Posts Tagged ‘massive pulmonary embolism’

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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