Posts Tagged ‘vsd’

Anatomically ventricles are separated by a single muscular wall namely inter ventricular septum.But physiologically it has to contribute to both ventricular function.

How does IVS  is able to achieve this ?

For the naked eye both ventricles appear to contract almost simultaneously , but there is an intrinsic delay , first the LV contracts , followed by about 70 milliseconds right ventricle generates the peak pressure. So the IVS is able to help in a sequential, & coordinated contractions.This is called ventricular interdependence. Please note pericardium also contributes to this  .

Final message

The mechanical function of  IVS is effectively  and intelligently shared by both chambers. The electrical  delay even in milliseconds is enough to facilitate this sharing .Such is the power of nature. From this concept it is obvious LV dysfunction can have an adverse effect on RV function & vice versa.Similarly any electrical delay( LBBB, RBBB  ) can impact the septal function. Fortunately the myocardium has much reserve function , bundle branch blocks in isolation rarely result in serious consequences unless there is loss of associated muscle mass.

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VSD is  the leading  cause  of   congential heart disease .

  • The natural history is hugely variable spectrum , from totally asymptomatic  , incidentally detected in   childhood to a fulminant cardiac failure  and death in early  infancy .
  • Many small VSDs get closed by year 10. None of the large VSDs close spontaneously.Few of the moderate sized VSD may get closed.
  • The site of the VSD is a major determinant of spontaneous closure. Muscular  VSDs are more likely to get closed .Of course many of the membranous VSD have  at least a rim formed by a adjoining muscular septum
  • Associated defects, RVOT obstruction and late onset AR also has a  influence  on the natural history.
  • Progressive PHT  leading onto   Eisenmenger  syndrome  occurs  has become a diagnostic curiosity in many countries .

It  is natural to expect  the VSDs   to share a  close relationship with  the conduction system which   fights for  “equal rights”  to occupy the inter ventricular  septum  , (In spite of   a defective septum ! )

How often we see conduction defect in VSDs ?

It is  rather surprising  to note   conduction  defects are not  common in VSDs .In fact it can be termed  rare . How  this is  posssible ?   VSDs , however large it maybe   ,  usually spares the conduction system . This is simply due to the fact , developmentally the two systems  , ventricular septum and the electrical  system  of the heart comes from different embryological focus and and are simply anchored together.

If the IVS is not formed properly ,the bundle  of His and it ‘ s major right and left branches  are  simply displaced  and not are  destroyed  ,  they  tend to occupy  one of the rims of VSD

*Further, a VSD located peripherally and distally towards the apex has little impact on the conduction tissue as it has already fanned out and small little twigs are affected ,while central , proximal,  and basal VSDs  can have more significance .

Classically ,  it has  major  significance   for the  surgeons than cardiologists  , as post operative blocks are more common than the preoperative blocks !

What are the  changes to the conduction system in various VSDs ?

Membranous VSD

  • Migration  of  A-V node   posteriorly toward crux of heart *
  • His bundle  courses  along  the  posteroinferior rim of defect

* This makes sure the compact AV node never comes into picture of VSD . It  also it explains the  rairty of   complete heart block  due to mechanical damage  to the  AV node  by the  VSD jet

How to avoid  injury during surgery ?

Sutures  are  made a few millimeters from postero-inferior rim,  Do not penetrate  the septum.  Suture along  RV side  of the  septum  as the  His bundle  is  often located on the  LV side of muscular septum.

RV approach to close VSDs,  make  postoperative RBBB a common issue but generally it has no great clinical significance

Location of conduction defect in various  VSDs

  • Membranous VSD  –  Conduction tissue runs along posteroinferior border of defect
    Muscular VSD
  • (Especailly with Inlet extension)  – conduction tissue is anterosuperior to defect
  • AV canal defects . This is the only type of VSD where serious defects of conduction occur  .Interruptions can also occur in the AV node.

Coming  soon . . .

Where  will the conduction system run in single ventricle where there is no IVS ?

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PAH  is  the major determinant of surgical outcome of left to right shunts. In this  modern era of cardiac care  allowing a child  with   left to right shunt   to progress to a  stage of   Eisenmenger syndrome  is  considered  as a  huge medical failure . But  , this is still rampant in many of the developing countries .

Cardiologists are divided over the issue of  operability of Eisenmenger syndrome .The confusion is largely due to the conflicting data of outcome in these patients. While  there is strong   data  when  PVR exceeds  SVR  ,  the death is imminent in the post operative period .

What has complicated the issue is   there are  many case reports  where severe PAH patients have been successfully operated. Most would think it is a statistical exception and one can  not alter the traditional criteria based on few case reports.

But ,it remains an irony as on 2009 ,  we do not have a proper methodology to assess reversibility of PAH in Eisenmenger syndrome . Further ,  there is a  significant number of  patients with high PVR  , who continue to experience  an  unabated left to right shunting .  We do not have an answer  for either the mechanism of such shunts and  how to manage these patients.

Click over the slide  to view full  PPT  presentation in PDF format .

This short paper was presented in the Annual scientific sessions of cardiological society of India 2009 regarding the usefulness of a new parameter to assess reversibility of PAH. This may not be called as  a study rather a report of  our experience  in  five  patients  with eisenmenger syndrome

Download the full PPT presentation in PDF  format.

pulmonary artery pulse pressure

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Biochemical diagnosis for PHT and Eisenmenger syndrome

Identifying reversibility of pulmonary arterial  hypertension remains a difficult clinical problem.Heath edwards grading of pulmonary hypertension is based on lung pathology .Grade 4 and 5 constitute severe obstructive vascular pathology including pulmonary vascular necrosis.

Lung biopsy is an invasive procedure and has a  huge risk in patients with elevated pulmonary artery pressure.

Do we have an alternative ?

Does the pulmonary artery  sheds  necrosed  endothelial cells  into the circulation  ?

Yes it seems so , This month’s Nature cardiology  reveals a breakthrough concept

The CEC (Circulating endothelial cells count )  can be used as marker  and  may be considered a non invasive equivalent of lung biopsy




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