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Archive for the ‘Echo library and gallery’ Category

Here is a patient with class 3  dyspnea  who was referred  for echocardiography

X ray chest showing cardiomegaly

         Moderate TR due to dilatation of tricuspid annulus.This patient had dilatation of all 4 chambers of the heart.LV EF was 24 %

Right ventricular dysfunction is major determinant of  clinical outcome in patients with dilated cardiomyopathy. The  myocardium of the  entire heart is now known to be a single sheet of muscle rolled into different chambers . So any primary disease of myocardium will involve the entire musculature . This is the reason  , all the  4 chambers of heart goes for dilatation in  primary cardiomyopathy . Of course there can be minor variations  due to differential hemodynamic impact.

But it is certain ,  RV  function will definitely be compromised  In  most patients  with  Idiopathic DCM (Less common in Ischemic DCM ) Rapid assessment of RV function is difficult  . Of course We have some clues .

2 d Features

  • Simple dilatation  of RV is suffice to say it is struggling with the  loading conditions
  • Septal bowing
  • Tricuspid annular dilatation
  • RV ejection fraction (Continues to be complex for routine usage )

TR jet

  • Dp/Dt
  • Morphology may be useful (Mainly for TR severity )

Tissue doppler

  • TAPSE
  • RV strain rate Imaging etc.

And  now  , we have observed a new echocardiographic  sign   ie  TR jet alternans  in patient with  DCM .

Note the changing TR velocity implying severe RV contractile dysfunction.

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The principles of pre-discharge EST  

This concept came about 20 years ago (1980s) to risk stratify patients following  ACS to triage early coronary angiogram and revascualrisation. Generally patients are discharged by 5-7 days after an MI  (May be  3-5 days in some hospitals)  . Doing an exercise stress test  early within  2 weeks has not been very popular with many cardiologist even though it was recommended by many guidelines.The type of stress recommended  here  , is heart rate limited sub maximal 70% of  THR (Usually around  140 /mt )  is performed . This is due fear of precipitation another ACS.

Still,  there are definite  advantages for  pre-discharge EST .It help us  identify  high risk  subsets of  STEMI and reduce the  intermediate term mortality .More importantly it  gives  us an opportunity  to  exclude  inappropriate  revascualriations  even without an angiogram . (The well known coronary dogma  ie  if a post STEMI patient performs > 10  METS ,  his  heart carries little  risk  for  future events  still holds good  !)

With the advent of liberal usage of CAG and improved techniques of revascularistion ,  most  patients  directly undergo pre-discharge CAG rather than EST !

Further reading

Does any cardiologist have guts to do a pre- discharge EST after  a successful primary PCI ?

Read a related article in this blog .

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I stumbled upon this image from the Heart journal. A good depiction of  IAS aneurysm in three dimension.

Image courtesy  : Heart 2012;98:79-88   Three dimensional echocardiography in congenital heart disease   by  Joseph John Vettukattil

Further  reading

Clinical implication of IAS aneurysm

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Echocardiogram in pulmonary HT has many aims .

  •  Identify the etiology
  • Assess the effects of PAH  on the right heart
  •  Estimate the severity of PAH.
  • Possibly prognosticate

Echo helps us to confirm the valvular, myocardial or congenital heart diseases in the evaluation of PAH. Apart from these etiological diagnosis of PAH predominantly lies in a systematic medical work up .(Read Dana Point classification )

2-D features

  • RA RV dilates
  • RVH*may occur (Dilation is more common )
  • IVS assumes  a D shape  ( RV pressure is close  to or   even > than  LV pressure )
  • Tricuspid annulus dilates

* For some reason RVH  does not occur commonly in pulmonary hypertension ,  while LV hypertrophies promptly in systemic hypertension .

Doppler

  • Tricuspid valve begins to leak  and RV ejects   with giant “cv”  waves into RA/JVP

Other Echo  findings

  • MPA may dilate
  • Pulmonary regurgitation

At what pressure RV begins to dilate  in PAH ?

It is  not known .It is highly variable . But most will dilate their RV at a systolic pressure > 50mmg.

It is also possible the onset of TR and the magnitude of  TR has a major say in the  timing  of RV enlargement .

We know RV is more sensitive to volume overload than pressure overload .

Paradoxically , it is often observed   acute elevation in RV pressure  dilate the RV faster than chronic ones.

Right atrium and right ventricle are significantly

The tricuspid annulus is dilated .Note the severe TR with twin jet morphology.

Estimating Pulmonary artery pressure

PA systolic pressure  :  TR jet + 10 mmhg

PA diastolic pressure : PR end diastolic jet + 10

PA mean pressure  :  Peak PR gradient

Other complex methods to arrive ar PAP in the absence of TR or PR

The Dabestani -Mahan  ‘s equation*   – The  mean PA pressure = 90 – (0.62 X acceleration time).

It is popular   for  calculating PAP by measuring pulmonary artery Doppler  acceleration  time  .

Many   believe  it is  neither  sensitive  nor practical  in real  clinical setting.

*Even though Dabestani is the first author of this paper   Mahan  got the full credits for the simple reason his name is easily remembered   !

Note the peak TR jet is around 50mmhg and predicted RVSP would be 60mmhg.One would have expected still higher RV pressure but since the RV is dysfunctional the true PAP may be underestimated.

The classical D shaped IVS during systole . D shape indicates RV pressure during systole is almost equal or even higher than LV. ( Please recall D shape occurs in Volume overload also but the timing is in diastole !)

Pulmonary valve  M-Mode

According to Wyeman  the following M mode signs are useful in diagnosing PAH.

  1. Presence or  absence and the amplitude of the “a” wave
  2. magnitude of the e-f slope
  3. presence of mid-systolic closure or notching
  4. fluttering of the posterior pulmonic leaflet

Currently ,  one may consider M-Mode echo to be  an obsolete  ,  but still the foundations help us understand the hemo-dynamics.

The most important principle in  the motion of  pulmonary valve ,   is  the relationship between pulmonary “a” wave and right atrial “a” wave

Normally atrial contraction produce an inward movement* on the closing pulmonary leaflet . This  happens because the MPA  end diastolic  pressure is usually lower than  right atrial a wave    .In severe PAH  the elevated pulmonary diastolic pressure  does not  allow  the atrial contraction to   intend the pulmonary leaflet in pre-systolic atrial contraction .Hence pulmonary valve  a wave in m -mode  is  diminished or even absent .

In PAH even   premature closure of pulmonary valve may occur resulting in mid systolic notch   .This  is referred to as flying “W” -Mid systolic notch.   (See below)

* The motion  we see in  short axis M-Mode is that of   left pulmonary cusp that moves  posteriorly.

Image source : Karmarkar SG. Pulmonary valve echocardiography. J Postgrad Med 1979;25:219-23

Absence of a dip is a hemo-dyanmicaly important sign pf PAH  but with one important caveat  .This absence of a dip is valid  only until RV failure occur.In th presence of elevated RVEDP a begin to appear again

Reference

1 Karmarkar SG. Pulmonary valve echocardiography. J Postgrad Med 1979;25:219-23

2.http://circ.ahajournals.org/content/50/5/905.full.pdf

4.Kitabatake A, Inoue M, Asao M, Masuyama T, Tanouchi J, Morita T. et al. Noninvasive evaluation of pulmonary
hypertension by a pulsed Doppler technique. Circulation. 1983; 68(2): 302-9.

5.Stevenson JG. et al, Comparison of several noninvasive methods for estimation of pulmonary artery pressure. J Am
Soc Echocardiogr. 1989; 2: 157-71.

 6.Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patient  with tricuspid  regurgitation. Circulation 1984; 70:657-62.

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We have thousands of  medical videos.When I stumbled upon this  one  ,from you tube which  I thought  will be immensely useful and   is crisply made.

It  proposes a 5  simple rules  to diagnose diastolic dysfunction .There is  also a new concept* discussed in this  video .

* What is super normal diastolic function ?  How can it be mis- interpreted as a pathological ?

Over to the video clip from  (123sonography 0

http://www.youtube.com/watch?v=qdLkbcFe_DI&feature=related

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We know,  electrical deaths constitute the bulk of sudden cardiac deaths in MI.  Mechanical deaths due to pump failure, muscle rupture , valve leak , also cause significant deaths   .(Surprisingly many of the mechanical deaths   may also   fulfill  the sudden death criteria !)

Free wall rupture is  invariably a fatal event. Papillary  muscle trunk  rupture  leads to severe LVF and unless intervened sure to result in fatality.

The ones who tear their interventricular septum  are some what blessed ! Here ,  the rupture does not result in instant death as there is  no loss of blood ,   instead , there is an  volume over load of right ventricle  followed by the  left ventricle  after a  few beats. Hypotension is the  rule. Even though this is a major complication there is something about  VSR which makes it unique.

Sudden giving way of IVS has  a decompressing effect on the ailing left ventricle.This many times  bring a  temporary relief to LV and if the patient survives the first few hour he is likely to stabilise  further . In fact , sudden deaths within 24hours after the onset of VSR is an exception.This defect always gives the cardiologists and surgeon some time to plan the management. We need to use this time judiciously.

The natural history is delicate . Five themes are possible

  1. Very unstable Instant death( Fortunately a  rare theme )
  2. Unstable – Deteriorating further
  3. Unstable to Stable * fit for discharge even without surgery
  4. Stable from the onset and  continue to be stable* .
  5. Stable to Unstable (Probably the most common theme )

* Pleasant themes occasionally witnessed !)

Here is 55 year old women came with extensive anterior MI with lower septal rupture.(She belonged to type 3 of the above scheme)

)

Note the septal rupture is visible even in 2D Echo

 

Color flow showing significant shunting from LV to RV.This shunt depends upon the LV contractile function, LVEDP and ofcourse the RV pressure

 

If there is severe RV dysfunction or bi ventricular dysfunction flow across the defect is inconspicuous.Brisk left to right shunting may be an indirect marker for good LV systolic function and absence of significant pulmonary hypertension.Both imply a better outcome.

The main determinant  of survival is the  underlying LV dysfunction and associated co morbidity(Renal function ) and complications .

Infero -posterior ruptures tend to be complex and  may have multiple irregular tracks  that makes it difficult to repair.

Investigations

Echo cardiogram is the mainstay .Serial echos should be done to assess the mechanical function and the progress of VSR.Hemodynamic monitoring may be done without injuring the patient .

Medical management

  • Often supportive , but  effective . Dobutamine infusion can maintain a life for few days.
  • Paradoxically , LV dysfunction and elevated LVEDP restricts volume overloading of VSD.
  • Associated MR, Arrhythmias  need to be taken care of .

Surgeons role

  • Very Vital.
  • Experience counts.(Individual as well as  Institutional )

Timing of surgery

Continues to be a controversy . Surgeons love to operate in a stable patient. But they need to realise , surgery is often needed to stabilise  many  patients. . The issue of tissue friability  is blown out of proportion in the literature .When a  life is  is at danger we can not worry about  friable tissues !

The rule of thumb could be

  • Operate as early as possible in unstable patient.
  • Post pone surgery in stable patient as late as possible ( Late here means . . .elective non emergent surgery )

Surgical options

  • Simple VSR closure without  knowing coronary anatomy
  • Simple VSR closure after knowing coronary anatomy
  • VSR closure with CABG ( total revascularization)
  • VSR closure with partial revascularization

In our experience  each of the above , has a role in a given patient depending upon the logistic , financial , social and even  the available expertise. (A good surgeon in bad Institution !)

Is coronary angiogram mandatory  before attempting to close VSR ?

Logically yes. If it is not available  just do not bother .  But, many times , when issue is saving lives , we can not afford to be too scientific , many lives have been saved by not following  such strict  protocols .A simple emergency  thoracotomy and closure of rupture site (Without even touching the LAD ) can be a distinct  and viable option in  a selected few .

Role of cardiologists

Contrary to the popular belief the role of cardiologists is minimal , except  to prepare  the patient and hand over to the surgeon.

Interventional approach to close  a VSR  is currently  be termed as an  adventurous option ! The VSRs  can assume unpredictable shapes  and the  tears can be multiple  in  different planes. The devices , catheters and  other hard ware are not specifically made to tackle these  issues  .An acquired VSR  should never be compared with congenital VSD.

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A female child aged 14 was referred for progressive breathlessness  and  abdominal distension

Abnormally dilated right atrium with significant pericardial effusion .www.drsvenkatesan.com

Can you guess the diagnosis ?

Apart form RA ,RV dilatation , the RV apex is seen filled with coarse treabeculations.This is believed to be a type of non compaction http://www.drsvenkatesan.com

Still difficult to conclude  ?   Look at the following Image.

Tricuspid regurgitation is significant . http://www.drsvenkatesan.com

If you have thought  . . .

  • ASD with TR
  • Severe PAH/COPD
  • RV cardiomyopathy

All are  acceptable  differential diagnosis

But the real diagnosis is none of the above .

Need  more time  . . . the following   Doppler tracing  will settle the issue !

Doppler velocity in RVOT at 88mmhg. http://www.drsvenkatean.com

The final diagnosis was . . .

  • Severe valvular pulmonary stenosis
  • Marked RV,RA dilatation
  • Acquired non compaction of right ventricle
  • TR -Moderate
  • Pericardial effusion -Moderate
  • This patient also had dilated IVC, Hepatic veins that  lead to clinical ascites.

Here , RV functional assessment becomes vital , but it is difficult many times. A simple clue is , as  the RV is able to generate 88mmhg pressure it implies ,   the   contractility  should be near normal .

RV EF %,  RV Dp/Dt , Tricuspid annular motion by  tissue Doppler are additional measures. Cine MRI can be a useful investigation prior to intervention.

Final message

  • VPS is a common acyanotic disease. Most are benign  and  milder  forms are the rule.
  • Dysplastic valves preclude balloon valvotomy. (In late stages   little  difference between dysplastic / non dysplastic VPS is noted  )
  • Severe progressive VPS  , like in this patient needs immediate balloon dilatation or surgery.
  • Long term outcome  is excellent except in advances cases where irreversible RV dysfunction sets in.

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