Posts Tagged ‘acute pulmonary embolism’

Mconnell’s  sign is a distinct echocardiographic sign that occurs in Acute pulmonary embolism , where RA and RV dilates. RV shows a distinct regional wall motion abnormality in which RV free wall shows akinesia (or severe hypokinesia ) with well-preserved RV apical contraction.This is visible in apical 4 chamber view.

This sign is explained by  both anatomic  and hemo-dyanmic reasons.

  • RV when exposed to  sudden pressure overload  it not only dilates , it’s wall stress increases (Laplace law : Wall tension = P x Radius  )   and end up mechanically stunned . But , since the RV has a complex shape the distribution of this stress  is not uniform .As the RV assumes more spherical  shape the apical  part is not exposed to this stress as it tend to abut under LV.
  • RV apex is anatomically tethered with LV apex and share significant amount of circumferential fibres .In patients with acute pulmonary embolism ,  LV usually is hyperkinteic  due to tachycardia .This pulls the  RV apex  along with it for a proxy contraction .
  • Rarely , primary RV ischemia  due to RCA under perfusion* may be responsible for this unique  wall motion defect . Since RV apex  is mostly supplied by LAD it is free from ischemia . (*Acute elevation of RV intramural pressure due to PHT , compromising RCA perfusion pressure  )


1.McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996; 78: 469–473.

2. Rachel P. SoslandKamal Gupta,McConnell’s Sign circulation. 2008; 118: e517-e518

3. Link to the Echo clipping of McConnell sign in echocardiography




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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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Acute massive  pulmonary embolism is a dreaded medical  emergency  . In the past,  surgical embolectomy was the main option . Now , we have thrombolysis as a viable option.But , it does not work in all cases.* (90% success ?). It is critical to evaluate the success of thrombolyis , before embarking upon rescue embolectomy.

As it is often in critical care  medicine , this decision making is not easy .

The key question is how long , we shall wait before labeling  thrombolysis a failure !

In-fact , premature  assessment is the commonest cause for failed thrombolysis. True failure is different from deemed to be a  failure . This  is often related  to  , lack of patience  among  the   members of  treating team . Unlike acute MI ,there is not a  strict time window to  follow .The issue hear is ,  not lung salvage but  restoring VP/VQ and  dead space ventilation . The assessment is made , by clinical ,   MDCT ,Echo  parameters.

When there is difficulty in judging success , clinical parameters will prevail over medical images !


Key clinical parameters for monitoring

  • Heart rate
  • Saturation
  • Blood pressure

There are  four  options  available to manage in  failed pulmonary thrombolysis.

1.Emergency embolectomy in an unstable patient *

2.Elective , planned embolectomy  in a sable patient **

3.Repeat thrombolysis ***

4.Continue Intensive heparin regimen  for up to a minimum of   72hours  and up to a week .

*  Dismal outcome .

** Best option (Ironically,  these are the  patients , who improve  with medical  management , as well !)

***This is especially useful  when  partial success  is noted in a stable patient . ( For rescue thrombolysis it is  logical tom use TPA if SK was used initially and vice versa.) The logic here is the initial dose was  either insufficient or ineffective  to lyse the thrombus completely. If TPA is not available /or not affordable,  repeat SK can still be considered .It can be  safely administered within the 5 days of initial dose.

**** Least popular and considered inferior but has worked wonders in many .

How to manage a relatively  stable patient with a large thrombus load  in his pulmonary artery ?

Option number 3 could be tried. Prolonged  monitored heparin

What  are the surgeons concern about  management in failed pulmonary thromolysis ?

Every  surgeon( Especially  the  cardiac  surgeons)  loves  to operate in a stable patient . If you hand over  a case  for pulmonary  embolectomy  ,  with  sinking  O2 saturation  and  falling  blood pressure  ,the outcome can be  easily predicted !

Further, RV dysfunction  is notoriously known    for pump dependency  .  CT surgeons are vastly experienced   in  the intra operative tips and tricks of  managing  LV dysfunction (They may not be  in  so  in RV dysfunction !)

Bleeding risk  is also high especially  in the milieu of   intensive anticoagualtion and thrombolysis .

The mortality could be as high  as 30 % in many centers.


Final message

  • The incidence  of failed pulmonary thrombolysis  is  often subjected to the whims and fancies of treating physician  and the imaging modalities used.
  • Timing of assessment is critical .One need to give a long rope for medical management  , in spite of the urge , to do something more. .
  • Clinical improvement should be the main guiding force.
  • Normalisation of tachycardia   ,  improving  trend  of  o2 saturation(  >90-95%)  , regressing  RV size are useful parameters.
  • Thrombus load  detected by a repeat  CT scan  ,  need not be  the   sole guiding parameter.In -fact , mobilising these patients for CT scan by itself is fraught with a risk of  worsening the hypoxia.
  • The issue of  tackling the source of thrombus should  be addressed separately .Luckily, the same anticoagulant protocol takes care of this issue also. It is rarely a emergent issue.
  • Deploying an  IVC filter as an emergency procedure is a bigger controversy .At best , it is useful in few high risk individuals with high risk mobile ileo-femoral clots .
  • Finally, not every one can handle this  situation .Ideally such  patients  should be  to be  shifted to a well established cardiac surgical  set up .

From Chest journal


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There were days when acute pulmonary embolism(APE) was almost always  diagnosed  post-mortem. We are in the era , where we can recognise most of  the  pulmonary  embolism  without any difficulty.

Experience has taught us ,  when to suspect this dreaded  syndrome . Any  unexplained, dyspnea, hypoxia, tachycardia , syncope* with  vague chest discomfort  and  a predisposing condition (DVT , post operative  state ,etc) will make  acute PE highly likely .

*Postural dyspnea and syncope is a classical finding in many.

Pulmonary Echogram

We have  advanced  multi detector CT scans  and MR angiogram , V/P scans and pulmonary angiograms  to diagnose and confirm Acute PE .What we fail  to realise  is we also  have a simple bed side tool  called echocardiography   to  rapidly detect,  assess the pulmonary  anatomy and its hemodynamic  status.  In fact ,  we can visualize  the entire  MPA, and its  bifurcation and to  certain extent RPA,LPA. It is strange  physicians  always  ask for pulmonary  angiogram to diagnose APE , when we have a totally non invasive  pulmonary echogram available at the bedside .It can  rule out almost all cases of  massive pulmonary embolism with a good festivity and specificity .

How often Echo miss a Acute PE ?

Echo may fail to image a thrombus if it is distal but it is very rare to miss a thrombus in MPA, and its bifurcation. Most of the patients with  massive pulmonary embolism , are likely  have a thrombus in the bifurcation.

Even if  echo  fails  to image a thrombus , the effects of  acute  pulmonary arterial  hypertension on the tender walled  right ventricle  is conspicuous. In fact, the  effect of Acute PE on the RV morphology and function  is  the  single most important feature to suspect APE . This is also  considered as an indication for thrombolysis.

The following  Echo features  suggest Acute Massive Pulmonary embolism.Imaging these patients may be difficult especially if they are acutely  dyspneic   .Luckily , pulmonary  artery short axis view can be obtained even in supine position  in most of the patients.

  • RV dilatation ( One popular criteria is End diastolic RV dimension > LV end diastolic dimension .It should be remembered ,  strict criterias  can not be followed in this high risk medical  emergency . Visual estimation of RV size is equally important.If in the para sternal long axis , RV is > 3cm it is significant . The only issue is, in patients with preexisting  COPD  RV size will not be useful to diagnose APE.
  • RA dilatation (this is also a usual accompaniment )
  • RV wall motion defect(Considered , as  RV SOS calls !)
  • Paradoxical septal motion
  • D shaped septum is  an absolute sign of distressed RV.
  • Tricuspid regurgitation(This depends upon the leaflet length and orientation, some may not develop in spite severe PAH )

Less common features

  • Pulmonary  regurgitation
  • RA , RA appendage , IVC ,  RV clots

Diagnosing  RV hypertension

TR jet

MPA  acceleration  time (Not useful in an emergency situation )

Other thinks to look in Echo

  • LV function (Hypoxic  dysfunction  or associated CAD )
  • IVC for  thrombus source .
  • IAS anatomy : PFO may increase the chance for stroke as these patients carry the risk of further  embolus. When the RVEDP, RA mean pressure raise to APE, the PFO becomes hemodynamcially patent and may develop propensity to shunt the incoming thrombus to left atrium rather than right ventricle  as LA pressure is considerably  less than RV

Unanswered questions

At what  pressure RV begins to dilate ?

This is not clear.The response of RV ,  to pressure overload is  not constant.  In acute raise of RV pressure ,RV tend to dilate  , while  in chronic PAH RV hypertrophies and dilates .It is  believed   , the first signs of dilation begin , even with a 30mmhg of PA pressure . So ,  even minor dilatation could become important in acute PE.

Can RV dilatation alone  , be taken  as evidence  for hemodynamic instability ?

Yes , but realise  ,  clinical , hemodynamic instability  is much more important than degree of RV dilatation  (Hypotension /hypoxia  )

The curious behavior of RV and TR jet in APE ?

Normal peak RV pressure is 25-30mmhg .In acute pulmonary  hypertension RV pressure is supposed to raise . But it does not always happen.It all depends upon how the RV respond to the sudden raise in its afterload.

Some RVs fight vigorously and take on the challenge  imposed by pulmonary  embolus.These are the  patients  who show strong TR jets which may reach 60 mmhg. More  often , the RV  is stunned and overwhelmed  by the unexpected sequence of events and  lose the battle from the beginning  .They become  flabby  and dilated.These  patients  do not  show any significant TR jet ,  in spite of raising PA pressure. This implies,  a  good TR jet > 3.5 could  virtually rule out  severe RV dysfunction.

(One  popular thought gaining ground is  , the primary determinant of   pulmonary artery  systolic  pressure  in Acute PE is the RV contractile force ,  rather  than pulmonary  impedance .)

Hypotension is common in APE .What is  the relationship  between PAH and systemic blood pressure ?

  • Inverse relationship is expected . This often result in syncope in these patients.
  • Bernhiem effect
  • Hypoxic LV dysfunction

Final message

RV  faces the brunt of the  hemodynamic attack of acute PE. .Differentiating simple RV involvement  from RV dysfunction  is a difficult and subjective  exercise. But ,  it need to be done accurately as  RV dysfunction becomes an indication  for thrombolysis  . RV dilatation  , wall motion defect, mild PAH, all  indicate RV dysfunction . Diagnosing RV dysfunction is  better  done by the  treating physician who has the  overall clinical data.

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Acute pulmonary embolism is a vascular  emergency.Massive pulmonary embolism needs immediate thrombolysis or embolectomy. Success rate  of  thrombolysis  appears good . But , the symptom improvement  is slower .

Sterptokinase is the commonly used drug to dissolve the pulmonary thrombus  . (Except in USA , where they  prefer the much costlier TPA )

The sterptokinase  adminstered with the following protocol

  • 2.5 lakh Unit bolus over 30 minutes
  • Follow with 1lakh unit /per hour for the next 48 hours (Up to 72 h)

When to start Heparin infusion ?

For TPA ,  there is no confusion .Heparin must be started immediately after the completion of TPA infusion (100mg in 2 hours)

Cardiology community is divided for heparin protocol with  streptokinase. Because , streptokinase is administered over 48hours it is thought heparin is not required during  this period.But in reality , it  implies , we  deny a role for this  powerful anti thrombin  in the critical hours of ongoing  intra vascular clotting . Hence  logic demands  to start heparin  along with  streptokinase.

There is further concern that,  the dissolved thrombus generate pro coagulant  debri , that will negate the benefits of thrombolysis. Oral anticoagulants  are supposed to be started  as soon as the diagnosis  of pulmonary embolism is made. In that case , heparin will be required  much earlier as  warfarin has to be overlapped with heparin.

We would  argue for  , a careful simultaneous infusion of heparin (May be 500units/hour ) .Strict monitoring of APTT is warranted.

What does the clinical  trials say ?

There are few studies address this specific issue .I am still searching the data base. Once i get it i will post it. The readers  may also try to find an answer .


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Pulmonary embolism is  one of the  important  causes of acute chest pain . It can mimic  acute coronary syndrome . In fact along with aortic dissection  , it forms  a  differential diagnosis for STEMI especailly if the ECG is not typical.

pulmonary embolism chest pain dvt d dimer ventilation perfusion

The Chest pain of acute pulmonary embolism can originate in one of the following structures  with different mechanism

  • Lung parenchyma ( Necrotic pain ?)
  • Pluritic pain in adjacent necrotic segment
  • Main Pulmonary artery and it’s branches
  • Right ventricular mechanical stretch
  • Right ventricular ischemia
  • Hypoxia induced LV ischemia with coexisting CAD.
  • Multiple contribution from any of  the above *

It should also be remembered , medicine never respects logic, as some times  an episode of pulmonary embolism can occur without any chest pain

Localisation of chest pain

One can imagine ,  how difficult for the  nervous system to zero in on the origin of this  pain as  the structures involved in acute pulmonary embolism are in different planes  and in different depths  within the chest cavity . Patients  often complain vaguely  the site of pain but  what is universal is severe resting pain deep within the chest . If the ischemic lung segment  transmit pain signals , the location and radiation depend on the  bronchpulmonary segment involved.This again adds on to the complexity in the  genesis of pain  .It can be virtually any where in the back or front of chest.

But , the central and retrosternal chest  pain are equally common as invariably the central pulmonary arteries go for a acute stretch which can be severely painful .In fact , current thinking is it could contribute maximum  for the intensity of chest pain. Similarly,  acute dilatation of RV result in mechanical pain. RV sub endocardial ischemia may   also contribute .An intact bronchial  circulation( From aorta)  can limit the  ischemic lung pain .

Final message

Analysing  the chest pain of acute pulmonary embolism can be an  interesting academic exercise . It could arise from multiple structures with different mechanisms. It may not be much significant with  reference to management . But it has a diagnostic role.  A pain which is severe , and  atypically located should raise the suspicion of acute PE especially  if the patient has associated dyspnea.

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Salvaging lung tissue is not the aim in pulmonary embolism , Hence Time window is a myth !

There is a time window for thrombolysis in myocardial infarction ( STEMI). This time window is to salvage myocardium before it dies.The average time window in STEMI is 12 hours. When does the lung start dying in Pulmonary embolism ?.Is salvaging lung tissue an aim in the management of pulmonary embolism ?. Not really .Lung parenchymal death occurs only in minority of patients with pulmonary embolism .

The bronchial artery continue to supply the lungs.

So the aim here is to restore pulmonary circulation and oxygenation. Hence there is no strict time window in the management of pulmonary embolism.

The General consensus is , one can attempt thrombolysis up to 7 days after diagnosing pulmonary embolism.

Beyond this time, it is believed thrombus gets organised and thrombolytic agents may be ineffective.

But this is only an assumption, in an individual patient thrombolysis may be done even beyond this period if warrented by clinical intuition .

Dr .S.Venkatesan .Madras medical college, Chennai.India .

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