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Can VF be a non sustained  arrhythmia ?   This question was raised and a single case report was presented

in the annual scientific sessions of  Cardiological society of India Meet in  year 2008 in  Chennai.

I am just reposting it from my archives .

Slide1 Slide2 Slide3 Slide4 Slide5 Slide6 Slide7 Slide8 Slide9 Slide10 Slide11 Slide12 Slide13

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Sinus node is the electrical high command of our heart .When it gets injured  seriously (or shot down   as in sinus arrest ) there is utter chaos in the lower ranks !

This is what happened  in this patient .

trigeminy group beating vpds sinus node dysfunction escape capture

The lower pacemkers can either passively release  themselves as escape rhythm or actively fire with a  ectopic focus  . Any combination of escape / ectopic  beats can  occur .If occasional sinus beats capture the ventricles things  can become further complicated .

It is obvious , this  random intra-cardiac  shooting  makes the life of the  myocardium miserable . It is a perfect setting for syncope, tachcyardic cardio myopathy , extreme brady induced VT , VF  even SCD.

*Meanwhile , It is  heartening to note  SND   rarely lead to  sudden death in spite of all the chaos .However  extreme  bradycardias  that occur in  complete heart block  does  not enjoy this immunity as fatal complications are common if not intervened .

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The irony of modern medical care is  9/10 times  medical negligence is  defined in terms of  acts of omission  in  required  level of care . In reality  most medical negligence acts are related to knowingly overdoing a futile diagnostic or therapeutic modality.

This irony was never understood by the public, the professionals or  even the judiciary .This remains  the most dangerous issue  facing modern medicine !

Finally some light is appearing in the horizon . A Missouri  Cardiologist is suspended for overdoing things he knows best  . . . namely coronary stenting ! 

This may bring chills over many cardiologist’s spine .

cardiologist stents inappropriate use interventional

http://www.stltoday.com/news/local/metro/missouri-healing-arts-board-issues-first-emergency-suspension-of-doctor/article_205eaffd-1825-5d7d-a9de-a289c010fd65.html

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Current prescribing information cautions clearly Prasugrel should not  be used in TIA  or recent  stroke (Even in  ischemic strokes -Embolic included !)

The warning  is perplexing and illogical to me.

What is your take ?

I would imagine the following  could be  the reasons.

Prasugrel  as an  antiplatlet agent is  many fold  powerful and could convert all  strokes into hemorrhagic one .

Does Prasugrel convert a TIA into stroke instead of curing it ?

Prasugrel may worsen the stroke  in case the TIA is going to end up as stroke.

Is there any thing called hemorrhagic TIA ?

Since we do not have any mechanism to diagnose Ischemic TIA from hemorrhagic TIA ,  it is better to avoid Prasugrel . It is still a mystery ,  why  clopidogrel which acts on the same receptor and can be safely given for TIA ( pro actively)

After thought

I think Neuro physicians must answer this question . ( Cardiologists  better limit their extended geographical terrain ! )

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Answer

Each of the above can be important in diseased heart .The most important component seems to be Inter- ventricular  synchrony .This is closely followed by AV synchrony .In dysfunctional  ventricles Intra-ventricular  synchrony  also becomes important .In  structurally  normal hearts  none seems to be important  (This statement can be debated  )

VVI pacemakers causes  both AV  and Inter-ventricular (VV ) dys-synchrony

DDD pacemaker  may still  induce  Inter-ventricular ( VV ) dys-synchrony  whenever  RV is paced for any reason .This may happen up to 60 % of pace making time in real world.

Some more facts

*Chronic VVI pacing may  induce adverse  remodeling of both atria and may worsen LV dilatation. In contrast isolated chronic organic LBBB is well tolerated and with paradoxical septal motion rarely worsen the LV function.

**Please note the paradoxical septal motion , which is  noted in  all LBBBs is  same as inter-ventricular  dyssynchrony .

***Inter atrial synchrony is a less discussed issue .It becomes  important in diseased atria which manifest gross   intra atrial conduction blocks  , atrial inhomogeneity and AF .Onset and offset  of AF has a major impact in the way DDD pacing is going to fire .

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This is an ECG of a 42 year old man .He was reported as  Left atrial  enlargement (LAE) and was referred for  echocardiography . His echo was normal . LA measured 2.5 X 3.1 cm .The consultant  called back the echo lab ,  to verify   the left atrial dimension .He thought he was very sure of LAE .It took  considerable time to convince him about the credibility  of the echocardiographer . He was  right after all  . . . still . . .  ECG was  also looked  convincing  for LAE !

left atrial  enlargement by ecg limitations sensitivity

left atrial  enlargement by ecg limitations sensitivity  echo la dimension

                         Is this phenomenon  of wide P wave with normal atrial dimension  common ?

Yes it is . It  underscores  poor sensitivity of ECG in the  diagnosis  of LAE .The P wave abnormality in the above patient is due to Inter atrial block (IAB ) . This widens the p wave .

What  are the types of Inter atrial block ?

inter atrial block europace 1999 de luna

 

P wave widening is not synonymous with LAE .(Here P waves  widened   due to sluggish inter nodal pathway and inter atrial pathway .It is something like QRS widening in  bundle branch blocks  )

Final message

IAB is an important differential diagnosis for LAE . The significance of which is not entirely clear . It  is possible  IAB   precede LA enlargement  .It can even trigger AF due to  inhomogeneity.

Even though IAB was reported in 1950s  (Puech P* ) ,  it was  rarely  considered important With  increasing incidence of atrial arrhythmia in aging population , IAB is expected to  come into the lime- light again . The sophisticated electro anatomical mapping  can unravel the mysteries surrounding this entity .

Reference

INTER ATRIAL BLOCK

*Puech P. L’activite´ electrique auriculaire normale et pathologuique. Paris: Masson, 1956; 206.

http://www.jecgonline.com/article/S0022-0736%2812%2900227-0/abstract

http://europace.oxfordjournals.org/content/1/1/43.full.pdf

Bachman bundle branch block

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We always look at the thickness of  Inter ventricular septum for LVH . The Normal IVS thickness is up to 11 mm in diastole .  LVH is definite if IVS measure > 11 mm .It is  certain if it is > 12mm . But , we need to realise LVH by definition is not simply wall thickness .

It is increased LV  mass .

LV mass can increase without wall thickening . This is  referred to eccentric LVH . For example in chronic  volume overload  states  (or even DCMs )  LV mass may increase without septal thickneing .

Final message

LVH is possible without IVS thickening .

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Guidelines are meant for simplifying  cardiologist’s life  as well as  ameliorating   patient suffering  . It should also  ensure  improving overall  outcome   with  efficient  use of human resources and  economy .

acc aha guidlines stemi 2013

These guidelines  are written from sophisticated centers  mainly for consumption  in developed countries .Though core  concepts will be same , many recommendations are neither possible nor desirable  at the exact point of delivery  in  less developed countries . Please remember these guidelines are not binding on you .Physician discretion is the ultimate principle in medicine.

So ,  let us read these guidelines apply our mind and try to  indigenise . Get maximum out of it  for the respective population .

Some  of the highlights in this 2013  guidelines
1. Therapeutic hypothermia should be started as soon as possible in comatose patients with STEMI and out-of-hospital cardiac arrest caused by ventricular fibrillation or pulseless ventricular tachycardia, including patients who undergo primary PCI.31–33
(Level of Evidence: B)

2 . Presumed or New onset  LBBB is no longer a Indication for emergency reperfusion

3 . Indication of Primary PCI has the following modification

Primary  pci Guideline in  2013 aha guidelines

Reference

http://circ.ahajournals.org/content/early/2012/12/17/CIR.0b013e3182742cf6.full.pdf+html

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Right ventricular function assessment has always been difficult in view of it complex shape and limited imaging planes in echocardiography .

Recently , we learnt tricuspid annular motion can give  a quick assessment of  RV function . This was accomplished by M-mode echo of tricuspid annulus. (TAPSE)  tricuspid annular plane systolic excursion . This simple parameter has  brought the  maligned M mode echocardiography into limelight again.

tapsee rca motion by coroanry angiogram rv systolic function tricuspid annulus motion right av groove atrio ventricular grrove mapsee m mode echo

Currently coronary angiogram is done just like a non invasive echocardiogram across the nooks and corners  of any country

Modern day  cardiologist is expected to  look  beyond the coronary artery  narrowing  when reading coronary angiogram.  If only we give little importance to how the coronary artery moves with  reference to  cardiac cycle we can  get  excellent information about  mechanical properties of heart.

Every cath-lab  work station has a DSA mode . With this one can measure the coronary artery swing and document   it  objectively  .Right coronary artery swing  faithfully reflect  RV longitudinal function . This motion is more accurate than the TAPSE by echo . We have found the normal excursion to be 15-20mm (Slightly  lower than TAPSE) . Similarly LCX motion give us an estimate of longitudinal LV function and LAD motion can tell us how IVS moves .

Final message

Coronary artery swing*  is a   new  method (  rapid  and accurate) to assess  cardiac  function  in cath lab !   We should utilise this more often .I feel it may throw more valuable  than the sophisticated but complex 3D reconstructed and post proceed  imaging modalities  to assess individual  chamber function .

* There is no published reference available for  modality  .It is so simple  concept  i think ,  it does not require any major experiments for a  proof !

Reference

RV  function assessment ASE  guidelines

http://www.echobasics.de/rv-en.html

Normal RV function Indices .

TAPSE (tricuspid annular plane systolic excursion) < 2 cm

TASV (tricuspid annular systolic velocity)< 15 cm/s

Tei-Index (myocardial performance index)> 0,50

TAPSE  can be correlated with coronary swing

Further research potential 

Now we   require  comparing  the  TAPSE   with the quantum of RCA swing by angiography.  I have asked my fellows to look into this  aspect . I guess TAPSE by  Echo over-estimates the true  motion ( normal 2 cm )   seems on higher side. It includes translational motion of echo which is eliminated in angiographic annular movement .

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Right ventricular infarction (RVMI ) is a  common  cardiac emergency in coronary care units. It can be termed as a mechanical complication of infero-posterior STEMI .However ,  around 10 % of anterior  MI do develop this complication . Onset of refractory hypo-tension in spite of correcting hypovolemia  suggests  RVMI.RVMI generally comes under class 3  (Cidar Siani /Diamond -Forester classification of STEMI )  , ie   silent lung with systemic hypotension.       (RV shock requires an unique definition , as it can not be included in traditional  definition of cardiogenic shock as the PCWP is likely to be normal.

How to manage a full blown RVMI  who is not showing  signs of improvement ?

Following is an extract  from our coronary care unit experience

(do not ask for evidence for everything !)

  • Consider immediate angiogram  to know the  anatomy of the problem .Try opening the RCA which is most  likely to be  the culprit (Any associated critical  LCX /LAD lesion  must be attended too ! )If  the duration of MI is beyond 36 hours  culprit lesion may be  left untouched or at least not our primary target !
  • Inotropic support (Doubtamine continuous infusion is preferred .Milrinone  for the rich !)
  • There is no specific RV assist devices available.(LV  assist device has no role in RV )
  • Restrict fluid (Opposite  to RVMI guidelines) There have been instances of  overzealous fluid therapy resulting intra-cardiac  hypervolemia. IVS encroaching LV worsening the cardiac index .
  • Pacing is  definitely required in severe bradycardia or CHB .  Dual chamber pacing is the  ideal  choice to maintain AV synchrony as we desperately need  the  atrial booster pumb  for a failing RV . (Please realise , VVI  pacemakers ,  can still save lives as it takes care of extreme bradycardias  effectively )
  • PCWP in the setting  of RVMI is an  unreliable parameter of true cardiac function.(In almost 90 % of RVMi some degree of LVMI is present ) . In RVMI  PCWP is determined by a  delicate balance between LVEDP and the  onward stroke volume from a failing RV .) The alter tend to bring the PCWP down former would keep it high . Which component is  operating at a given point is a  wild guess  . The situation get quiet complex in the setting of multiple vaso-active drugs , pacemaker , ventilator
  • Balloon Atrial septostomy  /dilatation might help ( Hypoxia may worsen as elevated RA mean pressure may shunt right to left  however cardiac out put might improve)
  • Pericardiotomy  or simple splitting  of pericardial  layers has been tried   (Improves RV restriction effect)
  • If the patient is on ventilator keep the PEEP well below the standard recommendations (RV will struggle more ! )
  • Pacing catheters  can irritate the RVMI in their  raw zone and trigger recurrent ventricular arrhythmia .( Often  labelled wrongly  as Ischemic electrical storm !)
  • Call  Nephrologist  consult  if  renal function  deteriorates . Peritoneal  dialysis is preferred  .  It  is worthy to know , deaths have occurred on hemo dialysis  table.

Final message

RV shock  carries a dismal  outcome , almost  reaching  as that of an LV cardiogenic shock. Ironically ,the most important prognosticator  in RVMI  is the quantum of LV involvement !

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