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Archive for the ‘echocardiography’ 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 !

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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Many modern  day cardiologists  consider  doing echo ,  a mean job and leave it to  technicians and fellows . Final report  often ends up with a cursory glance. The culture of reporting an  important aspect of LV  function is reaching a new low. It is common  to find the following terminologies  in  the  echo reports in many  parts of the country*     (Guess it is not used elsewhere ! )

  • LV function good
  • LV function adequate
  • Good bi-ventricular  function
  • LV function fair

what is adequate LV function

Among these , the term adequate LV function has caught  the  imagination  of young cardiologists ! Especially , this description  often appear in pre- operative  screening echo for non cardiac surgeries .

Recently ,one of my patient asked me what do we mean by adequate  LV function . I told  him it means nothing . . . it’s all  fancy words  !  but , generally  it is used to imply  normal LV function . . . I  clarified .

Think over for few minutes   . . . what do we  want to convey  by calling LV function  as adequate ?

Does it mean normal ?  or  Just less than normal  ?

If adequate LV function  is accepted ,  what is inadequate ?

Adequate for whom ?  For the patient ?  or  for the physician ?

Adequate  for daily activity  ?  or  Adequate to  with-stand  the proposed  surgery ?

Final message

Even  learned cardiologists indulge in this  term  frequently . This is  rather a fancy and unprofessional  way reporting LV function . They pass this  style to their residents  as well para medics .Adjectives  in medical science are not banished . . . but should be   judiciously used . In my opinion  the term adequate LV function should be removed from all echo labs .   Youngsters please  watch out.

Related links in this site .

LV ejection fraction fallacies

What is LV dysfunction ?

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Anterior mitral leaflet  has a classical M  shaped motion. Infrequently , M mode echo will record a triphasic pattern .

Triphasic AML motion

The exact  answer is not known . I guess it is a normal variant.

Often  it is recorded  when there is a long  and redundant AML , especially if the M-mode cut is too close to  the tips.

Though it is not common , I have seen in few the triphasic gets converted into classical M shaped pattern if the cursor is moved slightly away from the tip of AML.

Relationship to Heart rate

Some times it appears in slow heart rate and tends to disappear with tachycardia .

Triphasic Doppler filling vs Triphasic M-Mode

We do not know yet ,  how  the  triphasic AML motion  correlate  with triphasic Doppler filling pattern which  is considered a fairly good evidence for  LV dysfunction.

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Why should mitral  annulus gets calcified ? .  Degenerative  calcification can be benign in  elderly .  If it occurs prematurely (say < 55 years )   there is enough reasons to worry .  This may represent a systemic vascular inflammation and  is considered a surrogate marker for athero- vascular -sclerosis .  A study from Cidar Sinai  , Los angels  has well documented the link way back in 2003  !

mitral annular calcification mac cad link

This is a  large study involving  17 735 patients (who were investigated for symptoms of CAD )   were screened.

The incidence  of MAC was high (As expected !)

  • 35% > 65 years
  • 5 %  < 65 years
Angiography  revealed more surprises .
  • The incidence of angiographic  CAD among those who had MAC and no MAC   was  88% v68% respectively ,( p = 0.0004),
  • Left main coronary artery disease  was (14% 4%, p = 0.009)
  • Triple vessel disease  was (54% v33%, p = 0.002).
mitral annular calcification  www_drsvenkatesan_co_in

Image source  S.Atar ,  Heart 2003 : 89, 161-164

Conclusion
This study concluded ,  CAD is more aggressive in patients with MAC. It can  also be  an independent  predictor of  high risk CAD .
Further Implications  of MAC
  1. MAC is more common in women, especially diabetics .
  2. Degenerative Mitral regurgitation  is common ,rarely  mitral stenosis
  3. Recurrent VPDs and even  trouble some mitral annular VT is possible
  4. Extensive calcific lesions in coronary  artery is also reported with MAC.
Link between Stroke and MAC .
This was well proven by this paper  published in  NEJM in 1992.
MITRAL ANNULAR CALCIFICATION AND STROKE NEJM  EMELIA BENJAMIN 1992

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lsvc persisitence lsvc left superior vena cava

While 2D echo visualizes the LSVC , it is the color Doppler flow (in blue ) that confirms the flow going away from transducer towards coronary sinus .Please note , if the LSVC shows red flow it indicates the left vertical vein and the flow is from below up .This is supra cardiac TAPVC . It makes immense embryological sense to understand LSVC and and left vertical vein are both same entities only the connections are different .

Click over  for a high resolution Image

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VPDs are such a common cardiac arrhythmia . We also know most are benign .Still modern science demands to rule out structural heart disease in any patient with multiple VPDs.

When ventricles get irritated it reacts with VPDs . ( The irritants  can be anatomical , physiological or primary electrical)

Echo can detect only anatomical irritants .We are recognising  more such focus for VPDs . Hence idiopathic VPDs  may simply reflect our ignorance !  A focused  echocardiogram is  required .

The following conditions are often observed in patients  with recurrent VPDs

  1. Posterior Mitral annular calcification (Especially in women ) –Annular VPDs
  2. Aortic valve degeneration /Bicuspid aortic valve with calcification – Cuspal VPDs
  3. Mitral valve prolapse in young -Stretch induced  Pap muscle VPDs
  4. Minimal  pericardial effusions with adherent epicarditis
  5. LV false tendons-Stretch VPDs
  6. RVOT lipid focus -Subclinical ARVD
  7. LVH and Hypertension –Fibrotic VPDs    
  8. Asymmetric septal hypertrophy
  9. Scars in MI/ DCMs
  10. infiltrations in RCMs (Any Interstitial heart disease )

(Conditions 7 and 8 are  common disorders myocardium  just included to  complete the list )

**Please note ,above mentioned entites are anatomical irritants .There is a whole lot of physiological  irritants

that can induce VPDs .  ( Hypoxia, Excess catecholamines ,  K + fluxes ,  acidotic milieu etc ) .

*** Another group is primary electrical diseases inherited channel disease can induce VPDs

Also read

A crash course on ventricular ectopics

 

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Anterior  mitral leaflet (AML)  is an  unique structure  in the heart .It is the fastest moving structure inside the heart . It is the first structure visualised by echocardiogram by  Elder and Hertz in early 1950s .

While AML is known for vigorous motion , the PML motion is subdued . By tradition AML shows a  motion which resembles alphabet M .

But AML is not be taken lightly .  It can change it’s  motion  not only  in pathological states but also in health . One such  pattern is trifid   motion of AML . Following is a Echo Image in  a  perfectly  normal Individual .

mitral valve motion trifid m pattern  in m mode echocardiography

mitral valve motion in m mode echocardiography trifid

Possible mechanisms underlying Trifid motion of AML

  •    The plane of  M-mode cut  will change the  mitral valve motion .(May  be this is most common ).M-mode at tip of mitral valve may be trifid  ,however a little beyond may record a  bifid-M pattern .
  • Redundant  mitral valve
  • Mid diastolic AML drag
  • Signs of elevated   LVEDP
  • Finally ,  it could be a   sign of  mitral valve  fatigue after excrcise  . Some of these persons   revert back to M pattern after a brief period of  Trifid motion following exercise .

Does trifid AML motion  result in Tri-phasic doppler  flow as well ?

Mitral valve filling is classical E and A .

This usually correspond to M pattern of anatomical  AML motion .

Do the anatomy goes hand in hand with physiology ? Will the mid diastolic  AML  drag result in augmented flow ?

We are looking  at this phenomenon .

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