Posts Tagged ‘asd’

I stumbled upon this image from the Heart journal. A good depiction of  IAS aneurysm in three dimension.

Image courtesy  : Heart 2012;98:79-88   Three dimensional echocardiography in congenital heart disease   by  Joseph John Vettukattil

Further  reading

Clinical implication of IAS aneurysm

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Patent foramen ovale (PFO) is the new generation hole in the heart for  21st century  cardiologist. Present in about 20% of population  , would correspond to 140 crore  “man holes”  as  on  2012   in this planet. PFOs are embryological remnants across the inter atrial septum.

These minute  holes measuring few mm  are largely a  benign finding .In the recent  decades , it is being increasingly debated these holes  may  not  be innocent after all .Extensive  use of echocardiography in recent times   has contributed to  the awareness  as well as anxiety.

Evidence  is mounting  linking PFO to

  • Migraine,
  • Stroke and
  • Peripheral embolism.

While the above   observation may be true  ,  the  fact that >100 crore people have this entity   , raises  a serious question ,  as labeling  all of  them as heart disease will create chaos among the already health obsessed   population .

So , the main purpose should be ,  to identify the high risk subsets* of PFO population .(This will be a <5 %  at the most). People with PFO may  carry  a mental  stigma because it is referred to as a hole in  the heart by the  general  public .For many  the sense of living with a hole in heart is often more damaging than the hole itself ! (Incidentally , many develop  migraine only after reporting about this hole !)In a strict sense  PFO  is not a hole , rather  it is a communication it may be tunnel  or  slit like .It is argued physician should avoid calling PFO as a hole .

*What is a significant PFO ?

  • Large PFOs >5mm
  • PFOs that shunt blood
  • PFOs with septal aneurysms
  • PFOs with documented stroke or embolism
  • PFOs with atrial chiary network
  • PFO in  persons with systemic pro-coagulant states (Except probably in  pregnancy )

Final message 

PFO is a common residual congenital  atrial septal  anomaly . Usually  benign  . One can  live with it perfect harmony. Only occasional patients  are  at risk.

So the prime job of cardiologists is to not diagnose and create panic about  this entity. rather reassure  them (Is it better do not reveal to them if it is found incidentally ? Patient empowerment group would call  this a  foul !  I do not support blind empowerment  )

At the same time our main  aim is to identify the  high  risk subsets who are prone for events.

Closure of   PFO with device is required in a fraction . (*By the way ,  if   PFO is really dangerous ,  why It is never an indication for surgical closure ?  )


Your  search for best information  on PFO  would end here .  Here is  land mark   article  in JACC  by  Hara   also contributed by  Renu Virmani . A US  Japan  combines initiative  : A must read by every cardiologists



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It was those great  years  1974 -1976.  Even before the concept of  PTCA was born, few  committed cardiologists  of New  Orleans were on a mission. Closing the ASD in cath lab. They  achieved it successfully with a umbrella device.


But 35 years later as on 2010 ,the concept though proven still struggles to prove itself.

Link to related article .

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  • Second heart  sound is widely split because the pulmonary  hangout interval* is wide
  • Fixed because , the RV stroke volume does not show the normal  respiratory changes.

This is  due to  dynamic phasic   shunting across the IAS  ( For example  : During inspiration ,  if RA,RV volume gets augmented by 50ml from IVC  inflow  , in expiration this  IVC  augumentation is removed  but a  50 ml augmentation from  left atrium takes place  , this keeps the RV diastolic ,  as well as  systolic  volume relatively constant.) This makes the 2nd heart sound fixed .

* Hangout interval is the gap ( in time ) between the  arterial pressure curve and the  respective pumping chamber pressure curve (RV, LV)  at the level of incisura.

Incisura is the  notch   on the descending limb of arterial pressure curve  ,  when the  pulmonary  or aortic valve closure occurs . When we analyse  the simultaneous pressure  recordings of  RV ,LV/Pulmonary artery/Aorta , the arterial  pressure curves  faithfully accompanies the chamber pressure curve  along  the dome of the chamber pressure  curve  till it descends  , where  it dissociates  ,  from the chamber pressure curve and hangs out for a certain  milliseconds. This time interval is  called as hang out interval (Named by Shaver et all )

What is the normal pulmonary hangout interval and systemic hangout interval /

Pulmonary hangout interval  is  60-80ms

Aortic hang out interval  is    20 ms

Why does it happen ? What does it signify

It happens because ,   even as the chamber pressure falls below  the  arterial pressure  ( Note: Semi lunar  valves  close at this  cross over point ) blood continues to  rush  forward ,  with momentum in to the pulmonary and systemic circulation, in spite of the closed semi lunar valves. This keeps the arterial pressure  not only to be  sustained little  longer  but also  slightly higher .

This  interval  is an  indirect( inverse) marker for vascular  impedance  of the distal  draining  circulation .The impedance is same  as vascular resistance  for all practical purposes.Since pulmonary circulation is  a low impedance circulation , it has a wide hangout interval and  the systemic  circulation vice versa.

How much of S2 widening is contributed by RBBB in ASD ?

This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often  incomplete and  peripheral one  .( Pesudo RBBB due to RVOT dilatation )

What happens  to S2  when  pulmonary arterial hypertension develops in ASD ?

  • It  is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to  behave like systemic , hence the impedance becomes  high and the hang out interval is significantly lost  and second sound is narrowly split. (But fixity may  be maintained.)
  • It also depend upon the RV function and associated RBBB. RV dysfunction and  RBBB both tend to widen the split.

*Mild PAH usually does not alter the S 2 splitting



Is there any other cause for wide and fixed splitting of second heart sound ?

Having known the reasons for widening and fixity it is easy to understand  , a  patient with right heart failure and  RBBB   can have a wide and fixed split .

Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good  enough to handle the inspiratory augmentation of RV end diastolic  volume.)

Why in VSD the second heart sound is not wide and fixed  split even though  hemo- dynamically it fulfills the same hemodynamic scenario  ?

Guess the answer .It will be posted soon.

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Like in neurological disease, one can locate the site of block in bundle branch blocks. Though it has never been thought ,  to be clinically important to localise a BBB . (Unlike coronary lesions)

Generally ,  RBBB can be proximal  or  distal peripheral type.The commonest site could be the distal  type.

It should be realised , for over 100 years in  electrocardiology , we have been using some inaccurate terminologies just because it is easy to understand or being traditional .It is difficult  to assimilate a fact , even today that   “An electrical delay in conduction and block are one and the same ”

In fact,  bulk  of  the RBBB is nothing but delayed conduction over this bundle. So whenever we say RBBB  , we imply an incomplete block  ie conduction still occurring   over the  so called blocked bundle.(This dogma applies for LBBB and AV blocks also to a lesser  extent)

Examples of delayed  RV /RVOT conduction

  • Any disease where  RVOT dilatation  occur can cause a RBBB
  • Atrial septal defect
  • Many cases of RVH
  • Pulmonary arterial hypertension

What is the benign rSr’ pattern in V1 ?

This is nothing but a relatively late depolarisation of  RV outflow or conus that produce a terminal RV activity .

Many of the ostium secundum ASD may show just this rSr’ pattern   confirming there is no organic damage to RBB in ASD .

Calling rSr’ pattern as incomplete RBBB is not advisable (As many ECG books may suggest ) .This is because , even full blown RBBB pattern may actually be an incomplete one .Further , the degree of terminal r’ in V1 or s in lead 1  does  not always   determine the completeness of RBBB.

Is there a totally blocked right bundle branch block ?

Yes , it is not common .

  • It can occur in extensive anterior MI .
  • Some cases of Ebstein anomaly.

It can be an working rule , complete RBBBs  locate the lesion proximally and incomplete  ones distally .

What is the other evidence for RBBB in ASD  is  only a simple   delay  in conduction ?

After ASD closure  in many of the patients the RBBB pattern may disappear.This indicate RVOT regression .

Can you clinically differentiate the proximal from  distal RBBB ?

Ironically ,what is difficult in ECG may some times be possible clinically.The classical description of wide splitting S2 occur often in peripheral RBBB.

It represents a delay in the closure of pulmonary valve due to delayed electrical activation or increased hangout interval as in ASD .Logically S1 should also be split in RBBB. But this is not often discussed.

This is because , the split in S1 is lesser in magnitude and is not influenced by the hangout interval .(Hang out interval is the time taken for the blood ejected from RV to fill the pulmonary circulation. Due to the low impedence of pulmonary circulation the the blood that is ejected into the MPA continue  to run off for about 100milli seconds even after the RV/PA pressure crossover .)

S1(T 1) occurs  immediately with the onset  of RV contraction . Similarly M1 occur with LV contraction.It should be recalled it requires hardly 5mmhg of RV pressure to close the tricuspid valve and about 10mmhg for LV to close the mitral valve.

If for some reason if  there is a delay  in RV contraction , as in very proximal RBBB the T1 is delayed and hence S 1 split.

Note in most of the peripheral or distal RBBB the bulk of the RV free wall contraction is not interfered with . So , in distal RBBB it is highly unlikely the S1 will be delayed or split while S2 will be delayed.

What happens to S2 in proximal RBBB ?

Logic would dictate both S1 and S2 should be wide split.

Final message

There is a simple way (Some would call this an futile  academic  excercise  !)to  differntiate proximal from distal RBBB.If the first heart sound is split wide , it fixes the lesion proximally. This may  indicate a more adverse outcome than a simple peripheral delay in conduction.

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ASD is the most common acyanotic heart disease. Clinically distinguishing  ostium primum (OP-ASD ) from ostium secundum (OS- ASD) is not an easy  task . A Wide fixed split pf S2  , a short systolic  murmur and PA pulsations  in left second space, a loud P2 and a hyperdyanmic RV occur in both .  The following features might give a clue for OP -ASD .

  • While  OS-ASD is  often an  isolated anomaly , isolated  OP- ASD is very rare.It usually occur as a part of partial or complete AV canal .
  • Early onset of symptoms
  • Early onset of pulmonary arterial hypertension( PAH )
  • Extra murmur of  1.VSD 2.MR (Cleft mitral valve ) may be present
  • Biventricular enlargement (MR/VSD)
  • ECG -Left axis deviation -Structural defect in left bundle ?

Confirmation is by Echocardiography and angiogram is rarely required today . Documentation of  classical goose neck deformity of LV outflow confirms the diagnosis.

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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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