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A 60 year old man with chest discomfort and severe breathlessness  and  blood pressure of 160/110 was  wheeled into CCU. A diagnosis of  acute anterior  STEMI was made and he  was about to be  thrombolysed . Since  his blood pressure was high they were waiting for it to come down with IV  Nitrglycerin

I was called to see this  patient  .Here is his ECG .

Q-LVH INCOMPLET LBBB STEMI DIFFERENTIAL DIAGNOSIS 2

Though   ECG  suggested anterior  STEMI  , I  was  fairly  convinced  it  was  in fact  LVH and  incomplete  LBBB.

I confirmed with the  patient  about the onset of symptoms . It was primarily  breathlessness and only a  vague discomfort .Meanwhile , the troponin came as positive and CPK MB    was  normal. The combined troponin  positivity  and ST elevation  almost confirmed the STEMI ,  and  the  urgency for  thrombolysis was  intensified . One resident suggested  an  emergency PCI.

My self ,  in spite of  being a cardiologist was isolated among the physician team .  I  had to  urgently  prove to them it is indeed  not STEMI !  I did a bed side echo and showed  the  physician colleagues   a vigorously contracting  hypertrophied  left ventricle  with a EF of 68 % . There  was  negligible wall motion defect  . . .  if at all any !

They were still far from convinced ?  They  were  sort of  amused .There is   ST elevation ,  there is  troponin  positivity. . . what else you want  . . . they seemed to ask  ?

I asked them  . . . How can an  acute  extensive anterior   MI contract so well ,  without a trace of   wall motion defect ?

It took me considerable time and effort  to  convince them  that the whole thing was not a STEMI.  Finally they agreed .It was  a simple LVH with secondary ST elevation  due to incomplete  LBBB .  Troponin elevation  simply  represent minor myocardial  injury associated  with hypertensive  LVF . This  patient was discharged within 24 hours  in perfectly stable  condition . Since he had mild elevation of creatinine and was  sent for  nephrology  work up.

Final message

LVH with secondary  ST elevation in V1-V4 is a common situation that mimics  acute STEMI . Cardiac failure can result in non ischemic troponin  release .  Acute medicine is  an unique art . Some times it demands all your senses to be on alert mode . Realise ,  in the above case ,   in spite of the   the classical   triad of  chest pain ,    ST elevation , troponin positivity  it  almost led to a wrong diagnosis of  acute myocardial Infarction .

After thought : What  if they had thrombolysed this patient or taken for a PCI ?

When  the clinical suspicion is high and  circumstantial evidence  point to an ACS   ,   this error can be  justified . After all ,  5 % of   famous ISIS  study population were not suffering from STEMI  but got thrombolysis !

* One real possibility in this ECG is  old AWMI with re-infarction  or a dyskinetic septum lifting the ST segment .But both were excluded by the rapid bed side echo.

 

 

 

As I expected ,  my earlier algorithm “An Idiot’s approach to tachy-arrhythmias” has  elicited  mixed reactions  .Some  EPs calling it a dud while few  physicians termed it awesome . Here is  a follow up .

Heart rate of a tachycardia is the most neglected parameter by physicians .  They are often seen spending  hours together for decoding  arrhythmia , splitting the brains   for P wave  location , VA conduction, Fusion beats etc .Finally they end up  either administering  Amiodarone a broad spectrum anti arrhythmic agent or DC shock.

Here is an unusual algorithm  for arriving at a diagnosis in all tachy-arrhythmias  based only on heart rate and the width of he qrs complex.

(Click over the table for high resolution image )

approach to cardiac arrhythmias narrow qrs vs wide qrs brugada wellens criteria

General principles in diagnosis of tachycardia

Narrow  qrs tachycardias.

90 % rule : If regular It is sinus tachy if irregular it is A-FIB . Take some efforts to r/o sinus  tachycardia . (In children and young adult it can be extremely difficult at times )* Please note : Sinus tachycardia can show some irregularity due to sinus arrhythmia and  frequent  APDs and JPDS . Further at  fast rates P may fuse with T it should not be confused with  A-fib .

Wide qrs tachycardia

Common things  are common , if  you sight a large animal with a huge trunk  in a Kenyan safari ,  it is most likely to be an  elephant and not a Dinosaur !  Please diagnose VT  when you encounter wide qrs tachycardia by default especially when the BP drops  !

  Management issues

It  would be  foolish to split our heads for decoding an arrhythmia when a patient is unstable .Any hemo-dyanmic unstable tachycardia needs DC shock . (Synchronized will be better unless it is dire emergency )There are very few arrhythmia where DC shock is contraindicated   ( MAT/Dig toxicity/Underlying sinus node dysfunction )

Only if the patient is hemo-dynamically  very much stable   the  physicians  have enough time to  confuse themselves  and the real  ordeal begins .Please remember  the 5 arrhythmias  constitute 98  % of all known tachy-arrhytmia . So where ever  you practice ,  whether  in remote Nigerian village  or  sophisticated  Cleveland  university hospital , when you are  confronted with a tachycardia  the diagnosis  should be one among the  following  five  !)

  1. Sinus tachycardia .
  2. AF/A-fib
  3. Atrial tachycardia  with  or without blocks
  4. ventricular tachycardia /VF
  5. AVNR/AVRT with or without aberrancy

All  other tachy-arrhythmiaa  are  largely  academic !

Regarding  drugs

Knowing the mechanism of  arrhythmia genesis  is less important  at bed side . They are  triggered , sustained, and maintained by either functional or structural component .Ionic basis operates in every arrhythmia  , but it is the anatomical  substrate that maintains it .This happens in only diseased heart.The only point worth remembering regarding mechanism of arrhythmia  genesis  is ,  automatic and focal tachycardias  will not respond to DC shock . All other can be termed some form of re-entry . Micro reentry  for all practical purposes behave like  triggered  activity. Ischemic and electrolytic VTs are primarily ionic based and often polymorphic.Structural VT are commonly mono-morphic. Any VT just prior to degeneration to VF become polymorphic

Every patient with cardiac arrhythmia should be checked for hypoxia,acidois , electrolyte defect or exposure to any  pro arrhythmic drugs. (The commonest  cause of tachycardia in any  IMCU , is inotropic induced (dopamine /doubtamine ) tachycardia .

We  have  5  pharmacological options

  1. Blocking  adrenergic  receptors(IV Esmolol, Metoprolol)
  2. Blocking calcium channel (Dilitazem,Verapamil)
  3. Blocking potassium channel  (Amiodarone  ,Sotolol Adenosine  to a cetian extent )
  4. Blocking sodium channel . ( Procainamide , Lignocaine (Wonder drug almost forgotten now ! ) Flecanide Mexilitene etc)
  5. Digoxin ,Adenosine  magnesium are special  anti-arrhythmic  agent which  has very useful role in certain specific situations (Magnesium -Torsades/Polymorphic VT / Adenosine in LVOT/RVOT VT etc)

General principle is ventricular arrhythmias  are blocked successfully  by sodium or potassium blockade  Atrial and functional tachycardia are blocked by calcium or adrenegic blockade  .Of course,  there would be  some degree of overlap  when the arrhythmia  origin  hovers  around the junction  on either side of the AV  ring . This is basis of verapamil sensitive VT .Clusters of  calcium  channels are scattered  in the junctional  region

Refractory tachycardia

  1. Consider ablation  in AVNRT/AVRT
  2. ICD +Drugs  in VT
  3. Ablate and  Pace(Some A-fibs)
  4. Ablate and ICD (Some  incessant VTs)
  5. Surgery in minority

In AVNRT/AVRT 90 % success can be achieved  in most EP centers .VT ablation  is still a complex process  with  success rate around 60 % ICDs  are indicated in all recurrent VTs except incessant forms .(Where the battery will deplete within a month !) Surgical cure (Maze etc  ) is possible in selected few while undergoing mitral valve surgery.Contrary  to the modern scientific  mood ,  I can ay with conviction most A-fibs can be managed medically except a fraction will require pulmonary vein ablation / isolation .

Final message

Mastering the field of of  cardiac  arrhythmias ,  though  appear a daunting task ,  it does not  require   immense  sense  to understand real world problems are  only a  few and can be tackled in a simplistic manner !

Heart rate of a tachycardia is the simplest of all  . . . but   neglected parameter by physicians.  They are often seen spending  hours together for decoding  arrhythmia , splitting their brain for locating P waves ,  VA conduction, Fusion beats etc Finally , most end up  either administering  Amiodarone a broad spectrum anti arrhythmic agent or a DC shock  without arriving at a correct diagnosis.

Here is an unusual algorithm  for arriving at a diagnosis in all tachy-arrhythmais  based only on heart rate and the width of  the qrs complex with acceptable accuracy.

(Click over the table for high resolution image )

approach to cardiac arrhythmias narrow qrs vs wide qrs brugada wellens criteria

Caution :

The above table is  an extremely simplified approach for tachy arrhythmias. Not applicable for scientifically inclined . But in my personal opinion ,  in an emergency room  pure science matters less !

aortic dissection how safe is transesophageal echo tee

What is the mechanism of aortic injury by TEE probe ?

It is purely a mechanical  complication . The dissected/aneurysmal  segment   may  encroach the esophagus .The TEE probe if  faces any resistance  at lower esophagus , the procedure is to be abandoned .The false lumen  shares  a  intimate spacious  relationship with   esophagus and the probe can delicately hug the false lumen  ,  can  lift it accelerating the  tear. It is wise to  realise  coughing , retching or vomiting may amplify   the  frictional  force  between esophagus aorta  and the probe .

Reference

Risk of aortic rupture during tee in aortic dissection  tran esophageal echo

Final message

I would conclude the  risk  of aortic  rupture is negligible . If gently performed   TEE would remain a  simple ,  cost effective ,   vital bed side investigation inmost  cases of suspected aortic dissection.

The popular clinical  entity Idiopathic dilated cardiomyopathy   is often a  dust-bin diagnosis” . The fact is the word   idiopathic simply reflects  our ignorance.

For God nothing is idiopathic . . . he knows how each and every cell  would   behave  .

so , when a patient presents with progressive dilatation and  heart failure refractory to all medical  therapy he is termed as idiopathic and posted for heart transplantation. And only later , we realize the whole thing is due  a  terrible form of reversible  DCM  . That is  pheochromocytoma  induced DCM , which recurred again in the   transplanted  heart.  What a  costly  Ignorance ?

pheochromocytoma and dilated cardiomyopathy reversible dcm tachycardic

Image courtesy and source http://www.dreamstime.com.

Is sub- clinical pheo like situations rampant ?

We know  that  high levels of both epi and nor- epinephrine circulate  in cardiac failure . We presume it  to be a secondary effect .

How can  we  so sure about it ?  There  is a distinct  possibility  of   adrenal gland hyperfunction  and hyperplasia in all DCMs (Idiopathic or ischemic ! )  The dramatic beneficial effects of beta blockers in cardiac failure  will vouch for it .

So , It remains a fertile filed for the youngsters to explore . . . the hyper  adrenergic mediated reversible component of any cardiomyopathy and cardiac failure .

Final message

The default  approach  in any  patient with progressive / refractory cardiac failure   should  be  ,  to consider  whether they fit into  any form of reversible myocardial disease  .  What is idiopathic in remote clinic of   your distant  country side  may be  well recognized secondary cardiomyopathy . The irony is , even sophisticated university hospitals many times miss the true etiology as in the above case report .

                                  So, the term Idiopathic  dilated  cardiomyopathy  (iDCM )  may  aptly be named as  Ignorant  forms  of  DCM  , with an  attractive  abbreviation    . . .   iDCM

Reference

1.J Surg Educ. 2009 Mar-Apr;66(2):96-101. doi: 10.1016/j.jsurg.2008.11.004. Pheochromocytoma presenting as acute severe congestive heart failure, dilated cardiomyopathy, and severe mitral valvular regurgitation: a case report and review of the literature.

2.Kelley SR, Goel TK, Smith JM.Prog Cardiovasc Nurs. 2005 Summer;20(3):117-9. Pheochromocytoma presenting as heart failure.

3.Pheochromocytoma   masquerading as a cardiomyopathy. Garcia R, Jennings JM.  Am J Cardiol. 1972 Apr;29(4):568-71.

4.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1894695/pdf/20070600s00025p244.pdf

pheochromocytoma and dcm dilated cardiomyopathy .catecholamine induced dcm tachycardiac cardiomyopathy

5. http://downloads.hindawi.com/crim/medicine/2011/596354.pdf

pheochromocytoma and dcm dilated cardiomyopathy .catecholamine induced dcm tachycardiac adrenal cardiomyopathy

 

When I posed the above question  to few  cardiologists including electro physiologists , the answer I got was surprising .  In the process ,  I could understand why cardiology is such fascinating subject !   Each one gave a different answer and all the 5 responses were forth coming .

The following post in my blog which  I wrote years ago tries to decode the reason for such wide variation in our understanding of AVRT of WPW.

By the way ,  is there a  real risk   for an  ortho-dromic AVRT into anti-dromic AVRT by a definite block in AV node  ?

Mitral para-valvular leak

para valvular leak 002

How to manage para valvular leak ? 

Does  the terms  peri  & para valvular leak mean the same ?

Coming soon  . . .

Mean while , read this article from ESC journal  for an excellent discussion on the topic .

1. http://www.escardio.org/Para valvular leak

2. The ultimate  reference on the topic of prosthetic valve assessment by Echocardiography  http://www.asecho.org/files/public/pvtext.pdf

prosthetic valve echocardiography guidleines acc asecho esc

Here is some of the   highlights of my  presentation  in EUROECHO on  December 5th 2012 

At  the Mageron International Convention center  .Athens Slide1Slide2Slide4Slide5Slide7Slide3Slide6Slide8Slide9Slide10Slide11Slide12Slide13Slide14

CABG surgery is the commonest cardiac surgery done world wide .Right from the days of CASS study the  CABG was considered a major traumatic surgery to relive a small block in a coronary artery  (Not exactly relief  . . .it  just by-passes )

However , for more than two decades  till early 1990s CABG ruled supreme.Ever since coronary stenting grew in an  exponential fashion  the outcome of CABG  needed scrutiny .Surgeons had a compulsion  to explain  the world , CABG indeed has a  acceptable risk benefit ratio in the management of CAD .

Thus came the EUROSCORE  . First developed in 1995 .The initial score used a simple additive risk next it was modified

with logistic regression .

Limitations

Can you withhold  a surgery on the basis of high EUROSCORE  ?

Is it scientifically validated ?

EUROSCORE gives us  30day mortality

What is the acceptable EUROSCORE for CABG?

http://ejcts.oxfordjournals.org/content/early/2012/02/28/ejcts.ezs043.abstract

Click to access 1749-8090-4-32.pdf

What is the major limitation for EURO-SCORING system ?

It is ironical the most important determinant of any surgery is  the surgeon’s competence and institutional expertise in handling emergencies  and financial affordability  .They are  not included in the scoring .  This makes the EUROSCORE in most of the developing countries including India a futility .

This paper is to  be presented in the the Forth coming   Annual CSI meet New Delhi  December 2012

Beware of Primary PCI : Is there a Low risk STEMI where  pPCI is potentially contraindicated ?

Venkatesan Sangareddi  . Department of cardiology  . Madras Medical college

Primary PCI has proven to be the best  option for management of STEMI . But it need to be done early,  by an experienced team , in a good facility . It is not the individual expertise that matters !  Any treatment , which has great therapeutic potential  also  carries a hazard . So , these treatments  must be used with caution.  Not every STEMI patient , carry a high risk for death.  In fact , the mortality  in some of the subsets of STEMI  can be as low as 1%. If , a  STEMI patient , with a likely 1% mortality is going to get a procedure with  3 – 4 % ,risk it should (And Must !) raise a validity question  But,this issue is rarely addressed in the interventional summits.

In a case pool of 56  randomly collected primary PCIs from various institutes , the outcome  of pPCI  was analysed .It is a retrospective , observational study .STEMI was graded as high risk when one of the following features  were present and it was “low risk” when none of the feature  was  present ( Second STEMI , Extensive  anterior MI , Class 3 /4 killip, An episode of VT/VF, Complete heart block, Diabetic individuals )  High risk STEMI  constituted 22 patients .The overall in hospital  mortality  was (5/56) 9 % In high risk STEMI it was (2/22 )9.5 % in low risk  STEMI it was 3/34 6.4 % .In the corresponding period 40 patients with STEMI who were treated by only thrombolysis or heparin (If beyond time window ) was used a control . 15 patients  were in high risk In the this group the  mortality in high  risk STEMI  was (3/15 )19% and low risk STEMI  there was nil mortality (0/25) 0% .

There was an unacceptable moratlity  with  pPCI  in the low risk STEMI which fared worse than even simple administration of heparin.These data reveal a dangerous fact , that is , primary PCI does not differentiate in the procedural  risk with reference to the patient profile it deals with .While , it dramatically reduce the risk in high risk STEMI It confers a astonishing risk to low risk STEMI .The exact cause for this risk is not known . Common sense would tell , pPCI is  expertise driven driven while thrombolysis is not .Our analysis also suggest bulk of early hazard of pPCI is also logistics related.

Primary PCI could be  cautiously and consciously avoided  in  patients with  low risk STEMI even if it is technically and academically indicated. This can have a great impact in the overall outcome of STEMI management.It is suggested every STEMI patient need to be risk stratified on arrival.(It is still a mystery , why we do this for NSTEMI and not in STEMI ) . A change in the current PCI guidelines to this effect is to be considered.