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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 . . .

PTMC involves a critical step , where one has to cross  the IAS to reach the LA.The septal puncture remains  somewhat a blind procedure in fluoroscopy .(Echo can still assist us. )

Stitch effect is a rare complication where the needle pierces the intrapericardial space from the right atrial side and re-enter the left atria .This wrong way entry into LA may not be recognised  untill the sheath is withdrawn and a cardiac tamponade ensues after removal.

Where exactly the stitch  occurs ? What are  the anatomical planes ?

This usually  happens in the superior aspects of   IAS , abutting the roof of RA and LA . The alignment of IAS with reference to RA and LA is key a determinant.We know in mitral stenosis LA can outgrow the RA , bringing   superior aspect of LA  in a different  plane with reference to IAS  .The IAS puncture site may overshoot , enter the pericardial  space and  stitches the non IAS aspect of RA and LA together , of course  still guiding us  into LA through a false pericardial track (Which is not recognized )

stitch effect ptmc stich phenemenon

Note : The intra-pericardial track can be more complex than we realise as a significant part of posterior LA is extra-pericardial and transverse sinus of pericardium can get involved as well.

 

Our understanding(mis ?)  suggests at least four different stitches are possible

  1. IAS-Pericardial space -LA roof
  2. RA-Pericardial space -LA roof

Other complex tracts (Based on theoretical assumptions . Please note , in  some of the fatal punctures the exact  route was not identified by surgeons even under direct  vision . )

3.RA-Pericardial  space -Extra cardiac-Reenter LA

4.RA-IAS -Pericardial space-Extracardiac -Reenter LA  ?

What are the possible bleeding sites in stitch effect ?

There can be two sites of active bleeding .One from RA exit point and other from LA entry point of needle.Extra-cardiac oozing can also occur if the needle has pierced the outer pericardium before entering LA.

Management

  • Recognition is the key. It requires extra anatomic acumen to diagnose the false track before we insert and withdraw the sheath.Echocardiography should be liberally  used if you suspect a false track .
  • Tamponade  is to be  drained promptly and emergency surgery is usually required if re-accumulation occurs.
  • Closing the puncture site with devices has been successfully  attempted in few patients .A small ASD device (or a Plug ? ) is expected to close  the site of  puncture . Since the anatomy  can be complex ,one may need to  close with two devices , one on LA side and other one RA side .The radial force that closes the tear and long term retention of these device are not known .

Related topic

Other mechanisms of cardiac  tamponade during  PTMC

 

 

Mconnell’s  sign is a distinct echocardiographic sign that occurs in Acute pulmonary embolism , where RA and RV dilates. RV shows a distinct regional wall motion abnormality in which RV free wall shows akinesia (or severe hypokinesia ) with well-preserved RV apical contraction.This is visible in apical 4 chamber view.

This sign is explained by  both anatomic  and hemo-dyanmic reasons.

  • RV when exposed to  sudden pressure overload  it not only dilates , it’s wall stress increases (Laplace law : Wall tension = P x Radius  )   and end up mechanically stunned . But , since the RV has a complex shape the distribution of this stress  is not uniform .As the RV assumes more spherical  shape the apical  part is not exposed to this stress as it tend to abut under LV.
  • RV apex is anatomically tethered with LV apex and share significant amount of circumferential fibres .In patients with acute pulmonary embolism ,  LV usually is hyperkinteic  due to tachycardia .This pulls the  RV apex  along with it for a proxy contraction .
  • Rarely , primary RV ischemia  due to RCA under perfusion* may be responsible for this unique  wall motion defect . Since RV apex  is mostly supplied by LAD it is free from ischemia . (*Acute elevation of RV intramural pressure due to PHT , compromising RCA perfusion pressure  )

Reference

1.McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996; 78: 469–473.

2. Rachel P. SoslandKamal Gupta,McConnell’s Sign circulation. 2008; 118: e517-e518

3. Link to the Echo clipping of McConnell sign in echocardiography

 

 

 

During exercise stress test , systolic pressures should raise at least by 20-40mmhg.(Max 60 mm from baseline )  Diastolic BP will remain at baseline or show a marginal elevation or even a  miniscule fall.This is primarily due to increased cardiac out-put , mediated by demand and dilatation of musculature  in exercising muscle.

If the systolic BP falls or does not raise during exercise , it implies either poor LV function , vascular insufficiency or autonomic dysfunction.

If there is a fall of > 20mm , even in the first stage,  accompanied by  chest discomfort or giddiness with ECG changes ,it could be an  ominous sign of serious left main or a tight proximal LAD disease and test should be terminated immediately.

Paradoxically , If BP raises more then 200 at any time we call it hypertensive response and may be a risk factor for future onset systemic HT or even a stroke. ( Stress test not only help us  detect ischemia of heart ,it also can reveal  how the vascular system would handle  and adopt to increased cardiac output at time of  hemodynamic demands)

Physical de-conditioning is an important cause for hypertensive response , as the entire vascular system lacks dynamism (Vascular tone ) ,  a  precursor for  hypertension, endothelial  dysfunction and cardio vascular events..

We generally believe ischemia and it’s clinical counterpart  angina would  go together .It is not true .Most patients with ischemic cardiomyopathy do not have any significant  angina in spite of  having one or more critically  narrowed coronary arteries.

The reasons could be many ,

  1. Little viable tissue to generate Ischemia.
  2. Less contractile elements and less MVO2 consumption.
  3. Severe LV dysfunction makes these patients adopt a very restrictive lifestyle.
  4. Loss of nerve fibers  along with myocyte necrosis and apoptosis.
  5. Post CABG patients often have no angina due to denervation..

The benefits of revascularisation in ischemic DCM is not clear. As the cardiomyopathy  progresses , intensity of angina regresses and dyspnea dominates .Presence of angina makes the decision to  revascularise easy .To consider dyspnea as an anginal equivalent in ischemic DCM and advising revascularisation can not be  justified .

 

 

Human facial configuration  is formed by fusion and absorption of  different  tissue structures in a preplanned genetically programmed planes . The developing cardiogenic area  lies right in the cranial end of the  neural tube which enlarges to grow as face .The timing as well the location of facial plates are closely related to cardiac development. As the head end unfolds  to take it’s shape , the heart folds to form the chambers and the great vessels , septum and valves are subsequently  cleaved . Even minor genetic errors in the codes that  initiate and coordinate  the bio-genetic forces in the cardiogenic  area ,  results in simultaneous defects in  facial as well as cardiac contour .

There is a proposed embryonal classification for congenital heart disease (Clarkes ) The genetic  defect responsible for cono-truncal anomalies are located in  chromosome Q22.

 

cono truncal facies heart face abnormality catch 22 tof cardiac looping

 

cardiac development embryology of heart

Reference

1.Conotruncal anomaly face syndrome is associated with a deletion within chromosome 22q11.J Med Genet. 1993 Oct; 30(10): 822–824

Parallel reading
geentic basis of face development cono truncal facies

It is stunning to note some of the plant  species (Chinese Ginseng)  express unusual human phenotypes  , indicating the genetic codes responsible for  such things are beyond human comprehension . If one can  demystify  the genetic basis of this  perfectly smiling fruit plant with a human face ,  we may also know  what makes  it to go awry in human CHD  !

ginseng fruit cono truncal facies geentics of facial development

Interventional cardiologists in one way be labelled as intra-cardiac and intra-vascular civil engineers.Their primary  job is to create ,or close vascular tunnels and holes in various locations within the heart.How to deliver the  working hardware  to the  site of action ?. Temporary bridges ? .The vascular access is through long sheaths though which , wires, catheters, and devices , valves  are transported. It’s the key supply line to the ultimate battle field of life , right inside the beating heart.  .

So far,the sheaths  and catheters were rigid tubes with a fixed diameter.Innovative sparks come from  strange thoughts.As we struggled to take the per-cutaneous valve for  TAVR  through small caliber sheaths , some one thought why should the sheath be fixed and static .Why can’t it accommodate  liberal sized devices just by expanding its shaft like a python ,come back to its original state once the device passes by ?

Expandable sheath 164 solo path tavi tavr cathlab hardware

Thus came the expandable sheaths. Soon this concept is going to come in a big way and most complex and large device interventions will be benefited by this.

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

 

 

 

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