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Posts Tagged ‘rv infarction’

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 !

Reference

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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Myocardial infarction (STEMI)  occurs in two distinct arterial  territories .The anterior LAD circulation and postero- inferior RCA/LCX circulation.The incidence is equally shared.

There has been some  learned and unlearned perceptions about Inferior MI.

Inferior MI is less dangerous than anterior MI.  True or false ?

Answer: Essentially true in most situations.

Reasons.

Inferior wall of the heart (strictly speaking there is no walls for heart , only surfaces , which blends with adjacent areas)  inferior wall  is formed by diaphragmatic surface and posterior surface.Inferior MI can occur by either RCA or LCX obstruction.The outcome of inferior MI is determined by mainly by  the extent  of   LV myocardial   damage it inflicts.To  quantitate this  we need to know , how much of LV is supplied by RCA , or LCX or combination of both ? This depend on the coronary dominance .It is estimated , the bulk of the LV is supplied ( up to 75%  ) by LCA. This becomes further high in left dominant circulations . In fact , it is believed LV can never get involved in non dominant RCA occlusions. This has brought in a new terminology  called “Small inferior MI”.Inferior STEMI due to PDA  occlusion or in a co -dominant circulation is not yet studied

Apart from the above  anatomical considerations the following clinical observations  have  been made regarding inferior MI.

  • When thrombolysis was introduced , many studies  suggested the the ST elevation in inferior  leads toched the isolectric levels  in most situations even without thrombolysis.Technically, this implies spontaneous , successful thrombolysis are more common in RCA. Among the thrombolysed ,persistent ST elvation is a rare phenomenon.
  • The well known difference in the conduction defect between anterior and inferior MI  is an important contibutor for better outcome in the later.(AV blocks in inferior MI , are often transient, non progressive, supra hisian location rarely require permanent pacemakers)
  • During acute phase cardiogenic shock occurs in a minority (That too , only if RV shock is included )
  • Even in the follow up the ejection fraction in inferior MI is  almost always above  40%. In many EF is not affected at all.
  • Progressive adverse remodelling of LV is rare

When can Inferior MI be dangerous ?

Anatomical factors

Inspite of the  above  factors  inferior MI can not be taken lightly . Especially when it  extend into posterior, lateral , (Rarely anterior) segments.

While  posterior extension  is often  tolerated , lateral extension is very poorly tolerated .This is probably explained as  the extension involves the vital free wall of LV and the laplace forces could precipitate LVF. Free wall rupture is also common in this situation.

Posterior extension , predominantly involves the surface of RV which is less important hemodynamically. Of course incidence of MR  due to it’s effect on posterior mitral leaflet can be trouble some.

inferior MI ECG

High risk clinical catagories.

Out of hospital STEMI  are at  equal  risk irrespective of the territories involved  .This is because,  primary VF does not differentiate , whether  ischemia comes from RCA or LAD .

  1. In elderly , dibetics and co existing medical condtions  the the established  benign   character  of  inferior MI disappear, as  any  muscle loss  in LV has equally adverse outcome.
  2. Even though  inferior MIs are immune  to cardiogenic shock  , a equally worrisome  prolonged hypotension due to high vagal tone, bradycardia, plus or minus RVMI can create trouble. Fortunately , they respond better to  treatment. Except a few with extensive transmural RVMI outcome is good.
  3. Presence of  mechanical complications of  ventricular septal rupture , ischemic MR can bring  the mortality on par with large anterior MI.

How different is the clinical outcome of infero-posterior  MI with reference  to the  site of  coronary arterial  obstruction   ?

The sequence of  outcome  From  best to worse  : Non dominant RCA* → Dominant RCA but distal to RV branch → LCX dominant with large OMs

* It is believed   an  acute proximal  obstruction of a  non dominant RCA may not be mechanically significant, but can be electrically significant as it retains the risk of primary VF and SA nodal ischemia. The ECG changes  can be very minimal or  some times simple bradycardia is the only clue. One should be able to recognise this entity (Non dominant  RCA STEMI)  as the outcome is  excellent and these patients  would never require procedure like primary  PCI

** A inferior MI due to a dominant LCX and a large OMs have comparable outcome as that of extensive anterior MI. The ECG will reveal ST elevation in both inferior and lateral leads.

***In patients with prior CAD  and collateral dependent  multivessel disease  the  inferior anterior sub classification does not make much sense as  entire coronary circulation can be mutually interdependent.

Final message

Inferior STEMI  generally lacks the vigor  to cause extensive damage to myocardium in most situations .Further they respond better to treatment. Risk stratification of STEMI based on the location of MI has not been popular among mainstream cardiologists. This issue needs some introspection as  the costly and complex treatment modalities like primary PCI  is unwarranted in most of the low risk inferior MIs.

Related posts in my blog:

1.Why thrombolysis is more effective in RCA?

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