critical decision making cardiology cath lab tricks coronary  angiogram primary angioplasty ptca vs cabg acc aha guidelines esc guidelines


While our brain perceives  whatever option  we  choose is the best for the patient  , in reality it is rarely true !

The only comment I wish to make,  there is nothing called standard guidelines for complex and unusual problems .We need not be obsessed with protocols  !

Please remember , If you apply standard guidelines  in  non-standard situations  9/10 times we  are going to err !

So my  choice  would be, to  go with your gut feeling , of course  your gut should  be alive ,  up to date and periodically maintained !

If you don’t have the guts  . . . don’t worry  you have plenty of other options !


Here is a  video recipe  !

Please click here to  see more videos from my you tube site

Answer  is question is wrong : RAA clot do occur in AF and severe right heart failure.It is less often recognised , since echo views are difficult and clinical events are silent.

RAA right atrial appendage clot tee echocardiographyBrief account of RAA clot formation

  • RAA is broad flat ,thin , broad   chamber comparable to elephant’s ear.The ostium is not that distinct as the body as it  blends  with crista  terminalis .
  • Rough pectinate muscles  should make it prone for thrombus.Further , RAA has more sluggish flow than LAA  increasing the propensity for thrombus.However , the flat nature of the chamber , absence of tortuous tracts , constant  SVC flow which is abutting the  RAA can counteract this.
  • RAA clots are  less recognised as echo views are difficult .TEE is often required.
  • Overall RAA clot is 50% less common than LAA.
  • RAA clot should be specifically looked  for  in chronic AF and any severe right heart failure. (Unlike MR jet TR jet has less efficiency in flushing the  Right atrium )
  • Finally,clinical events from RAA clot are less conspicuous as the emboli reaches the pulmonary  bed silently.Unlike its colleague on the left side it  neither triggers TIA nor a stroke !


right atrial appendage clot raa clot in af atrial fibrillation

1. Buğan B, Baysan O, Demirkol S, Güngör M, Yokuşoğlu M. Right atrial appendage thrombus in a heart failure patient with sinus rhythm. Gulhane Med J. 2011; 53(3): 214-215.


2.Subramaniam B, Riley MF, Panzica PJ, Manning WJ. Transesophageal echocardiographic assessment of right atrial appendage anatomy and function: comparison with the left atrial appendage and implications for local thrombus formation. J Am Soc Echocardiogr.; 2006; 19(4):429-33.

3.Sahin T, Ural D, Kilic T, Bildirici U, Kozdag G, Agacdiken A, Ural E. Right atrial appendage function in different etiologies of permanent atrial fibrillation: a transesophageal echocardiography and tissue Doppler imaging study. Echocardiography;2010; 27(4):384-93

4 .Ozer O, Sari I, Davutoglu V. Right atrial appendage: forgotten part of the heart in atrial fibrillation. Clin Appl Thromb Hemost; 2010; 16(2): 218-20


A tense anesthetist  calls for help !

I had an unusual cardiac consult last week .A middle aged man who was to undergo routine ortho surgery wanted  a cardiac clearance.

It was  a through and through fracture of clavicle , why do they need a cardiology opinion , it seemed a  simple  procedure I asked over phone

The anesthetic  fellow who was  in charge of the patient told me ,”There is a wire just going parallel to the clavicle sir .I  believe it is pacemaker lead” I agreed to see the patient immediately

This was the X-ray

pacemaker lead clavicle fracture electro cautery surgery

It was obvious why they got tensed up  as the pacemaker wire criss -crossed surgical field . His ECG showed own rhythm of 80/minute but occasionally VVI pacemaker was capturing his ventricles.

I suggested

General precautions

  1. Strict Intra-operative  ECG monitoring
  2. Keep another temporary pacer ready .
  3. Hold a cardiologist on call and  pacemaker programmer on site.
  4. Surgical field  kept small with  minimal   manipulation .
  5. Issue of cautery : Free to do as long as it’s  bipolar and good earthing plate.
  6. Ensure the cautery is  applied in one or two second pulses with a gap of 10 seconds pause in-between
  7. Wiring the clavicle – Signal interference  are  very rare  as the wires are inert

Use of magnet in such situations  (Link to magnet and Pacemaker)

Keeping a magnet over the pacemaker generator removes the pacemaker sensing function and is an option if  prolonged electrical interference.

*Caution : Response to magnet can be quiet variable .Should be done only with cardiologist supervision.

What happened to this patient during surgery ?

Nothing alarming.When anesthesia was induced he was entirely  on pacemaker rhythm . limited cautery was used with ease. Patient  tolerated well.

Final message.

One need not  panic when a pacemaker patient is taken up for non cardiac  surgery .It is not a major issue .Few precautions are required .

Read a related article in this site .Electrical cautery  in pacemaker patients.


pacemaker and electrocautery diathermy







Reperfusion arrhythmia was described originally  in the thrombolytic era .

It can be any of the the following .

  • AIVR(Accelerated Idio Ventricular rhythm)
  • Sinus bradycardia (In Infero posterior MI )
  •  VF can occur as  Re-perfusion  arrhythmia.

Does these arrhythmia occur following primary PCI ?

It should  isn’t ? 

In fact it  must be  more pronounced  as we  believe PCI is far superior modality for reperfusion !

Busy Interventional  cardiologists  of the current era  either do not  look for it or fail to document it . These arrhythmias occurs only  with early Primary PCI (Say less than 2-3 hours) .If re-perfusion arrhythmias are  really less common with primary PCI , are we missing some thing ?



As we practice this Noble  (&  Delicate )  profession ,we often tend to Ignore the  warnings  even from our learnt colleagues , Why ?

Wisdom ego quotes brainy best dr s venkatesan top inspirational




Primary VF is the arrhythmia that occurs within minutes to few hours after acute coronary ischemia .This is most common fatal arrhythmia following STEMI accounting for 90% of all pre hospital deaths.

It  occurs within  4 hours after onset of symptom and the risk rapidly fade as the hours go by.One variant of primary VF is the re-perfusion arrhythmia after thrombolysis  .This  can occur up to 12 hours or so.Primary VF responds  well to prompt defibrillation.Follow  up anti arhythmic drugs are not required in most situations.

What is secondary  VF ?

  • As a rule secondary VF is  not related* to  index event of ischemia but to the anatomical substrates of Infarcted myocardium or pump failure
  • It generally occurs after 24 hours .Response to defibrillation is less favorable .Continued anti- arrhythmic  drug therapy  is required.
  • Few of them may end up with ICD.

(*However,a role for ongoing ischemia can never be disproved ! What about a small re-infarct  trigggering another episode of primary VF ? )


A STEMI patient arrives late after 48 hours with chest pain .There is  persistent ST elevation.

What is the likely mechanism of this chest pain ?

  • Index infarct pain continuing . . .
  • Post infarct Angina-IRA territory
  • Re-infarction following intermittent re-perfusion  and re-occlusion
  • Remote  ischemia from a branch of IRA
  • Ischemia from a possible  non IRA lesion in a multivessel CAD

If this patient  comes to a non PCI eligible centre. Will you lyse him  ?

If post infarct angina is  unstable angina  . Isn’t  thrombolysis  contraindicated in UA  ?

How to differentiate Post Infarct Angina from Re-Infarction ?

A very tricky issue indeed.

Unless fresh ST elevation with fresh enzyme peak is documented these entities  cannot be differentiated.

(Even  fresh ST elevation can be related to infarct expansion ,stretch or early acute remodeling.Fresh enzyme  release or new peak  may not represent new infarct always .It can be due to intermittent re-perfusion of IRA .It may  simply represent a  enzyme  flush from the index infarct zone)

What is the practical , realistic , (Unscientific !)  solution  ?

Why break our head ? Never bother to differentiate PIA   from Reinfarction  etc . Let  it  be any thing . Do a emergency CAG .Stent  whichever  lesion looks good  for the same . Of course , make sure he has enough insurance coverage .


This  query often  evokes  confusion  among fellows and General physicians .

              The answer is simple .Yes ,  you can.(With few conditions)

  • Thrombolysis  or PCI  is  done  with reference to  the  presence  or absence of ST elevation and chest pain.
  • If there is ongoing chest pain  and  significant new onset ST elevation  thrombolysis or PCI is indicated whether there is associated q  waves or not.

Clinical situations 

 Ischemic  q waves: Q wave can occur  with transmural ischemia which result in electrical stunning and loss of R waves . (Many of them  regenerate this R within few days after STEMI ,  indicating the q  waves can be  ischemic  in origin)

Reinfarction : Patients with  old  MI can develop fresh ST elevation  in q leads due to tachycardia and dyskinetic infarct segment .This group  of patients  should be carefully evaluated before labeling them as  re-infarction

* q RBBB in early hours of  anterior STEMI is fairly common which  may revert later. qRBBB is not a contraindication for re-perfusion .

Final  message

Presence of q waves does not  imply one should not  entertain  thrombolysis or PCI .The decision  to reperfuse  , rather  goes with  presence of  chest pain , ST elevation and  of course  within the  acceptable   time window!


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