the pulm.
    Vascular bed will likely be normal.
  • If the shunt is large (flow ratio gt2.51), the
    left atrial ventricular volume overloaded
    occur, as well as right ventricular pulm.
    Arterial hypertension.
  • The pulm. Arterial trunk, left atrium, left
    ventricle are enlarged because of the large
    volume of pulmonary blood flow.

12
Clinical Manifestationssmall defects with
trivial left-to-right shunts NL. Pulm. Art. Pr.
  • Asymptomatic.
  • Cardiac lesion is usually found via a routine
    physical exam. (harsh ,loud ,blowing,left
    parasternal holosystolic murmer on left lower
    sternal border .
  • The systolic murmer maybe not audible via the 1st
    few days(limited left-to-right shunt d.t.higher
    right side pr.
  • CXR usually normal .
  • ECG usually normal but may suggest LVH
  • (RVH suggest pulmonary HTN , large VSD ,or
    associated symptom as pulmonary Stenosis)

13
Clinical Manifestationslarge defects with
excessive pulmonary blood flow pulmonary HTN
  • Dyspnea , feeding difficulties , poor growth ,
    recurrent pulmonary infections cardiac failure
    in early infancy (cyanosis is usually absent but
    duskiness is noted during infections or crying.
  • A palpable parasternal lift , a holosystolic
    murmer , less harsh more blowing d.t. absence
    of a significant pr. Gradient across the defect.
  • CXR showed increase broncho-vascular markings
    ,gross cardomegaly with prominence of both
    ventricles , left atrium pulmonary artery,
    frank pulm. edema pleural effusion.
  • ECG shows bi-ventricular hypertrophy , P wave
    maybe notched or peaked.

14
Diagnosis
  • Two-dimensional echocardiogram
  • position size of VSD.
  • By Doppler examination used to diagnose very
    small muscular septum defect the degree of
    volume overload of the left atrium left
    ventricle.
  • Pulsed Doppler calculate the pr. Gradient across
    the defect.this will allow estimation of right
    ventricular pr. help to determine whether the
    patient is at risk for the development of early
    pulmonary vascular disease.

15
Diagnosis
  • Cardiac catheterization
  • indicated when clinical evaluation leaves
    uncertainly regarding the size of the shunt or
    when lab. data dont fit well with the clinical
    findings.
  • It is useful for detecting the presence of
    associated cardiac defects.

16
Prognosis Complications
  • (30-50) of small VSDs will close spontaneously ,
    most frequently during the 1st year of life
  • the vast majority of defects that close will do
    so before age 4 yr..
  • One of the long term risks for these patients is
    that of infective endocarditis.

17
Prognosis Complications
  • Endocarditis occurs in fewer than 2 of children
    with VSD , is more common in adolescents , is
    rare in children under 2 yr. of age
  • it is less common for moderate or large VSD to
    close spontaneously , even defects large enough
    to result in H.F.(manifested in infants as
    F.T.T.) may become smaller rarely will close
    completely.
  • Large defects ass. with recurrent chest
    infections C.H.F.

18
Treatment(small defects)
  • Reassure parents
  • allow the child to live a normal life
  • surgical repair is not recommended
  • protection against infective endocarditis
  • follow up screening for pulmonary HTN or pulmonic
    Stenosis indicated by RVH.

19
Treatment (large VSD)
  • Medical treatment has two aims to control CHF
    to prevent development of pulmonary vascular
    disease.
  • Patients show signs of recurrent chest infections
    FTT.
  • Pulmonary vascular dse is prevented when surgery
    is performed within the 1st yr. of life.
  • Large defects ass. With pulmonary HTN should be
    closed between 6 12 mo. of age.

20
Treatment (large VSD)
  • Surgical risks are higher for defects in the
    muscular septum , particularly apical defects
    multiple (Swiss-cheese type) defects,they may
    require pulmonary artery binding.
  • Catheter occlusion devices are currently being
    tested to close apical muscular VSDs.
  • After obliteration of the left-to-right
    shunt,catch-up growth occurs in the majority over
    the next 1-2 yr.
  • Systolic ejection murmurs of low intensity may
    persist for months.

21
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