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How common is ischemic SVT ?

November 4, 2009 by dr s venkatesan

Ischemic ventricular tachycardia is a  too well recognised clinical  entity  . But , ischemia triggered atrial arrhythmias are less often encountered .

Does that mean , atria are relatively protected from the effects of ischemia ?

Not really  . . .  It  is possible  it may not be  that rare ,  as we think .

And then ,  the semantics play  a major  role !

Atrial fibrillation  is the commonest supra ventricular  arrhythmia  in human ,  we also know CAD is the leading cause of the AF apart from HT & Cardiomyopathy . So technically , ischemic SVT  is  more common than Ischemic VT ,but we do not call it so !

If we analyse the triggers for AF it is more often hypoxia  (than ischemia )  . . .yes there is huge difference between the two .In the ventricles it is more often ischemia that  trigger a VT.

Atrium is very sensitive to systemic  oxygen saturations especially in elderly and COPD patients. This is the reason we get many of the complex atrial arrhythmias in hypoxic situations ( Ectopic atrial, Multi focal atrial , etc) .These arrhythmias are difficult to control unless oxygen saturation is corrected. While  many of AF episodes are transient and disappear after correction of hypoxia.

If the ventricle also  responds with fibrillation  at times of systemic  hypoxia ,  one can  imagine the disastrous consequence ! God is kind enough , systemic hypoxia per se  rarely trigger a VF ,  though  it can maintain a VT which was initiated by some other mechanism.

So what are the causes of  narrow qrs tachycardia in the coronary setting

Apart from AF ,  Ischemic SVT  can occur in the following situations

  • STEMI -RVMI
  • Atrial infarction -Focal AT -Atrial flutter /AF
  • Post Pericarditis
  • Refractory , ischemic JT (Junctional tacycardia ) in elderly , perioperative , hypoxic patients

*Atrial arrhythmias are very rare during unstable angina for some unknown reasons . Atrial scar induced ischemic focal AT is underdiagnosed.

** Never  diagnose AVNRT /AVRT in a patient   who has an ACS. It is likely you will be 99.9% wrong.

*** Preexcited AVRTS are very rare in elderly CAD patients even in those with a history of SVT  .This is because as the age advances the accessory pathways undergo degeneration either by ischemia or  the wear and tear  and get self ablated .

Many times the associated , HT and diabetes may contribute to the arrhythmia.

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What is the difference between isoelectric P waves and absent p waves ?

November 4, 2009 by dr s venkatesan

P waves represent atrial depolarisation. The p wave height  and width depends not only the size of the RA and LA but also the site of  origin of atrial  impulse .A normal SA nodal origin of P wave produce the normal shaped p waves.

We know  ectopic  p waves can have a wide variation of morphology.(Fully inverted, partially inverted, slurred, bi phasic, notched, rounded , deformed, etc. The morphology is dictated by the direction of p wave vector and thus it is quite variable in different leads. Further  it is also determined by the inter atrial and intra atrial conduction.So in summary , an ectopic p wave can have any morphology we can think off !

What is isoelctric P waves

It is rather a surprise we have not thought about so long,   like a low voltage QRS ,  a  p wave can also be very low amplitude and it may be entirely isoelectric , which could actually mean the p waves are as good as absent.This can happen in all leads or in few leads. .Atria gets electrically activated but fails to inscribe a p wave .This is termed as isoelectric p waves

The importance of isoelectric p waves

It  can  happen , both  in sinus rhythm  and in ectopic atrial rhythm . Absent p waves should be differentiated form isoelectric p waves. It is typically described in focal atrial rhythm arising from the right side  of  the  inter atrial septal near the   perinodal  tissue.The atrial tachycardias arising from this site are classically have isoelectric p waves in most of the leads especially  V1 .

Other causes of absent p waves

  • Atrial fibrillation

The classical example .in fact here p waves are replaced by fine or coarse fibillatory waves

  • Sinus arrest  plus Junctional rhythm with retrograde VA block

Not all junctional rhythm result in absent p waves .Many record inverted retrograde p if there is VA                            conduction.

  • Sino ventricular conduction .P waves appears  absent in surface ECG. It occurs in hyperkalemia /renal failure is due to high levels of pottassium   which suppress the atrial activity sort of atrial electrical paralysis but still impulse originates in SA node traverses  the inter atrial pathway and reach ventricles.typically P waves are absent or can be termed isolectric.
  • Atrial  stunning following cardioversion

Long standing atrial tacycardias may fail to resume it’s mechanical (or even electrical ) activity after  cardiversion  .If it is electrical stunning the p waves do not immediately appear  but occurs later .In fact this could be termed as failed cardioversion.

* Note  p waves are failed to identified in many of the VTs AVNRTs

Final message

Absent p waves ,  isoelectric p waves , hidden p waves, merged p waves , low voltage p waves , unrecorded p waves,  selective absence of p waves in some leads all can happen in clinical cardiology practice.

One should realise the importance  differentiating   absence of   p waves in the given strip of ECG from failure of p waves to  get recorded by the  ECG machine .This has diagnostic significance.

Posted in Cardiology-Arrhythmias, Uncategorized | Tagged , , , , , | 1 Comment »

How to estimate right atrial pressure with echocardiography ?

November 3, 2009 by dr s venkatesan

Estimation of right atrial pressure (Often referred to as  central venous pressure (CVP) is a common hemodynamic excercise both at the bed side and in echocardiographic lab. A venous catheter inside the right atrium is probably  the best way to measure it accurately .But, there are  practical issues  for  putting and maintaining a CVP catheter. ( & We also know , what happened to the concept of routine  swan  catheter in critically ill patients !).

A  rapid bed side echocardiography  can give us a fairly accurate estimation of RA pressure . We  don’t even need look into the heart , what you need is imaging the inferior vena cava , it’s size and it’s  behavior  with respiration  . You don’t require  a doppler probe either ! With these two parameters one can decode the mean RA pressure. This  modality is rarely used in the ICUs , it can be a simple aid to fluid management .

RA pressure echocardiography ivc collapse hepatic veins

ivc collapse ra pressure right atrial mean pressure

Shrewd clinicians would argue , we have a natural catheter inside the right atrium, ie the   internal jugular vein   This gives us a unique opportunity to study the moment to moment RV, RA pressure . And .  .  . yes ,  we know it but we rarely respect the neck veins !

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Does the esophageal spasm get relieved by sublingual nitroglycerine ?

November 2, 2009 by dr s venkatesan

Esophagus and the heart are closely related structures. Both can generate chest pain that can mimic each other. The squeezing substernal pain  is very characteristic of esophageal spasm  .The smooth muscle of esophagus can exactly mimic a vascular smooth  muscle  .The relief of chest pain following nitrates  though very classical of angina it can very well alleviate the pain of esophagal spasm also. This has important clinical implication

Also read

Cross talk between heart and esophagus

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Origin and location of chest pain in acute pulmonary embolism

October 21, 2009 by dr s venkatesan

Pulmonary embolism is  one of the  important  causes of acute chest pain . It can mimic  acute coronary syndrome . In fact along with aortic dissection  , it forms  a  differential diagnosis for STEMI especailly if the ECG is not typical.

pulmonary embolism chest pain dvt d dimer ventilation perfusion

The Chest pain of acute pulmonary embolism can originate in one of the following structures  with different mechanism

  • Lung parenchyma ( Necrotic pain ?)
  • Pluritic pain in adjacent necrotic segment
  • Main Pulmonary artery and it’s branches
  • Right ventricular mechanical stretch
  • Right ventricular ischemia
  • Hypoxia induced LV ischemia with coexisting CAD.
  • Multiple contribution from any of  the above *

It should also be remembered , medicine never respects logic, as some times  an episode of pulmonary embolism can occur without any chest pain

Localisation of chest pain

One can imagine ,  how difficult for the  nervous system to zero in on the origin of this  pain as  the structures involved in acute pulmonary embolism are in different planes  and in different depths  within the chest cavity . Patients  often complain vaguely  the site of pain but  what is universal is severe resting pain deep within the chest . If the ischemic lung segment  transmit pain signals , the location and radiation depend on the  bronchpulmonary segment involved.This again adds on to the complexity in the  genesis of pain  .It can be virtually any where in the back or front of chest.

But , the central and retrosternal chest  pain are equally common as invariably the central pulmonary arteries go for a acute stretch which can be severely painful .In fact , current thinking is it could contribute maximum  for the intensity of chest pain. Similarly,  acute dilatation of RV result in mechanical pain. RV sub endocardial ischemia may   also contribute .An intact bronchial  circulation( From aorta)  can limit the  ischemic lung pain .

Final message

Analysing  the chest pain of acute pulmonary embolism can be an  interesting academic exercise . It could arise from multiple structures with different mechanisms. It may not be much significant with  reference to management . But it has a diagnostic role.  A pain which is severe , and  atypically located should raise the suspicion of acute PE especially  if the patient has associated dyspnea.

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What is being rescued in rescue angioplasty ?

October 18, 2009 by dr s venkatesan

Rescue angioplasty as a concept in PCI is advocated for the past  two decades. Rescue angioplasty  continues to enjoy the  controversy over the years. A procedure which fails to shrug off the controversy for so long   inspite of multiple studies ,  would indicate there is something seriously wrong in the  procedure  or in the conceptualization.

The fundamental question   that  is often  and not answered properly is :

What is being rescued in R angioplasty ?

Is it the

  • Patient’s life ?
  • Myocardium  ?
  • Rescues ischemic myocytes
  • Infarct related  artery ?

*Or it simply rescues physician  from the legal issue arising out of  labeling his patient as  failed thrombolysis

The term rescue generally implies  tackling an  impending crisis .The threat is either  to the patient’s life or to the myocardium or both.

In STEMI when the initial reperfusion strategy fails (Usually thrombolysis)  R -angioplasty is considered. Here the aim is  to  rapidly  rescue  and salvage  myocardium . The problem  here is   , contrary to our expectation   the population of failed thrombolysis is not a homogenous one .In one end of the spectrum ,  is a patient with  persistent ST elevation ,   totally comfortable and pain free and  hemodynamically stable.The other end is , deteriorating blood pressure , tachycardia , progressive angina and impending cardiogenic shock. Considering the above situations it is very simple to guess who will  require the rescue  and  who will benefit more. In fact,  R -angioplasty  in   patients with  asymptomatic  failed thrombolysis  without ongoing  ischemia defies logic and conveys no meaning !  .This is especially true if the patient has crossed 12 hours of time since the first symptom.

In deteriorating patients R- PCI has a role where one can potentially  arrest the progression of cardiogenic shock  or even reverse it.

A third  group  among failed thrombolysis have  predominate  angina  with  hemodynamic stabilty. This group will benefit from R angioplasty  irrespective of time window , as the pain is often due to a critical non IRA lesion .Technically again we can’t call this PCI as rescue as nothing is done to salvage the myocardium . (Of course one wish to call it so ,  as the  patient is rescued from angina !)

A tricky issue is to know where does the pain come from in a post MI patient ?

It should be realised a post MI patient can have variety of source of chest pain. There has been instances where a persistent  pericardial pain has resulted in emergency  R-PCI !

The critical question that  has not  been  answered by cardiologists is

How long a STEMI pain last and when does post infarct angina begin in a  susceptible patient .

 

In other words how do differentiate present(Index event)  infarct angina from post infarct angina ?

Studies on pain signal transmission (medullated type c)  would suggest a dull aching retrosternal pain may occur in a substantial number of  patients  following STEMI .These pain signals come from  necrosed cells and not from  ischemic cells. This pain ceases after complete  ischemic destruction of nerve endings . The threshold , duration and central perception of this pain is highly variable.

One can imagine the importance of the above issue ,  as   there is a potential  to  misdiagnose recurrent post MI angina   for the relatively benign infarct related pain. Though experience have suggested a 12 hour cut off to define post MI angina ,  it is too empirical .

Final message

  • Rescue angioplasty remain as  disputed entity in vast majority of  post MI population .
  • It is most useful when  it is done in  impending cardiogenic shock .Note the word. Impending  . . . not established cardiogenic shock. (After prompt recognition of failed thrombolyis ,  within  overall time window < 6h*  ideally ,  but may be done  to up to 12h) There is no role for routine rescue in all failed thrombolysis patients , for the simple reason there may not be any clinical or  live myocardial  targets for rescue.

Need for seperate time window for rescue angioplasty

* Even this 6 hours is emprical . We need  seperate evidence based time window exclusive for rescue angiopalsty .I would personally believe this could  be as short as 1-2 hours .

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Can medical mangement convert a patient with positive stress test into negative ?

October 16, 2009 by dr s venkatesan

Exercise stress test is the most commonly used non invasive  diagnostic test for CAD.

It is also useful in the functional capacity evaluation.Even though medical management of CAD is a proven and accepted  method of therapy in CAD . There  is always a   perception  even   among the  cardiologists  medical management  is an inferior form of treatment.  This is primarily due to peer group  pressure rather than based on solid scientific concepts.

What is the effect of medical  management on  the common CAD parameters ?

Relief of angina  . It is a simple , and easy parameter to assess.

Functional capacity . Increased exercise capacity  is a good marker of successful medical therapy

The effect  on stress ischemia could be most objective way to assess the success of medical therapy.

But , unfortunately this does not come in the regular scheme of things  for many  cardiologists following medical  management. If we are able to document reversal of stress  test positivity it could be the ultimate marker of success in medical revascularisation. EST is an approved method of assessment of efficacy of optimal medical  management .Still ,  in day to day cardiology practice this is rarely done for the simple reason the patient often stumbles upon an  interventionist and lands up in a PCI or CABG !

Following  things can happen over EST following medical management

  • Complete correction of inducible   ischemia
  • Delayed appearance of ST depression with increased exercise capacity
  • Duration of ST depression can be reduced
  • Convert painful  ischemia into silent ischemia*
  • No response **

* Conversion of painful episodes into silent episodes may not be a real success  in physiological terms.But in patient point of view it is .It should be  recalled  even in  CABG  pain relief  is a major clinical  outcome .

** Could be termed as failure of medical management , but there  is a  group of patients who have increased exercise  capacity but still EST is positive

Real world experience of large case studies (Individual communication : Large community based stress test in over 9000 patients ( Gnanavel et all Ganesh clinic Thiruvannamalai ,India ) strongly suggest optimal medical management would indeed reverse exercise induced ST depression.

Why can’t we call medical therapy as a revascularisation procedure ?

Human mind does not accept certain things. Simply swallowing few drugs can never make us believe ( Especially the current generation cardiologists !  )  it can be  equivalent to a PCI/CABG

While , restoration of  TIMI flow ,  %  stenosis , Net luminal gain,  are the popular   scientific parameters fro effective revascularisation , the following are  the  desired outcomes  clinical well being , relief from pain, reduction of plaque volume, plaque stabilisation, maintenance of  collaterals , microvascular patency ,  reduction of recurrent events .The irony in CAD management  is  in many points clinical endpoints can be achieved without mechanical  the above  mechanical end points !( As we learn from the OAT, COURAGE trials where we learn t arterial patency is nothing to do with major  clinical end points )

While PCI and CABG inherently convey they are revascularsation procedures , realistically looking medical  therapy also does improve the vascularisation espcially where it is needed (Micro)

In the overall interest of  CAD community , and with good scientific basis ,  it is vital  to  emphazise medical management of CAD  is  also a  form revascualrisation .It is better to call OMT(Optimal medical therapy )  as medical revascularisation .This will help us  to neutralise the unfair” semantic  advantage” the PCI and CABG enjoys as   revascularisation modalities !

 

Refer: 1.AVERT study :Atorvastatin equals PCI .2.Regular excercise equivalent to PCI (esc2009)

Final message

Medical management , do reverse  the positive EST in most of the patients provided the drugs are optimally used

Stability provided by  medical management   in coronary micro and macrocircualtion is  often  significant and it can either directly  or indirectly improve coronary perfusion .  attenuate ischemia ,  improve exercise capacity and relieve symptoms. To confirm this , every patient  with medical management should periodically undergo exercise stress testing.

* One may argue , without knowing coronary anatomy  it is dangerous to  assume things and every patient with positive EST should udergo CAG. Yes ,  It may be true, ischemia due to  critical lesions in proximal locations can never be corrected with drugs

Posted in Uncategorized | 5 Comments »

Routine Thrombus removal during primary PCI is it safe always ?

September 25, 2009 by dr s venkatesan

Current data from TCT

TCTMD – The Source for Interventional Cardiovascular News and Education

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How to humiliate medical therapy for CAD ! Learn how COURAGE and OAT trials were disgraced by the mainstream cardiology community !

September 25, 2009 by dr s venkatesan

Medical profession has  evolved over centuries with humble discoveries by genuine researchers in the past . As we  pursued  science vigorously  , we  looked  for innovations , when innovation  work ( or many times shown to work !) we jump to sky , even as  some of these  innovations fail and crash down  to earth , many times  we continue to be in the clouds . This is the fundamental problem of modern medical science . When  our expectations reached  unrealistic proportions ,   we tend to lose the common sense . Prolonging life and reducing human suffering may be the ultimate aim of the medical  profession , but  If we try to fight the death with science and money without application of mind , our current  life may become  miserable ! Thats what is happening for the majority of the population of this planet . After all ,  death is an essential and final  component of life !

Coming to the issue of CAD ,  in our country , a  rich gets a 4th generation drug eluting stent for a insignificant  asymptomatic PDA lesion , and poor fellow with left main dies without any intervention .This is  fairly acceptable   to this uneven world  , where a rich westerner  dies due to obesity related disease and a  poor African dies to malnutrition .

This article is in   response to  my  recent  experience  when  . . . I advised

Simple life style modification &   few drugs   for a patient with chronic multivessel   CAD  , I was  made to look   ordinary , inferior  and funny   by  many of the current generation cardiologists .

Further , the term optimal medical therapy(OMT)  for chronic stable angina has evoked laughter in one of the interventional cardiology  conferences  I  attended !

It is a sorry state of affairs  for the whole cardiology community , a  genuine scientific  fact , proven by  real life experience  as well,   is  being  ridiculed.

Richard  Conti tells in this excellent editorial in his journal   Clinical cardiology about the issue of medical management of CAD

“Respect in clinical trials”

Chronic stable angina pci vs cabg vs medical courage trial oat trial ethics in cardiology

Click here to reach the article  http://www3.interscience.wiley.com/cgi-bin/fulltext/122512853/PDFSTART

A similar study which  suggested  exercise  could be  better than PCI in the recent 2009 ESC is suffering the same fate !

What if regular exercise were as good as a stent for stable angina?

http://www.theheart.org/article/1000047.do

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Great medical web sites : How to innovate medical education ?

September 23, 2009 by dr s venkatesan

Internet has revolutionised  in sharing our knowledge . But  , the  freedom it gives  has a trade off .Identifying   genuine  knowledge  in the  vast cyberspace is like searching for lost treasure in the ocean bed.

Have a look at this site which innovates medical teaching

great medical videos top cardiology web site drsvenkatesan

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