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Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !

myths-truths-300x300

When false truths are synthesized to conceal a true myth . . . where will the poor myth complain ?Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !

  • Primary PCI  is a greatest innovation  in modern day cardiology .Without this modality  most  STEMI patients will buy Instant  tickets to grave yard !
  • A cardiologist who intends to  thrombolyse  a STEMI is considered as a low quality cardiologist .
  • Streptokinase should have  no place in the crash carts of modern coronary care units.
  • There is nothing called “Time window” for rescue angioplasty.
  • VVI pacemaker  will convert an electrical problem of heart block into a mechanical one by depressing LV function .
  • Digoxin is an obsolete  drug even in well established cardiac failure with dilated heart.
  • Beta blockers not only fail to control  blood pressure smoothly , it often converts  a hypertensive individual into a unhealthy one  by it’s prohibitive side effects !

 

Here is a  video recipe  !

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

” This is post is 5 years old , Newer developments should be given considerations”

 

STEMI is the “Numero Uno” of  cardiovascular emergency .The  treatment has evolved over decades,  right from   the primitive  arm chair approach to the  air dropping of  patients  over the cath  lab  roofs  for primary PCI ! We realise by now ,both are extreme forms of treatment and  may  have unique  hazards. What we forget is the , the natural history of STEMI is too  much dependent on the degree of initial damage to the myocardium , and it is very difficult to alter this,  however good is the therapeutic strategy .  We are yet to find an answer regarding the mechanism of primary VF and modes of preventing it. We also have no answer for  ,  why  some  develop myocardial damage  very fast and  the  cardiogenic shock occur in an  accelerated fashion. (Fate ?)

Many would consider  ” non availability of   infrastructure and expertise ”  is the major issue  for  primary PCI . But the real problem is much more than that .When an  illusion of knowledge is  created by constant bombardment of data  , it is natural for human beings to believe whatever is told or printed in books and journals. We cardiologists are made to believe thrombolysis is a far . . .  far  inferior treatment than primary PCI in STEMI .  It is not so in any stretch of imagination !

The fact that,there is no entity called ” Failed primary PCI ” in cardiology literature  , would  suggest how biased we are against thrombolysis. Every cardiology  resident will  recognise  thrombolysis fails  at least 40% of time .Yes , it is  a  fact  , but the irony is , this   is  often  used   to convey a surrogate  meaning , that  is , primary PCI is  near 100% successful !

How  do you assess success of primary PCI ?

Unlike elective PCI where the criteria is too liberal, we can not afford to adopt the same in an emergency PCI. Here the aim of the procedure is entirely different (Salvaging dying myocardium vs pain relief  ).

It’s still a  mystery ,  while  thrombolysis is vigorously assessed  for it’s  effectiveness   primary  PCI is rarely  subjected to the same scrutiny  . A check angiogram  after the procedure ,  is all that is done . . . and every one  leaves the cath lab happily. The  effect of primary PCI on ST segment ECG resolution must be documented immediately after PCI. While ,  It is mandatory to take ECG after 60 -90 mts after thrombolysis , this sort of protocol is rarely  followed after PCI.

If the ST segment  fails to retract  > 50% immediately  following PCI  the procedure  should be  deemed to have failed . Further , unlike thrombolysis  in primary PCI , the ST segment has to regress within 10  mts , as IRA patency occur instantly .If we apply this criteria , the success rate of primary PCI would be far less than what we believe*

* Not withstanding the official lesion , hardware, related failure. If we encounter a severe triple vessel disease , with a bifurcation lesion and thrombus it’s  a tough exercise as we are racing against time .

Primary PCI  Camouflaging  in semantics

  • A successful but  delayed   primary PCI  is actually a failed PCI
  • A  complicated  primary PCI  often  reach the equivalence  of   failed PCI
  • No  reflow is almost synonymous with failed primary PCI as successful correction of no reflow occur in minority.
  • Not all TIMI 3 flow is converted into myocardial flow.
  • Renal dysfunction following excess dye has a  high  morbidity
  • If patient  develops significant  LV dysfunction following primary PCI it is a failed PCI.
  • Finally if the cost of primary PCI exceeds the insurance limit it is  economically a  failed primary PCI as the patient  has to spend double or triple  the amount of sum insured .This stress has resulted in many recurrent coronary events .

Why is it important to recognise failed primary PCI ?

For failed thrombolysis we have a strategy . Unfortunately , even in this modern era  we have  no useful  strategy for failed primary PCI . Handing over a patient to a surgeon in a such a situation is considered by many as a great rescue strategy but in real world it does no good in most of the patient.

Doing an emergency CABG in a sinking patient with a battered coronary artery is no easy job /Many times it only rescues the cardiologists from the embarrassing situation of facing the relatives who ask for explanation.

So , what can be done at best , in failed primary PCI ?

  • CABG can be an option but still questionable !
  • Most times  there is  no other option except to fall back on the medical management.
  • Intensive anticoagulation and one need to consider even a rescue thrombolytic treatment !
  • Some times we can only prey !  Failed primary PCI for a patient in cardiogenic shock with IABP support is near death sentence !

Final message

  • Remember ,  success of primary PCI   is  not in  wheeling out a  patient  alive out of cath lab   , with a TIMI 3 flow  in the IRA ,  but in  garnering significant   myocardial salvage   which  should have an impact on   intermediate and long term  outcome .
  • Do not ever think primary PCI is a sacred treatment modality in STEMI  and the job of the cardiologists ends there. It is vested with  lots of important complications – defined, undefined , recognised,  unrecognised, reported, and unreported ,  concealed ,denied, poorly understood, etc etc.
  • There are  equally  effective, less dangerous treatment modality available .
  • Decision  to do primary PCI  must not be based   only on the  “affordability and  availability”  of  cath lab and expertise !
  • In  clinical cardiology practice,  no  procedure  is  great   & nothing is inferior either  !  Every thing has to be used judiciously , appropriately  and  intelligently (Intelligence is synonymous with common sense many times!)

Coming soon

Surgeon’s real time experience of operating  on a failed primary PCI. To our surprise , only a handful of surgeons  have this experience

It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

We have been taught right from first year cardiology residency  how to trouble shoot a pacemaker .It has been a real complex thing for us. Now looking  back ,all the troubles we took to understand seems to be redundant.Here is a summary of my thought process on the issue. It can be approached  with reference  to time, symptoms and ECG features.  With due respects to all those brainy hardworking   EP experts  , I have taken few academic liberties!

pacemaker trouble shooting

Timing

  • Within 24 hours -100% technical or procedural Issues , like lead dislodgement/Screws and nuts.
  • Within 1-2 week – Again technical , Pocket issues , Infections.
  • Within 6 months – Benign pacemaker syndrome ,Threshold settings, Scars
  • After  first year – Generally Issues are rare , Lead issues , Associate disease progression.
  • Beyond 8-10  years /Near end of life – 95% Energy depletion leads issues .( Please note , pacemakers do not stop all of a sudden it has a intrinsic end of life indicators .We have to look for it. May be ,we can expect a  warning siren in the future ? )

Symptoms

  • Vague dizziness – Pacemaker syndrome ? Anxiety ?
  • Near syncope – Show some concern (For many , Impending true syncope is a non existent entity )
  • True syncope  – Real emergency*

* Syncope can be unrelated to pacemaker but always consider  them electrical  unless proved otherwise . Few patients  may continue to have significant symptoms  in-spite of   normal pacemaker parameters. This would  mean , the original symptom for which  pacemaker was put is not related to the Brady-arrhythmia .It could   suggest alternative hemodynamic explanation  like vaso-depressive component of vagal syncope ,autonomic dysfunction , orthostatic intolerance or  a coexisting neurological /systemic condition.

**Never forget syncope is not an exclusive symptom of bradycardia .A new onset  tachycardia  , which is either a part of  brady- tachy syndrome or separate arrhythmia can continue to provoke the symptom.

Gross ECG findings

Bradycardia /Often implies back to original rhythm –  Indicates real trouble . Since ,in a paced patient HR cannot be less than programmed rate of 70.

Tachycardia -No spike.( Not to worry ?) A common  situation if the original indication was  sinus node dysfunction . Many of them are  in own sinus rhythm or AF . Just ensure spikes reappear when the rate falls below 70 . If the rate never goes down , what to do ? Try a carotid massage or observe a nocturnal ECG  or call analyst and increase the rate to document pacing . (In DDD mode we have a rare PM mediated re-entrant tachycardia , which is mainly used to grill cardiology fellows in their board exams with all those PVARP stuff !)

Simple pauses – Any pause more than the pacing interval is a definite concern .

Spikes more than QRS  – Indicate capture failure.

No spikes (Can be so benign  to ultimate danger )

  • No spikes , but  excellent own rhythm – Good  functional  SA node
  • Regular  spikes ,but intermittent own rhythm or only random spikes with good own rhythm – Needs bedside hairsplitting and  EP assistance !
  • “No spikes -No Own rhythm” -Most dangerous .Sudden lead issues or hyper sensing .(Emergency  switch off  by magnet  application before inserting temporary pacing advised )

* Anatomical issues like lead dislodgement , fracture , compression ,  perforation are to be ruled out in every pateitn with intermittent capture or failure .This is done by combinations of imaging as well physiological assessment.Dislodgement must be visualized .The term micro dislodgement may not exist.

Other Investigations

  • X ray
  • Echo for any new structural lesion (RA,RV dilatation , TR RV clots or vegetation )
  • Holter
  • Event monitors ,Loop recorders.

Pacemaker analysis

  • Battery life ( Very important parameter .Usually around 10 -12 years.Unexpected early drain can occur.)
  • Threshold (Most failure to capture associated with high threshold Note :Threshold will be normal in battery depletion Acute threshold can increase marginally .Should be reasonable other wise battery will drain.New protocols like auto capture and managed pacing will help optimal threshold
  • Impedance – Normal in battery depletion , dislodgement and exit block,  Increased in lead fracture and loose screws.Decreased or lost in insulation failure.

Management

The principle of management are simple. Few logical questions ,

  • Is the pacemaker generator is alive and has has enough energy ?
  • Are the  leads okay ?
  • The problem is in the settings ? can it be rectifies by the programmer
  • Or should we replace the pacemaker ?

Technical jargon like  under sensing , over sensing or no sensing  , fusion beats , micro dis-lodgement  etc are important for  academic reasons . We may talk any thing , realistically , what  the ventricle want  is a non stop heart beat  every second or so !

Emergency

Bradycardia – Insert a temporary pacemaker /Call the analyst  /Inform the  electrophysiologist /Senior cardiologists /(Please realise ,  some fellows  can be better than the personnel mentioned above in tackling emergencies !)

Tachycardia : Native or machine induced ?

Native – Mostly safe ,  Ignore  or treat with drugs.

Machine induced :(very rare) Switch of the pacemaker . No off switch available as in a mobile phone ? *What to do ? if unclear about the  whereabouts  tachycardia origin . If hemodynamically unstable no harm in shocking .Nothing will happen .Call the EP  guys on hot line and decide.

Elective symptom guided.

  • Asymptomatic -Normal ECG : Reassure and send home.
  • Vague symptoms   -Do Holter and Observe
  • Syncope -Normal ECG needs extensive all system investigation.
  • Syncope -With pauses /Bradycardia /Asystole  – Ironically ,decision  making is easier. Temporary pacing is the  ultimate savior. Later , check the lead,  generator .One may need to change  either one or both of of them.

** While the above principles apply  for both single  and dual chamber pacemakers , the later doubles our thinking burden . While atrial tracking is a great technological advancement , what to  do with those sensed event can be really  tricky .The response of  ventricles and the AV intervals  can be tentative at times. Cross talks from unexpected atrial and ventricular arrhythmia can occur.  Further , mechanical atrial lead  issues are far  more common . When confronted with recurrent atrial lead related  problems , one  simple solution is  silently convert the mode to  single chamber VVI mode.

Final message

Pacemaker trouble shooting appears complex at the first look .It’s all common sense.Thinking with simple state of mind and  being clear about the intended  goal is vital. Electrical intricacies are tough to understand  but most situations do not require them. However ,If the initial indication was for complete heart block one has  to be very alert.

Principles of medicine argue us to make an exact diagnosis before treating . But,realise  this is rarely  possible or even desirable in emergency .Curiously , most pacemaker troubles can be solved successfully without making a proper trouble shoot !

If  we can summarize in one line  , a prompt emergency  back up temporary pacemaker insertion  is key to  management most of the serious  pacemaker related problems.It ,not only tackles the emergency ,  buys time till we decode the real problem . . .  if we wish to !

Related article.

Role of magnet application in pacemaker trouble shoot

 

 

 

We know , any wide QRS tachycardia  would argue us to make a default diagnosis of VT.But,  one has to be extremely cautious to apply this rule if  wide QRS  tachycardia shows  significant irregularity in RR interval .

All classical VTs are fairly regular tachycardia (Note the  key words , fair and regular) . Small cycle length variations are observed in VT,  but they are usually not discernible in surface ECG.

There are no practical rules .A well  appreciable  irregularity in RR interval will seriously  question the diagnosis of classical VT. To make an another statement, most of the  irregular wide QRS tachycardias infact turns out to be  atrial fibrillation with some form distal widening mechanism .(Preexisting blocks, or rate dependent  or antidromic conduction through accessory  pathways)

However , irregularity  is still possible during VT .(May be less than 10% of times)

When can VT can be irregular ?

  1. Irregularity is observed  immediately at the onset of VT as the re- entrant circuit warms up and tries tosettle down
  2. AV dissociation  can make the VT irregular but it is subtle .(This AV dissociation is absent if retrograde VA conduction is intact)
  3. Multiple reentry circuits with two morphological VTs dissociating themselves
  4. VT with multiple exit points and epicardial breakthroughs
  5. A drugged VT.Amiodarone modified VT can be irregular as it can variably lengthens  the re-entrant  circuits and inducing VA block and precipitating AV dissociation.
  6. Multi- focal VT  (We have MAT in atria do we really have MVT ? (Why not , are we missing it ?)

Final message

Statistically , as well as realistically  , the commonest cause for  any highly irregular tachycardia turns out to be AF , whether  QRS is wide or narrow !

ICDs are primarily life saving devices.Whether single or dual chamber  it does this function  effectively.They will also  take care of  bradycardia by  default  back up pacing .For most indications single chamber ICDs are good enough.

My professor used to tell us , dual lead  means ,  dual expertise , dual cost , dual caution and  dual set of complication . One should avoid it whenever possible. Make things as simple as  it could be , without compromising the main goal (Here prevention of SCD) . The incidence of inappropriate shocks being lesser with dual chamber ICD  has not been truly  realised in real world scenario.

Recent studies  tend to give  credence to this  perception .(Peterson JAMA 2013)

Dual  Chamber ICDs  may have an edge only in few situations .

  • When there are both indication for pacing as well as ICD like heart block and LV dysfunction.
  • In extreme LV dysfunction were benefits of dual chamber pacing may have advantage.(If CRT is not an option )

Reference.

1 .Peterson PN, Varosy PD, Heidenreich PA, et al. Association of single- vs dual-chamber ICDs with mortality, readmissions, and complications among patients receiving an ICD for primary prevention. JAMA 2013; 309:2025-2034.

2.Medscape review

 

single vs dual chamber pacing indication

 

 

We are aware  , modern day cardiologists literally live within the patients coronary artery and vascular system .  It ‘s not at all surprising then , man made cardio vascular accidents  are becoming more common  , where pieces of hard ware like guide wires catheters and stents  get trapped .

Knowing about the hardware and techniques of retrieval of foreign bodies within vascular system is so important .It would appear  indulging in cath lab work with out proper salvage hardware and expertise is a  near  serious offense.Apart from this , many complex procedures require intentional snaring of wires and gadgets .

How to retrieve a foreign body from  coronary artery ?

There are few snares availablew  with  single or multiple loops  and comes in various sizes .

1.Goose neck EV3 snare (Covidien /Medtronic)

2.En snare -Multiple loops (Merit Medica)

3.Micro elite snare (Vascular solutions)

 

 

ev3 microsnare covidien

The snare is constructed of Nitinol cable and a gold plated tungsten loop. The pre-formed snare loop can be introduced through catheters without risk of snare deformation because of the snare’s super-elastic construction. The snare catheter contains a platinum-iridium radio opaque marker band.

  • Nitinol Shaft for durability and kink resistance
  • Super-elastic and shape memory properties of nitinol provide kink resistance.
  • Ideal for challenging or unplanned foreign body retrieval and manipulation cases.

goose neck snare amplatz ev3
True 90° snare loop remains coaxial to the lumen

  • Snare loop forms a true 90° angle.
  • Device remains coaxial to the lumen for proper insertion and successful retrieval or manipulation of atraumatic foreign bodies.

 

Hardware specification

ev3 goose neck

2.Ensnare

 

coronary snare ensnare merit medica

 

 

Micro elite snare

micro elite coronary snare vascular solutions

 

micro elite snare

Other retrieval devices

  1. Bioptome* (Cook medical)
  2. Needle and eye snare
  3. Multi snare
  4. Welter loop catheter
  5. Expo retrieval catheter
  6. Curry snare
  7. Simple  alternate option : 2 or three wire guide wire trapping  technique.
  8. The cheapest option :To make a custom made snare with  .014 PTCA   guidewire  with a flexible loop .
biopsy forceps

Intra cardiac biopsy forceps may help to retrieve some of the foreign bodies

 

Final message

At least few of  these retrieval devices  should be  available in  every cath lab .  Attempting to do sophisticated procedures  in your cath lab without essential hardware is akin to driving a car with defective breaks  or like flying airplane with a single engine .

Acknowledgement

Image source , content and courtesy respective manufacture web site

I was recently asked to suggest a topic for debate on STEMI in  a major Indian cardiology conference. I wished , this is what we  should be mulling  over, with a set of  virtual  guest lectures and special invitees from heaven ! Plenary  session : State of the Art  STEMI care             Time :  11.AMSpeaker : Dr Hippocrates Topic : Aren’t  we erring   on either side of the  Noble profession ? Moderator:  Dr. William Osler Chairperson :  Dr .Harvey Cushings, Dr,Sir Thomas Lewis ,Dr Paul Wood , Excerpts : “While , vast number of  our country-men’s  culprit artery doesn’t even get that  mandatory  Aspirin on time . . . an urban rich  man’s  distal non-culprit artery  is decorated with a fancy  bio-vascular scaffold making  that innocuous lesion vulnerable in the process as well !  Aren’t  we erring   on either side  in the  Noble profession ?

Atrial fibrillation is the most  common arrhythmia we encounter in clinical cardiology .Ironically it is  uncommon during ACS and extremely rare in association with UA/NSTEMI. Surprisingly , an entity ” Ischemic AF” is not to be found in cardiology literature.

The incidence of AF in STEMI is less than 5%. Occurs more often due to factors other than primary ischemia of atrial musculature. Of-course , AF in association with Infero posterio MI and RVMI is an important trigger for AF.LCX disease is more often associated with AF as it gives up a consistent branch to left atrium.

Though it is tempting to implicate ischemia as a trigger for AF ,most often it occurs , in elderly ,associated COPD ,hypoxia preexisting atrial disease .Acute elevation of LVEDP and stretch of left atrium could be a more logical mechanism.

Hemodynamic impact

  • AF can bring down the blood pressure.
  • Worsen ischemia by increasing the MVO2
  • Could be very destabilising in RV infarction
  • Surprisingly it is well tolerated in many STEMI patients.

AF in STEMI- Is it an emergency  ?

It would appear so. But , if hemodyanmicaly stable one need not panic.Many times they are transient .Correcting  hypoxia, optimizing beta blocker would help.

Role of DC Shock  , Precautions before shocking  & Post shock events

  • DC shock is done only if there is hemodynamic instability  or ongoing ischemia .(Very difficult to rule out the later )
  • Mural LV clots can form even within 24 hours and DC shock embolic strokes may ensue .
  • Hence it is mandatory to do an echocardiogram prior to shocking.

Drug of choice

  • Betablocker
  • Class 1c -Flecanide.
  • Class 3 -Amiodarone./Ibutilide/

Role of Digoxin

There used to be a concern about usage of Digoxin in the setting of ACS as it pro-arrhythmic , but it remains useful in the management of AF .There is no other  anti-arrhymic drug available to control, the heart rate without depression of  the LV  function

Rate control vs rhythm control

Always aim for rhythm control in the setting  of ACS.Rate control is may not be a  logical concept in acute settings though Amiodarone does both.

Wide QRS Atrial fibrillation

As we know , AF in STEMI can conduct with aberrancy , and we have a traditional teaching all wide qrs tachycardia are VT in the setting of MI making our patients statistically vulnerable.

After all , both entities lack discernible p waves. At high rates it may be difficult  to identify irregularity  RR interval. However , one would shock such patients  and both AF and VT would respond .All is well that ends well.

Summary

AF during STEMI is a risky arrhythmia and needs urgent intervention , but one need  not be alarmed .There is a set of protocol . Only hemodynamically unstable AF require DC shock .Many times it is just transient.There has been instances of  physician panicky that has resulted in more adverse events .

Cardiologists do magic inside the human coronary artery , that too in a  live beating heart , unlike the surgeons.Blocks are removed , holes are closed, valves are inserted ,  scars are burnt, new electrical connections  are laid .They do this with relative blind vision with good degree of success. Still, as we aim for more precise interventions we require excellent imaging  modalities to assist us.

In  PCI of CTO(Chronic total occlusion)   the critical element to know  is  the morphology of the  tissue plane , what  exactly  we borough ?  as we navigate  through complex, often hard shapeless tortuous tissue tunnels  . Our patients will be  surprised to know we are currently doing this with our eyes shut. If only we have a camera guide in the tip of the wire it give us tremendous advantage .

CTO pathology

The CTO morphology .Image source : Kenichi Sakakura ,Eur Heart J. 2014 Jul 1;35(25):1683-93.

The exiting IVUS technology can only look sideways . Now a new vision is added by annular array of transducer at tip with CMOS sensor .The technology is just coming out it would be  use for us in the near future .

Anatomy of the forward looking ultrasonic eye

ivus forward loooking cto intervention

Reference

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