ventricular septal defect l.
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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 functional circulatory system has been established by the 4th week ; the ventricular septum is fully developed by the 8th week.

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  • 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.
  • 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.
  • This septum is muscular & is an outgrowth of the ventricular wall itself.
  • It doesn’t 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).
  • 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 .
  • 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
  • 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.
  • When a small communication is present (usually < 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 > 1.0 cm2), right & left ventricular pressures are equalized.
  • 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.
  • When the ratio of pulmonary to systemic resistance approaches 1:1, 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
  • 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 <1.75:1), the cardiac chambers will not be appreciably enlarged & the pulm. Vascular bed will likely be normal.
  • If the shunt is large (flow ratio >2.5:1), 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.
clinical manifestations small defects with trivial left to right shunts nl pulm art pr

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)

Clinical Manifestationssmall defects with trivial left-to-right shunts & NL. Pulm. Art. Pr.
clinical manifestations large 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.

Clinical Manifestationslarge defects with excessive pulmonary blood flow & pulmonary HTN
  • 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.
  • Cardiac catheterization
  • indicated whenclinical evaluation leaves uncertainly regarding the size of the shunt or when lab. data don’t fit well with the clinical findings.
  • It is useful for detecting the presence of associated cardiac defects.
prognosis complications
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.
prognosis complications17
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.
treatment small defects
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.
treatment large vsd
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.
treatment large vsd20
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.