Archive for the ‘acute pulmonary embolism’ Category

The right ventricle  is considered as a docile cardiac chamber with passive filling and  emptying  properties .

This belief  was reinforced when Fontan  in early 1970s suggested a principle in the management of  cyanotic heart disease  when  the right side of the heart is underdeveloped. He  proved  RV can be by-passed safely , with  great veins  (IVC/SVC)  by  themselves  take care of filling the pulmonary circulation  without the need of RV pumping function.

While it is true for few complex cyanotic heart disease, largely this a misleading  concept. In clinical cardiology practice  ,sudden or non sudden  RV deaths happen every day in the form of . . .

  • RV Infarction
  • Acute RV dysfunction in massive pulmonary embolism
  • COPD with RV dysfunction
  • Most cases dilated cardiomypathy  the terminal event is due to RV  failure.

So , RV function can never be dispensable in day to day cardiac hemodynamics.

RV has some unique properties in terms of shape , size and  hemodynamics . We are getting more insights from  modern blood pool imaging by MRI , about  how the RV handles the blood volume .

We know RV has a unique shape  triangular ( partially  pyramidal ) . It can be inferred the RV cavity is formed by fusion of  many  eccentric spacial planes. We have always believed  RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.


right ventricle physiology anatomy hemodynamics

It is curious  to know  RV inflow is connected to the outflow by an invisible   physiologic Bridge . About 44% of  blood traverse the RV in this fashion.


RVOT blood flow right ventricle

Note : RV blood flow preferentially enters the RVOT with out transiting RV body and apex.Image courtesy http://ajpheart.physiology.org/


Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)

After reading this article it seems to me , the mechanical  function of RVOT could be most  vital. If it fails to handle the first increment  which  comes directly from  RV inflow, stasis  is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.

Clinical implication of this study

  • Differential dilatation RV chambers to pressure or volume  overload is observed .
  • We need to analyse why RV dilates in some   but   goes for hypertrophy in others when confronted with pressure overload (VPS vs PAH)
  • RV apical clot in restrictive cardiomyopathy  is a direct consequence of stasis  of blood  in RV apical zone .
  • RVOT pacing  may have a hemodynamic advantage  over RV apical pacing  . However , for anatomical reasons RV apical pacing  is  far safer than RVOT pacing where the lead  is subjected to constant life long strain due to this busy RV inflow to outflow express  high way !

Final message

Traditionally we have labeled  RV  as a  passive venous chamber .It is clearly a misnomer.It  has to handle both the venous and pumping function beat to beat with precision  without  back log .Obviously ,  RV has to think and work  more than it’s  big brother !


I wonder , if  there is  any other site other than APS . . . to  find crucial  answers in cardiac physiology  !


Right ventricle physiology blood flow  3d 4d analysisAfter thought

  • There is huge gap between physiologists  who work in research labs and the physicians at bed side .
  • I appeal all young cardiologists  to visit  APS  once in a while ,between your busy cath lab schedule and help narrow this gap.
  • Without understanding the physiology properly how are we going to intervene the pathology ?


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IVC filter usage has increased many fold in recent years.Please note , it is not indicated in every case of recurrent DVT/or PE. There are specific indications.

Permanent IVC filters

  1. Patients at risk for DVT /PE  with  absolute contraindication to anti-coagulants.
  2. Recurrent DVT/PE in spite of adequate  anti-coagulation

Temporary /Retrievable filters*

  1. It is used during high risk periods  for DVT following major trauma or Bariatric/Spinal /Neuro surgery (PREPIC 2 study ) .*Some of the retrievable filters can be kept for months ,years or even permanently. (If the risk period extends or it has trapped a huge clot.)


indication for IV filter prepic study

Outcome  of IVC filter (PREPIC  -8  year follow up study )

  • Reduces risk of PE
  • Increases risk of DVT
  • No impact on long term  survival
  • Clogging of IVC remain  an important Issue


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A 25 year man ,  hotel  manager  who had a documented DVT , since 2011 was on tablet warfarin . He discontinued  the drug by sheer miscommunication as he was told he should stop the  drug  beyond INR 3 by his general practitioner.He stopped it permanently  instead of titrating the dose of warfain .Six months later he landed  in August 2013 with an episode of minor hemoptysis . Clincally he was normal .His lower limbs were fine.

He was investigated and  his image file showed .

pulmonary embolism  3  total occlusion of LPA

pulmonary embolism  3  total occlusion of LPA

pulmonary embolism total occlusion of LPA

Living with one lung

  • He is comfortable with one lung function (Akin to  Pneumonectomy )
  • His saturation was 100 % at room air
  • Pulse -80/mt .BP 110/80mmhg
  • His physical activity  did  not show any significant limitation (At worst class 2)

One of the cardiac surgery consultant wanted to do pulmonary embolectomy and endarteriectomy .

In fact , he was admitted in the critical care unit driven by the dramatic CT images.

One enthusiastic cardiologist wanted  thrombus aspiration and pig tail catheter based thrombolytic  irrigation within LPA !

How did we manage ?

  • The risk of major vascular surgery was considered high in an absolutely asymptomatic individual .
  • Intervention was considered too adventurous.
  • He was  put on oral anticoagulant with target  INR 2.5-3.(After a 1 week Heparin overlap)
  • We hope the thrombotic CTO will open up gradually but for surely .As the power of  natural lytic  molecules should not be underestimated as we have witnessed in LV and LA clot disappearing over months.
  • However the option of putting IVC filter was strongly recommended for him , as he has only  functioning  lung  which  is threatened by a potential  embolus from DVT . The patient wanted to come back for IVC filter next month.
  • He was also worked up for all those protein C, S,  Lieden mutation stuff.
  • The patient was discharged in stable condition (By the way he  was never unstable either !)

* Meanwhile the hemoptysis  did not recur. CT scan showed a small wedge infarct in left lung that was in the healing mode.

Final message

This is a perfect example of  CTO of pulmonary artery being  managed conservatively* .We will let you know the follow up .

Link to related topics in this site.

Deep vein thrombosis-Therapeutic dilemmas

What do we mean by conservative management ?

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The  commonest  cause for death in massive pulmonary embolism is 

  1.  RV shock
  2.  Massive Hemoptysis
  3. Primary VF   originating  right ventricle
  4. Refractory Type 1 Respiratory failure

Answer : 1  .(RV shock , RV standstill and RV , RV stunning  is the unequivocal  cause for sudden death in pulmonary embolism . This RV shock occur very early .Once the patient survives the initial  RV scare (say 24-48 hours) usually do well if prompt thrombolysis and anti-coagulation is administered  )

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Conventionally  pulmonary embolism is classified as massive, sub massive  based on

  1. Severity of obstruction
  2. Level of  obstruction in pulmonary anatomy (MPA,Branch PA, Segmental etc )
  3. Thrombus burden
  4. Quantum  of pulmonary vascular bed  compromised

But it is always intriguing ,    the clinical outcome was not linearly  correlating with the above parameters.

Instead the outcome seemed more dependent on the following .

  1. Degree of RV dilatation
  2. Systemic hypo-tension
  3. RV shock

Image courtesy .www.smartdraw.com

So ,  whatever be the quantum of pulmonary embolism , it is the behavior of RV that is going to determine the outcome.  The current  wisdom   demands , all hemo-dyanmically unstable pulmonary embolsim may be considered as massive or high risk pulmonary embolism and  aggressive treatment  is  to be undertaken.

Counter point

There is  one major diagnostic issue  if we depend more on hemo-dynamic instability . What is that ?

There is no valid method to identify Acuteness / chronicity of   RA, RV dilatation . Consider this  example , a patient with chronic thrombo -embolic PAH presents with  acute deterioration  due to a transient arrhythmia  or  non cardiac  cause of hypotension . He is at  risk of being labeled as  acute pulmonary embolism  since he may  show   some thrombus  in his pulmonary circulation in  CT scan .  However ,  no great harm is done as long as he receives only heparin.



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