Posts Tagged ‘cath lab’

Years ago ,  I  remember asking my professor during  a balloon mitral valvotomy workshop .

How  is that ,  you  are able to  puncture the  IAS  effortlessly and efficiently sir ?

Every thing is in the feel  Venkat ,  he used to say !

What  feel ?  I  used to wonder !

Now , I  realise the guide wires  and catheters are just an  extension of our hand and fingers.

When we   tackle  CTO lesions we should   be  able to feel  and differentiate the  capsule and dimple .

More sensitive hands (Brains)  can tell whether the guide wire  is poking the vessel wall or the lesion .

Of-course ,  now  we have sophisticated OCT, IVUS, and camera  tipped ( Is it really there ?)   guide wires to guide us.

Still ,  a cardiologist  who  is able to feel the  lesion intimately  . . .  would be  a clear  winner !

How to feel a lesion ? (Plaque palpation ,  Hitting the calcium  , Feeling  the  thrombus  !   Cuddling the  foramen ovale  etc )

Key word : Guide wire tactile sensitivity .We are familiar with   guide wire torque .Now , a new technology  that can transmit the feel of the target lesion  ,  to the hands  of  the operator  would be very much desirable .

Two point discrimination  and temporal cortex  plays a critical role here. Irrespective of  the hard ware  used   , how  the  brain  perceives  touch is going to determine whether you are going to cross  a difficult  lesion .

Can you electronically amplify tactile feeling like sound amplification ?

It may be possible in near future. But it has  other issues  like   hypersensitiveness

Can a physician with defective cortical sensory  system  face difficulty in catheter based  interventions ? 

I have observed at least  two  cardiologists with diabetes  , acknowledging  major  difficulty  to  feel the palque and  cross  the  lesion   (Due to autonomic  neuropathy ?) With many  cardiologists  rapidly aging  , the quest  for intervention  goes unabated   (Still  unwilling to quit !   )  one may  experience  cortical dementia  as a hurdle for  guide wire manipulation . These issues need  to be tested  in  real  world .

Final message

It  is   fascinating  ,  how the feel  of  coronary plaque  reaches  our brain . It is picked  by the tip of  guide wire , travels about 150cm , handing over the weak signals across the  gloved fingers ,  reaching all the way through cervical spinal cord and spino-thalamic tracts ,  brainstem  and finally to the  cortex.

There are  multitude of factors that determine   the success of   complex  angioplasties . I realised  suddenly , Intact  cortical sense  could  be an  important one,  among  them . Let us train our brain  centres for this specific sensation of cath lab hardware . After all ,  the brain is  maneuvering force in any cardaic intervention !

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Chronic total occlusion is the cardiologist’s  daymare .Here is an article that adds on to 1ooth technique to cross the chronic total occlusion within the coronary artery !

If only we succeed in  this  Arabin magic , in the cath lab we can open the doors of  all CTOs .

This technique is based on the principle  to push the hard plaque  into the adjacent side branch like a sliding door,   if the pateint has one !

The only isssue  with this  technique  could be the    “cave door”  may close again immediately  as it did for Alibaba    !




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There are millions of  articles in cardiology . Some  simply  occupy   valuable spaces without any purpose  . Some give us knowledge . Some enlighten  us. While few are  so vital , it is almost a crime  if we do not read such articles and apply  it in day to day  practice .

This an article  written by Henri Justino that has a immense importance for the patients as well as the physicians .

Do not think  the article which came in pediatric radiology  is not applicable in adults !

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atropine leafsAtropine ,  the extract from the  Belladona  plant  is an important cardiovascular  drug. It’s  presence is vital  in every crash carts .  This  unassuming molecule  probably has   saved more cardiac lifes than any other drug . It provides immediate  remedy for many of the bradycardias .It  works like a magic.  The physician buys  time with this molecule  and  proceed  on to resuscitate or  plan other interventional  procedures. It is most powerful antiarrhytmic agent known .It is an irony , many of  the standard cardiac texts do not even mention this while discussing anti arrhythmic agents .

In  this  era of  hyped  cardiac  care   , the  sartans ,  2b3a inhitors   , the fondaparinux’s  making merry !  we  have no spare time  to realise  ,   more  cardiac  deaths  have been prevented by atropine  than  all these   drugs    put together.  It is still working like a bull  across the coronary care units and cath lab world over. While  many mediocre  drugs  enjoy a  big  bash  time for  possibly  saving   few occasional  lives   , the atropine  like drugs never get the due recognition among cardiac literature for the simple reason ,  it being a  cheap  generic drug.This drug is available  for few  rupees , no marketing no advertisements, no celebrations.

Mechanism of action

The  biochemical  mediator :  Acetyl choline

Site of action :     It blocks the M2 (Muscaranic receptors) .

We will confine to the cardiovascular  actions.

  • SA nodal acceleration
  • AV nodal accelerated conduction

Effect on ECG

Sinus tachycardia

Short PR interval

Life saving situations in cath labs  in CCU.

Vagus  nerve richly innervate the heart and blood vessels . Acute coronary syndromes   especially involving the infero posterior territory  raises the vagal tone  , and can  in severe bradycardia and hypotension.  In cath labs , as we  manipulate  cardiac  structures with wires and  catheters  there is always  a potential to elicit the vascular reflex .It can occur  any where between the  access point , femoral or radial  artery to coronary arteries .

Further ,  whenever the  pain  intensity is more , the  central pain integrating  centre in  brain stem  and thalamus has a spill over effect into the vagal nucleus .

What happens if a vaso vagal reaction is left untreated ?

We have often  made  the term “vaso vagal  reaction” appear as an  innocuous  entity. The main reason for this perception is   due to the common occurrence of  “vaso vagal  syncopewhich  is largely a benign entity in the general population .This fact  has sensitised our brains . One should distinctly realise the vaso vagal syncope that occurs in  healthy people standing  in erect posture ,  from  vagal reactions that  occurs in  lying patient with a diseased heart  in a  cath  lab  or CCU.In the classical vaso vagal syncope , assuming the recumbent posture is the treatment and it  counters the hemodyanmic imbalance .No drug is required here. So the common vagal syncope can never be compared with potentially dangerous  vagal reflex that occur in CCUs and cath labs. If not recognised earlier and  immediately countered  it can lead on to asystole and death .Many of  the delayed deaths post PCI during sheath removal or an episode of vomiting are directly related to this.


Atropine is the Savior here . Can you imagine a  world without atropine .

The other reason we had always considered vaso vagal   reactions lightly is that the poor atropine is always available  in the side selfs and it acts   rapidly  and promptly with almost  100 % success  reversing the vagal action  in less than  60 seconds .

How often we here  this  “Oh it’s a brady . . . push  2cc atropine . . .  given sir, the rate has picked up . . .”

If only atropine has a failure rate of say  50%    we  would have  realised the full impact of   vaso vagal shocks (See … how we struggle with No reflow   with no effective drug available !)

Is there any other alternative  treatment  for vaso vagal shock other  than atropine ?

No.   (I guess so . . .Readers may correct me )

Other uses of atropine in cardiac practice

  • During stress testing along with dobutamine  to  increase the heart rate.
  • It can be used to differentiate AV blocks the two types of 2nd degree AV block. The mobitz type 2 worsens while type one accelerates.

Non cardiac uses.

Ophthalmology, pre anesthetic medication, bronchial asthma, various poisoning.

What is the future for this molecule ?

Remain bright .  But only very  few companies make this molecule.  It is a drug that can not  fill the cash boxes but  it is a drug to keep the human heart running at times of crises  . The only  threat to this drug  is  the  possibility of it being replaced with a  modified patented  version of this great  molecule  !

Final message

The evolution of medicine is based on strong foundations  put upon by clinical acumen   by great medical men of  past generation. Atropine was developed by such people   and it has withstood the test of time. This drug  probably  has saved ( and  continue to  save)  many  lives  than any  other drug  in cardiology . It should be recalled ,  another great cardiac drug   called digoxin  has almost succumbed to modern medical  forces  .Let us  keep developing   new molecules  ,  we shall also pay  tributes  to some of   the  unassuming drugs in cardiology .

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Scientifically ,  the  indication for coronary revascularisation   should be  based on following

  1. Patient’s  symptom ( more specifically angina , dyspnea is less important !)
  2. Prov0kable  ischemia  ( A significantly positive stress test )
  3. Signifcant LV dysfunction with  documented  viable myocardium &  residual ischemia
  4. A revascularisation eligible coronary anatomy * TVD/Left main/Proximal LAD etc ( *Either 1, 2 or 3 should be  present  in addition )
  5. All emergency PCI during STEMI /High risk NSTEMI

Practically ,

A CAD  patient  may fulfill  “Any of the above 5 or  “None of the above 5” ,  but ,  if   a coronary obstruction  was  revealed  by coronary angiogram  and if he  fulfils The 6th criteria , he becomes  eligible for  revascualrisation

6th criteria

If the patient has  enough monetary   resources (by self  ) or by  an  insurance company  to take care of PCI /CABG *

*The sixth  criteria overrides all other criteria in many of the cath labs .Of course , there are few genuine ones still  fighting hard , to keep the commerce out ,  from contaminating cardiology !

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A poorly deployed drug eluting stent is far inferior to a properly deployed bare metal stents

  • Doing a plain old balloon  angioplasty ( POBA)  is not a scientific crime , millions of coronary lesion just  need that! ( Click here -Why POBA is important ? )
  • PCI is most effective during an ACS than a chronic coronary syndrome
  • Primary PCI is a race against time and muscle , not a race against money ! Don’t do it  for a  evolved   MI
  • Recognise , from the patient point of view  the term no reflow is  generally  synonymous with   failed primary PCI( It is semantics !)
  • Side branch  can be more important than main branches , so don’t sacrifice it often
  • Attempting a trifurcation  angioplasty is generally not in  the interest of the patient but  to show interventional expertise
  • Make sure surgical back up means, a table is reserved with a surgeon fully informed and ready

When in  doubt , it is always  better to err on a longer stent than a shorter one

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This paper was presented in the just concluded 60th Annual scientific sessions of cardiological society of India , Chennai.India


Venkatesan  sangareddi , G.Gnanavelu, R.Alagesan,V.Jaganathan.

Department of cardiology, Madras Medical College, Chennai.


                          Radial  artery  has become the  major access  site for the interventional cardiologist in recent years. Radial approach has provided increased patient comfort and  less access site complication. Many  of  the   complications  are  unique to radial approach mostly due to  anomalies of origin, and course while others are  hardware related .Unlike femoral arterial access ,  compromise of blood supply to hand is never considered a  threat because of dual blood supply to hand  .But the fact  is that,  it  could be sub-clinical  and the hand is rarely assessed for vascular insufficiency after a radial procedure.

             The aim of the study is to assess the  impact of   radial  procedures  on the  blood flow  to  hand . 20 patients who had undergone routine  radial coronary  angiogram  formed the study population. All patients had negative Allen’s test prior to the procedure. The mean procedure time was   25mts (18-45) .Standard  hardwares were used. Difficulty in crossing at forearm and   subclavian   was observed in  4  patients. Extravasation of dye  in forearm was observed in two. Allen test  was  done 24 hours  after sheath removal and  repeated 48 hours after the procedure .  4 patients   showed positive Allen test  at 24hrs. One  patient   regained  Allen negativity at  48hours. The incidence of positive Allen test at  24 hours is 20%. The compromised blood flow was correlated with the  procedure time, and a difficult catheter course .

                 We propose,  radial procedures especially , when prolonged has a potential to compromise palmar arch flow .This phenomenon  is  either  permanent  or transient  and  may be attributable to enhanced  endothelial tone and sheath related injury. Irreversible  compromise  of blood flow to  palmar arch  may  also occur  in radial dominant hands. Further enhanced  sympathetic tone can  spill over to ulnar artery as well . 

             It is concluded, interventions through radial route has hitherto unreported adverse effect  of  “Post procedural  positive  Allen test”  . It  implies , radial  procedures  could  convert  a dual blood supply  pattern of the  hand to ulnar dependent  uni-modal  blood flow  in a significant  subset of patients. This is important   to recognise, as it   precludes further radial procedures in the same patient.


Final message

Hand function could be as vital as our heart’s ,   please handle with care to avoid this complication


Click on the slide to download PPT presentation


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