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Archive for the ‘Echo library and gallery’ Category

5 minutes crash course in cardiology : Echocardiogram in Pulmonary arterial hypertension

Posted in Cardiology - Clinical, Echo library and gallery, echocardiography, pulmonary hypertension, tagged , , , , , , , , , , , , , , on April 13, 2012| 1 Comment »

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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A 8 minute video crash course on diastolic dysfunction .

Posted in Echo library and gallery, echocardiography, Uncategorized, tagged , , on February 8, 2011| Leave a Comment »

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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5 minutes crash course on Ventricular septal rupture !

Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Echo library and gallery, echocardiography, myocardial disease, tagged , , , , , , , , , , , , , , , , , , on January 14, 2011| 2 Comments »

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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Rare encounters in echo lab : Abnormal right atrium and right ventricle

Posted in Echo library and gallery, echocardiography, Uncategorized, tagged , , , , , , , , , , , , , , , , , , on November 5, 2010| 3 Comments »

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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Rare encounters in echo lab : Left atrium

Posted in Echo library and gallery, echocardiography, tagged , , , on November 5, 2010| 1 Comment »

A young women  with Rheumatic heart disease .

 

LA aneurysm

Giant left atrium in rheumatic MS . http://www.drsvenkatesan.com

Mitral regurgitation is significant .www.drsvenkatesan.com

 

When do you call  a left atrium as   giant  ?  When it is referred to as  Aneurysmal dilatation ?

It is all semantics. Whenever LA becomes more than 6 cm ,  at least in two diameters  many prefer to call it giant .

In India , 6 cm LA is such a common finding , we have kept a  cut off at an  arbitrary 9 cm .

What factors determine a LA to dilate like a balloon ?

The exact mechanism is not known.It could be  the  intrinsic weakness of LA wall ,  as very few with RHD develop this. Many LAs resists dilatation even in the midst of extreme LA pressure. But , it is a well-known fact , mitral regurgitation provokes greater LA dilatation than MS alone .This implies volumetrics  play a major role than  pressure dynamics  in determining LA size. Acuteness of hemodynamic insult is  inversely proportional to LA size.

By the way, what is the purpose of  recognizing  the LA as Aneurysmal ?

  • In plain X -ray chest , LA may  form the right heart border  over shooting the RA.
  • When LA becomes huge  , there is a  chance for mechanical complications  like dysphagia, phrenic nerve , bronchial compression etc .
  • Giant LA invariably increases the chance of LA clot.

Electro-physiological Issues

  • Atrial fibrillation , a usual accompaniment of giant LA ,  is often refractory . There is no  purpose  to convert to sinus rhythm . In fact ,  one should not attempt this. There was a time when surgical incisions  ,corridors , mazes were quiet popular.Now it is believed all these are adding further injury to the ill-fated LA .Electro-physiologists should be restrained . Pulmonary vein ablation should never be attempted in such cases as the focus of AF is elsewhere .

Implication in cath lab

During PTMC LA size can be an issue  as the plane of IAS is distorted and make things difficult for septal puncture . Further the balloon , guidewire  may often slip  back into RA .

Implication for the surgeon.

For the surgeon the implication could be more. As a cardiologist I can’t comment about that .One thing we have observed is when LA becomes huge , the size of mitral annulus is too fictitious and funnily enough we have recorded up to 6 cm of mitral annulus . No valve is available for this size . We learnt from the surgeons ,   large LA  rarely pose a  problem as they suture the much  smaller valve in a larger annulus .(Which  makes the task  that easier )

Does the LA size regress after surgery ?

In many  it does regress  , in as many it doesn’t. We have seen giant LAs continuing to trouble the patient even after a successful mitral valve replacement.

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