Posts Tagged ‘ventricular septal defect’

The following  questions  are asked frequently  in clinical cardiology classes on congenital heart disease.

What are the chambers that dilate in ASD ?

Right atrium and  right ventricle .

What are the chambers that dilate in VSD ?

LA, LV , ± RV,

* Image courtesy Wikipedia

While there is no controversy about ASD, The chambers that enlarge in VSD ,   is  by and large  poorly (or rather wrongly ) understood .  Whenever we  diagnose  VSD , our brain is tuned  to think  this way : Blood  will be  shunted form LV to RV.  RV  would  handle more blood and it  should   enlarge . In reality it does not happen.

The VSD  shunts  the  blood from  LV to RV outflow*   or even directly into  pulmonary artery  .  Hence , VSD even if it is large  , does not dilate  the RV until the onset of  pulmonary hypertension and RV dysfunction sets in . It is surprising to note , even the RVOT ( The entry point of most VSD jets) does not significantly  enlarge

Importance of diastolic shunting in determining RV size in VSD

It is also important to recognise, the VSD shunt predominately occur in systole .(90% ?) In systole , the RV is also contracting along with LV  , so it’s size is diminutive  and hence RV can not be volume overloaded in  most of the VSDs however large it may be. Instead in ASD , there is diastolic overloading   involving  all regions(Inflow, Body, Outflow) of  RV   .This enlarges the RV   in a classical  fashion.

Significance of  anatomical location of VSD and RV enlargement

When VSD shunts blo0d into RA as in Gerbode defect it is bound to enlarge RV (like ASD) as there is diastolic volume over load of RV.

In some large muscular VSD , RV body can be  volume  overloaded. This is because the VSD and RVOT are well separated geographically .The  blood that is coming in from LV can enter the pulmonary artery , only in the next cardiac cycle  . So , RV needs to accommodate the shunted  blood till the next beat. Hence RV enlarges.

What are the situations RV can enlarge significantly in VSD ?

  • Rare VSDs of inflow or large muscular VSDs.
  • Eisenmenger syndrome.
  • Tricuspid regurgitation
  • Pulmonary regurgitation
  • Associated RSOV.

Final message

Right ventricle   does not enlarge  significantly in uncomplicated  VSD .This is in contrary to the  traditional teaching and understanding  for  many years. It enlarges only in specific sub types of VSD  or  after the onset of PAH and cardiac failure .

Coming soon

Katz-Wachtel phenomenon is not  due to  bi -ventricular hypertrophy !

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Aortic regurgitation complicating VDS  is an important clinical  entity in congenital heart disease.It is  also  a popular case for the cardiology fellows in their  final clinical examinations . AR is a  late manifestation of VSD (usually in early  adolescent  or adult hood) .This develops due to loss of aortic valvular support provided by the inter ventricular   septum.

In fact ,   IVS can be termed  as a foundation stone  on which  a  part of  aorta (Mainly its anterior part) rests . So, it is not surprising VSD patients  are prone to develop AR especially,  as they grow when aorta tires to outgrow the septal support . Further,  the hemodynamics of VSD has a crucial impact on the AR progression.(See image below)

Pulse /Blood pressure

Large volume pulse,  may be collapsing

Peripheral signs of Aortic run off usually present

Apical impulse

Shifted down and out Hyperdynamic


To and fro murmur (To -Systolic , Fro -Diastolic )

It is differentiated from continuous murmur by a distinct reduction  in the intensity of murmur towards the end systole and a different murmur  appear  in diastole  . While , a continuous murmur  is  a single murmur  that peaks  around sound  heart sound , overlaps the second  heart sound and spills well into diastole.

Other useful diagnostic clues

  • Usually the VSD  is  restrictive  .Left to right shunt is often below  2:1
  • With the onset of AR  ,there is  further reduction in the left to right shunt of VSD
  • Hence,progressive pulmonary arterial hypertension is uncommon and Eisenmenger is reaction is very rare in  VSD with AR.
  • Presence of AR makes  LV dilatation disproportionate to VSD  shunt  (LV size  is not useful to assess the  hemodynamic  significance of VSD)
  • LV dilatation invariably means significant AR rather than VSD.  VSD induced LV enlargement  is  usually less conspicuous as it is  represents  physiological flow across mitral  inflow .  While , AR is a high gradient leak  from a non-physiological chamber (Aorta)
  • ECG volume overload of LV   is  evidenced by  more prominent * q waves in  V5 V6

*Double dose of volume overload (AR +VSD)


  • If AR is mild ,only VSD closure is advocated *
  • If AR is moderate  , repair of aortic valve is  considered along with VSD closure.
  • For severe AR , Aortic valve replacement or repair with VSD closure mandatory.
  • Device closure of VSD and percutaneous  aortic valve replacement  not feasible at the moment .May be a future possibility.

* If both  VSD and AR are very small ,  simple follow up , and observation (Leaving the patient happy!)  could be a distinct option !

Pathogenesis of AR in VSD : The landmark article from Japan in 1973 by Tatsuno  and Sakakibara


Thanks to circulation .Such articles are made available .


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Ventricular septal defect(VSD) is one the commonest congenital heart disease . Right from the days of Gasul , Abbot, and Keith we have analysed the natural history for nearly a century . VSD is an intriguing congenital heart disease where a child can develop a florid cardiac failure within weeks of birth in one end to a totally asymptomatic adult with a benign cardiac acoustics defect (Namely a systolic murmur in the left parasternal area.) But for this murmur , the patient would be labeled absolutely healthy.

 In between these two spectra is the huge population of VSD that gets closed spontaneously. A rough estimate says 60 % of all small VSDs get closed by age 10 .

So ,what we are supposed to do once a child is diagnosed of VSD ?

Should we close or should we wait ?

The indication for closing a VSD is discussed elsewhere ( Read this link )

 What are the factors that determine VSD closure ?

  • The size
  • The site
  • Age of the child
  • The Rim morphology
  • Associated lesions*
  • Hemodynamic stress
  • Inherent tissue factors
  • Infection **

* Associated defects like PDA, RVOT obstruction are strong deerrants against spontaneous closure

General rules of VSD closure


VSDs <5mm have great chance of closing Large VSD > 1cm is rarely get closed .

Supracristal VSDs located sub arterially are immune to spontaneous closure however small the size is .

Location & Site

 VSDs that are located exclusively within the membranous septum rarely close . VSDs which are located in the perimembranous area (With at least 50% circumference is fenced by muscular or trabecular septum has the greatest potential to close by natural forces.)

Isolated muscular VSD if large can not get closed . Inlet VSD has anatomical difficulty to get closed.

Rim Morphology

 Small muscular VSDs have a potential to close , but it is believed differential cellular lining of VSD rims (Eg : A combination of muscle, membrane , is more likely to close .)

 Process of tissue growth As the child grows the it is expected the heart will outgrow the lesion . This is thought to be the commonest mode of VSD closure. As the IVS mass increases as he child grows it brings he rims together . But logic would suggest unless some degree of neocardiac proliferation occur a VSD may never get closed completely .

Some times even large VSDs try to close with the help of the neighboring structures like septal tricuspid valve leaflet . Indeed this can be the dominate mode of closure in many. This can induce a tricuspid regurgitation .

**Role of infection

Paradoxically an episode of infective endocaditis in the edges of VSD accelerate the process of approximation of tissue plane and healing .

 Relation with Pulmonary arterial hypertension (PAH)

 Once PAH sets in the VSD never gets closed spontaneously , This may be due to all VSDs that result in PAH has to be significantly large

 Can a VSD get larger progressively?

In physics and hydraulics a hole under hemodynamic stress is destined to progress In human biology this is thought to be rare .Post MI VSRs can behave in an unpredictable manner as he edges of the defect a often softened and prone for tissue plane dissection and extension .

Why some VSDs never close ?

It is clear , size and location matters the most , but there are other issues some of them may be unique tissue properties .

Why is it important to know the biology of VSD closure ?

In this era of interventional cardiology we are using mechanical devices to close VSDs and ASDs .It is fraught with many technical issues. If there is a biological glue or membrane that can be delivered by catheter to close small VSDs or ASDs .

 So for no therapeutic approach to hasten the natural closure of these defects has been practiced .Further research is required to explore the cellular adhesiveness and help accelerate closure of these defects.

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