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Why P wave becomes “tall” in RA enlargement and “wide” with LA enlargement ?

September 20, 2009 by dr s venkatesan

Normal P waves

normal p wave ecg rae lae

What are the components of Pwave ?

RA component : The SA node depolarises the RA first  , so the initial part of  P wave represents  RA  current .After about 40msec  the wave front reaches LA and it begins it’s depolarisation .LA component :By the time LA is maximally depolarised the RA  already starts its repolarisation.So there is  overlap and also a short time lag between these two wave forms . This is very important to recognise as , even if the RA conduction is prolonged in pathology the RA component of P Wave still falls within the LA wave .Hence it is not shown in the ECG and P wave is not widened in RA enlargement. This is in contrast to LA enlargement , when the terminal half of P vector delayed it stretches the P wave wide beyond the normal 110ms .Hence LAE widens the Pwave.

Why P wave becomes taller in RA enlargement ?

In classical P pulmonale , the P waves are  tall >2.5mm. It is easy to explain why it not getting wide than  why it is getting taller ! The atrial vector has two components .The initial RA vector  is directed  anteriorly .The main reason for tall p with RAE is  due to the anatomical proximity of RA to the chest wall Further ,the  Initial atrial  electrical dp/dt is steep . Any RA voltage increase is easily picked up by the chest leads and P wave voltage increase and becomes tall. We need to realise LA is not only left of RA its equally posterior of RA. Hence LA enlargement rarely brings (Never ?)  it closer to chest wall ,and hence high voltage tall P is almost unheard of with LA . Note , deep negative late P wave activity is typical of LAE , consistent with its posterior location as well its late depolarisation compared to RA)

rae right atrial enlargement ecg tall p p pulmonale p tricuspidaleright and left atrial enlargement how to differentiate lae rae

Why LAE can not produce tall P wave ?

The Left atrial vector which  follows RA vector  is mainly directed posteriorly and hence inscribe a  descending  limb of   P wave . This causes the P terminal force .  So  the direction of vector forces  and the anatomical locality  make a  tall & positive P  deflection highly improbable in   LAE .

*Of  course  when LAE is   huge , where a antero -supero vector from  roof of LA may inscribe a positive wave .

What happens in bi atrial enlargement ?

It can have features of both . Tall & wide P waves .

Can RA generate a Q wave ?

Yes . When RA assumes a huge  size  , especially if the RV is also at high pressure as  in severe PHT or valvular PS   a  q wave is generated in the lead V1 .This q wave is nothing but the intra cavitary potential of the enlarged RA.

What is the difference between atrial enlargement, atrial dilatation, atrial hypertrophy, intra atrial block and inter atrial  block  ?

The p wave morphology has no  specificity to identify the various entities. In any pathology of atrium the first thing that happens is a conduction delay ! It is now realised the bulk of the changes we see in atrial enlargement especially in LAE is due to intra and inter atrial  blocks or more subtly conduction delay.

It is  obvious , a wide P wave can occur either  due to LAE or simple conduction delay .In elderly  hypertensive patients atrial fibrosis is more common , one can not confirm LAE  without echocardiogram .

A notched P wave  can be a very specific sign of   inter atrial block .Which is more common in severely diseased left atrium. A notch , slurred p wave is a good marker for impending AF or atrial flutter.

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Posted in Cardiology - Clinical, cardiology -ECG, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , , , , , , , , | Leave a Comment »

Medical pharmacology is not simply learning how a drug acts , it is also about “How a drug company acts*” !

September 19, 2009 by dr s venkatesan

Pharmacology is a major discipline in medicine where we learn how a drug acts in our body for various ailments . Now  in this era ,  doctors need not only how a drug acts but also how a drug company acts ! This has become vitally important   for the welfare of the mankind .

In this context one of the best books on medical pharmacology is from the

Famous Editor of New England  journal of medicine

A must read for all genuine medical professionals

ethics hippocrates ebm

Watch Marcia Angell  talk http://www.youtube.com/watch?v=ouF3ISihHLM

Full lecture of Mercia Angell  http://videos.med.wisc.edu/videoInfo.php?videoid=940

Click to buy/read the book  http://www.amazon.com/Truth-About-Drug-Companies-Deceive/dp/0375508465#reader

A Review  about the book  http://calitreview.com/176

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Should we not clarify what exactly we mean by wide qrs tachycardia ?

September 18, 2009 by dr s venkatesan

Wide qrs tachycardia has a unique place in clinical electrocardiography .It is  a much fancied and glamorous entity for the simple reason , it continues to be the  cardiologist ever solved puzzle .For over three decades of research, clinical debates , symposiums , seminars have effectively failed to take away the uncertainties in decoding the wide  QRS  tachycardia . (Specifically ,  VT vs SVT with aberrancy)

Some wondered , should we really waste our efforts in differentiating the two . In emergencies it never matters , in fact one need  not attempt to do this often futile exercise !

Few dedicated criterias like Brugada etc have helped us .

While the difficulties in differentiating between VT and SVT with aberrancy remain over the decades .A less reported  , but more common issue is  confronting  us .

It is  the big question of  differentiating a  wide  QRS tachycardia from a narrow QRS  tachycardia

wide qrs tachycardia vt svt aberrancy

This  occurs  more often than we realise  ,because we define wide  QRS  tachycardia in a vague manner

  • Normal qrs width between Up to 80 / up to 100 ms acceptable  ?*
  • Narrow qrs tachycardia 80 ms?
  • Wide qrs tachycardia i> 120ms  ?
  • Definitely wide qrs >140msec

* The confusion is mainly because 20ms difference between limb leads and chest leads .

In reality one may not be able to all  tachycardia into narrow or wide .

There is big  overlap zone that need to be labeled a intermediate qrs tachycardia

If we can  triage the tachycardias into three instead of two it may help us arrive  fast  ,  to the  correct diagnosis

Narrow QRS tachycardia ( qrs 80ms)

  • Sinus
  • All svtS (avnrt etc)

Intermediate QRS tachycardia 90-120

  • Most of the SVT with  aberrancy  ( Except antidromic SVTs which are really to wide !)
  • Septal VTs*
  • Fascicular VTs*
  • VT in PPM and ICD /CRT patients **

*  Any VT that arise near the major conducting system of ventricle conduct  fast and hence qrs are relatively narrow.

**These are rare entities where  base line wide QRS getting narrower with the onset of VT . (Ref : http://europace.oxfordjournals.org/cgi/content/full/eun254v1)

Wide qrs tachycardia >120ms

  • Most of the genuine VT (Ischemic , myocardial origin)
  • Post MI VTs
  • SVT aberrancy especially AVRT
  • Any SVT with preexisting BBB
  • Marked electrolytic disorders

Unresolved questions

  • Which lead we should look for measuring the width of qrs ?
  • Should we take the narrowest qrs or widest qrs or should we take the average ?
  • Should we calculate how much the tachycardia has widened the qrs from the baseline  width of a given patient ?  Is it not possible , what is wide for some may be normal for another !
  • If  there is no isoelectric line  and ST segment  blends with qrs complex  how to mark end of qrs ?
  • If  limb leads show a narrow qrs and chest leads shows  wide qrs what is the significance  ?
  • In precardial leads  if one lead alone shows a narrow qrs , what is the significance ?
  • Can a narrow qrs VT conduct  with aberrancy and making it  really  wide ?

Final message

When we are  able to solve   complex electrophysiological  problems  , we must also realise  even   simple  tasks can be demanding in medicne ! It is proposed to create a  new  group “Intermediate QRS tachycardia “that can help solve the issue where we have difficulty in labeling these  tachycardias which fall  in the  greyzone .We can try &  apply the modern EP based VT criterias  to this group and find out the hidden truths !

Posted in Uncategorized | Tagged , , , , , , , , , , , , , , , , | 1 Comment »

Why is absent RS complex in precardial leads is very sacred to diagnose VT ?

September 17, 2009 by dr s venkatesan

The most popular criteria to differentiate VT from SVT aberrancy is  formulated by Brugada in 1991.

The greatness of  this  criteria is that  a single question asked  is able to confirm VT in vast majority of cases.

Is RS complex absent all  of the pericardial leads ? If  the answer is  yes  it is VT 100%

How is that,  we have been struggling for so long , a single question is able to solve the issue quite easily ?

wide qrs tachycardia vt svt aberrancy brugada

This is because , the term  “Absent RS complex ” actually means

Presence of  one of the  following three typical complexes Of VT.

  1. QS
  2. QR
  3. Monophasic R

Two of them  actually imply ,  q waves throughout   V 1-V6 .This  means a badly damaged ventricle and  with  little electrical activity coming towards the chest wall .This situation  almost always occur in VT.*

The third complex is Monophasic R .

A  monophasic , wide  QRS  complex  again indicate VT  as monophasic aberrancy is very rare as the supraventricular  impulse invariably conducts with  RSr’  (The right bundle  refractory period sees to that  at least a small r’ is inscribed however fast the SVT is !  )

So if there is no RS complex  it must be VT !

What  are the  difficulties  faced in applying this   first step of Brugada criteria ?

It is funny to note , in medicine criterias  often work perfectly in  text books only !

Is there a RS complex seems to be a very easy question ? There lies the catch !  .Even though this criteria may be 100% specific , differentiating RS from QS complex even by an experienced cardiologist may be difficult in a significant number of VT tracings.This  realistically ,  reduces    supposedly  100% specificity  of this criteria !

In fact we expect Brugada to develop an  another limb  to his now famous algorithm

Is there  absence  RS complex in precardial leads  ?  Yes / No / May be ,  not sure !

Posted in cardiology -ECG | 3 Comments »

What is protected left main disease ? How good is the protection ? If good , why should it need another protection ?

September 15, 2009 by dr s venkatesan

Left main disease  is an important subset of CAD , and it has special interest for the interventionist. Traditionally cardiologist have   a fear to touch this lesion , as they thought a sudden occlusion within this vessel is life threatening   . Later on as  they gained experience  it was thought  we could intervene safely at least in protected left main . Subsequently  it was realised this fear was largely unfounded  , after all  the proximal LAD is equally  dangerous and we spend hours together inside an LAD ! .Now we have technology and expertise to do successful PCI any where in LM. And  unfortunately , the same expertise is not applied in selecting the ideal patients who will benefit the most . LMD has become a glorified indication for PCI.

The terminology of protected and unprotected LMD is in vogue for many years . Unfortunately it do not convey a uniform meaning . In next few minutes ,  I shall share  my views on the nuances of protected and unprotected LMD .

The term   protected was  not  coined by  cardiovascular physiologists   but by   interventional  cardiologists . Hence it connotes a  anatomical  meaning rather than physiological.  Protected LMD  meant there must be a at least one  graft to either LAD or circumflex . And this graft should be functional . The presence of this graft is supposed to increase the comfort levels of the interventionist as well as  the patient.

A left main coronary artery disease angiographically  can be  classified  as

Common types of Left main lesion

  • Asymptomatic , non flow limiting , angiographically insignificant disease(< than50%)
  • Ostial
  • Ostio proximal
  • Shaft : Mid, distal or diffuse Left main
  • Bifurcation

Unprotected left main

  • All the above lesions
  • Non functional GABG grafts ( eg: LIMA occlusion makes LAD unprotected)

Protected left main

  • Post CABG  with atleast one functional graft to LAD /LCX
  • ? Left main   with total  LAD and very good LAD collaterals from RCA /LCX

Partially protected Leftmain

It could mean any of the following,     Left main Plus  .  . .

  1. Incomplete occlusion of single  LIMA graft
  2. Occlusion of  SVG-LCX and patent LAD-LIMA
  3. Occlusion of LIMA-  LAD graft but patent SVG-LCX  graft
  4. Patent LIMA-LAD  but a  critical  LM / LCX  bifurcation lesion with no grafts for LCX*

The above 3  situations may demand a  PCI .But logic would  suggest one would try to open up the partially occluded graft rather than open the left main . Of course the decision involves status of RCA .

*The only indication for a  PCI  in protected  LMD could be 4

Unusual ( Crazy !) questions  about  left main disease

Can left main be protected by collateral circulation ?

It is very common to find Left main   bifurcation  lesion   with LAD having  very good collaterals from RCA sometimes filling up to proximal  LAD .This can be considered   “protected left main equivalent”

As on today , cardiologists would rather   believe  a surgeon’s graft  rather than a naturally grown  collateral from RCA however extensive it may be !

But logics and real case experience would indicate in a patient  with LMD and an  extensively collateralised LAD can in fact be  considered a protected left main.

If a  left main is well protected by a functional LAD graft , why should we do a PCI for left main at all ?

This question was risen in one of our cath conferences , a patient   who had functioning  LIMA to  LAD graft.His   RCA had a functioning  venous graft  and his circumflex had a partially functioning  graft.The left main had a near total  obstruction and the proximal  LAD was  faintly visible .

Since the  patient  had class  2 angina Options were discussed .He  satisfied  the  current criteria of protected LMD .Just because he fulfils the criteria of protected left main , he  does not  become eligible for  left main    PCI .  After all he is having this LMD for many years. Protecting again the left main which is already protected is not a big deal in terms  of outcome .  Double protection is waste of resource at additional risk. It was decided to attempt a PCI to SVG graft to LCX. If it does n’t work leave him with medical management.

Does  every patient  after a CABG   has a high chances of developing LMD ?

What is accelerated atherosclerosis of Left main following LAD /LCX  grafts ? It is  true  left main  has high risk of  accelerated atherosclerosis and it   undergoes  gradual obstruction once the LAD and LCX is grafted.This is due to low flow across the native left main as distal grafts maintain the flow . This is all the more likely in good bulk of patients who had undergone  CABG  where   LMD  was the indication .

A typical scenario

A left main patient   who undergoes a CABG  a follow up for a suspected  angina  angio after 5 years show the  totally  or near totally occluded native left main . Sudden   Visualisation of worsened leftmain disease    makes this patient eligible for  a  PCI as he fulfills the criteria for  protected leftmain .

Final message

A well protected left main  with a good  functioning graft especially to LAD   most often do not require a fresh revascularisation  procedure  irrespective of the tightness of left main disease . Most of such patients will be candidates for medical therapy .Contrary   to the popular belief ,   left main  intervention   could  be    confined  to   ” unprotected LMD   rather than well protected LMD” as the  potential benefits are more .Further interventional resources need not be wasted in giving second alternate protective channel  for an already protected vessel !

Of  course it should be remembered  in any given patient  with  protected or unprotected  LMD  the indication for  revascualrisation  is based on  the severity of lesion , symptoms,  LV function ,  residual ischemia, viability  etc .

Suggestions  , comments  and  corrections  welcome

Posted in Uncategorized | 7 Comments »

What are critical differences between complete heart block and AV dissociation ?

September 13, 2009 by dr s venkatesan

CHB and AV dissociation are often confused with one another . While CHB is an important cause for AVD , there are distinct differences  which have clinical implications. This table is an attempt to simpify the understanding of the two. Corections and suggestions welcome.

This is a high resolution image , to read better  right click on the table  copy image and open in any image viewer

complete-heart-block-chb-av-dissociation-avd-va-associationn-va-block-sinus-node-dysfunction-ecg-ep-study-interfernce-avd-aivr

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias | Tagged , , , , , , , , , , , , , , | 3 Comments »

How the presence of atrial fibrillation influence the effectiveness of CRT therapy ?

September 12, 2009 by dr s venkatesan

Atrial fibrillation and CHF are close companions. Either it   precipitates  CHF  or  follows it.In advanced heart failure of any etiology  the incidence of AF can be up to 40% .Medical therapy of AF is fairly effective in patients with normal LV function  .But when associated with refractory cardiac failure  it becomes  too complex to control .

Currently CRT with ICD  is becoming the standard OF care for advanced CHF. The efficacy of CRT is being rigorously being assessed . Even as the controversy  about  the wideness of QRS is being settled , the issue of optimal  timing of CRT has risen  . Now ,  the MADIT-CRT has answered this issue “Earlier it  is better , it can be  indicated even for  class 1 patients”

While MADIT -CRT will increase the number of CRT implants , we  have no clear cut answer for the  efficacy of CRT in patients with AF .( Of course , the MUSTIC and CARE HF sub group analysis suggested AF has no significant impact on CRT efficacy )

atrial fibrillation crt cardiac resynchronisation therapy icd madit crt care chf

Why is AF important in CRT ?

There are two issues that need analysis

  1. A patient who  has chronic AF at the time of CRT
  2. Development of  new onset AF after CRT implantation.

Impact of AF during CRT

  • Inter atrial synchrony is lost. ( Significance not clear . . . makes AF permanent)
  • AV synchrony is lost
  • Rapid AV conduction : May trigger   too much of Bivi pacing if sensed by LV lead

Presence of AF at the time of CRT gives us an opportunity to tackle this issue.

How to tackle  sudden AF induced CRT response ?

There are variety of algorithms available to

  • Ventricular sense response
  • Conducted AF response
  • Atrial tracking recovery

In dual chamber pacing mode switching converts DDD into VVI  .This happens  at the cost of loss of AV synchrony .This may have profound implication in CRT .

Then the big question comes  . What is the use  of  having Intraventricular  and interventricular  synchrony without AV synchrony ?

When nothing works .The best strategy is ( Rather deemed to be best ! )

  • To ablate the  AV node  pace  the atrium and ventricle  (RV & LV)  .

Note : Ablation of AV node and putting a dual chamber pacing can never guarantee a physiological pacing as the atrium continues to fibrillate and AV synchrony is rarely there .

Final message

For CRT is to be successful , there should be maximal Bi-Vi capturing , of course this capture has to optimally timed , and must reverse the three pathological asynchronies , namely intraventricular , Interventricular  and  atrio  ventricular  asynchronies.

It is obvious , presence of AF complicates the issue as it demands  constant monitoring and programming of the device (Of course  now most  of them are automated) . It may   require  knocking down of AV node , which  not only carries a risk of SCD *  ,  it also make these  patients   permanently  dependent   on the RV pacing  . This  adds on ,  another  risk ,  for an  acute complication   if the RV lead fails for some reason.

Reference :

*Sudden death after radiofrequency ablation of the atrioventricular node in patients with atrial fibrillation
Journal of the American College of Cardiology, Volume 40, Issue 1, Pages 105-110
C.Ozcan

EP experts generally take  too much liberty in adopting this  strategy for the simple reason it solves the nuisance of atrial impulses  interfering with   ventricular  leads  function that result in  inappropriate ventricular capture fusion or ultimately poor BiVi pacing . But it is not an easy decision  atleast for the patient ! This article , emphasises the dangers involved in ablate and pace strategy for uncontrolled AF.

Further reading

  • Fung, J. W H, Yip, G. W K, Yu, C.-M. (2008). Does atrial fibrillation preclude biventricular pacing?. Heart 94: 826-827 [Full Text]
  • Khadjooi, K, Foley, P W, Chalil, S, Anthony, J, Smith, R E A, Frenneaux, M P, Leyva, F (2008). Long-term effects of cardiac resynchronisation therapy in patients with atrial fibrillation. Heart 94: 879-883 [Abstract]
  • Buck, S., Rienstra, M., Maass, A. H., Nieuwland, W., Van Veldhuisen, D. J., Van Gelder, I. C. (2008). Cardiac resynchronization therapy in patients with heart failure and atrial fibrillation: importance of new-onset atrial fibrillation and total atrial conduction time. Europace 10: 558-565 [Abstract] [Full Text]

Posted in Cardiology - Electrophysiology -Pacemaker, Uncategorized | Tagged , , , , | Leave a Comment »

How paroxysmal nocturnal dyspnea differ form orthopnea ?

September 11, 2009 by dr s venkatesan

orthopnea paroxysmal nocturnal dyspnea pnd www.drsvenkatesan.com

Some Infrequently asked questions in (iFAQ) in PND

What gives relief from PND?

The classical description is, the patient wakes up from sleep. sits up, often to stand up, and go to the nearest window and try to breathe fast and an episode of dyspnea settles down in a few minutes. The relief is completely in many unless the ongoing trigger and baseline cardiac defect overwhelms the reserve mechanism.

What is the hemodynamics behind relief?

Since symptoms are due to sudden unexpected congestion during sleep, assuming erect posture slows down the venous return of 400 ml instantly. It is equivalent to an IV diuretic push. Further standing up (even sitting up is sufficient)  brings the left atrium in its natural superior position, compared to LV. The gravitational forces emerge* and aid in LV filling and improve stroke volume and relieve the congestion backlog. Apart from this two more factors contribute. V/Q mismatch improves as more lungs get perfusion in an erect posture . Finally seeking the window is spontaneous, in search for better fractional oxygen content from the atmosphere. (One more related question. How do pillows give relief of dyspnea in acute LVF? Few of the above mechanism operates)

*Postural changes in LA mean pressure is a complex topic of physics involving lungs, pulmonary circulation, and LA mean pressure.

Is basal rales mandatory during episodes of PND?

Yes. Most will have. But it should be emphasized in orthopnea patients, rales are rare since it takes some time for lung congestion take place. If rales appear immediately after lying down it may Indicate severely compromised LV function.

PND vs Orthopnea: Which is a reproducible symptom?

Obviously orthopnea. PND can never predict which day its going to come as there is CNS component to the circuit in triggering this. (REM sleep, Dreams etc)

How many episodes of PND can occur in one night?

Usually one. Because PND requires a time lag of at least few hours.Usually, these patients will not sleep thereafter or the usual wake-up time ensues.

Can episodes of PND be prevented?

Since its a volume-dependent pulmonary hemodynamic stress, a diuretic at dusk will prevent these episodes in many.

What is the sensitivity of PND for predicting heart disease?

It has low sensitivity( <30% ) but up to 75% specificity to diagnose heart disease.(Class 3 Non-Expert Evidence)

Is PND sign of advanced heart disease?

No.It has very low sensitivity to predict severity of heart disease.

Can PND and Orthopnea occur at same patient at same time a same day ?

Orthopnea has no time lag.It occurs immediately hence it is obviously more severe. Many of these patients, however, do get into sleep after some time as some sort of compensation or adaptation to neural signals of dyspnea take place.

These patients, later on, can get into the same cycle of PND . However, as heart disease (as in cardiomyopathy ) worsens the pulmonary interstitium shows some reactive fibrotic changes resist water logging in the lungs.

Since PND and orthopnea share a close relationship in terms of pathophysiology, we cluster it together in symptomatology. However, they are temporally separated in most patients in natural history.

PND : is it equivalent to acute heart failure?

Yes, it can be called so (If it is due to heart disease*) . It fulfills all criteria of cardiac failure. LV/LA filling pressure raised, forward output (Cardiac Index may still be normal ) .PND is a transient, acute, left-sided failure that results in acute oxygen debt for the body which is self-corrected usually.

* In volume overloaded, CKD patients PND can occur

What is the relationship between RV dysfunction to PND /Orthopnea?

There is a complex fluid regulatory mechanism in the failing heart. The lung can be congested if and only if the RV function is adequate enough to flood the lungs and at the same time LV function matches it with its inadequacy resulting in persistent congestion. In other words, a very high RVEDP is protective against pulmonary edema (However the patient will feel the dyspneic still due to hypoxia /VP VQ etc !)

Its prudent to give importance to PND/Orthopnea with reference to the balance of RV and LV function. One may recall why pericardial disease where right heart filling is impeded rarely lead to lung congestion.

Can PND be associated with Angina ?

Yes, it can but generally its not. Angina occurs due to nocturnal sub-endocardial Ischemia. This combination occurs in critical Aortic valve disease.(Both AS/AR)

Is PND a cardiac emergency?

Difficult question. Most times, no. Since its self-limiting especially if the patient knows he is going to settle with his past experience. But it can trigger dangerous events in severely compromised hearts.As expected, the first episode creates much panic and invariably elicits an emergency alert.

PND has sinister significance if is due to nocturnal ACS.Its a sign of ischemic LVF and requires immediate care.

Which is the most benign form of PND and Orthopnea ?

Students should know, medicine is a funny science. PND as a symptom is benign in some, while it denotes impending death in others.

Benign PND : Obese men, women, in pregnancy may experience terrifying dyspnea at night when they turn around or stretch. This is due to the upward movement of the diaphragm encroaching lung space.

If you record mitral inflow Doppler filling pattern during an episode of PND what will you find?

It’s quite simple logic. You do it yourself and find it as a learning exercise.(Please don’t make the patient suffer by doing echo at times of distress. One of your colleagues to attend to him as you simultaneously do an echo for academic purpose)

Try calculating LVEDP with various echo formulas.

Posted in Cardiology - Clinical, Tutorial in clinical cardiology | Tagged , , , , | 1 Comment »

Why ECG evidence for AV dissociation does not occur in majority of patients with ventricular tachycardia ?

September 10, 2009 by dr s venkatesan

AV dissociation is the specific marker for diagnosing VT. Evidence for AV dissociation manifest in many ways in ECG. *Random p waves unrelated to qrs complexes , fusion beats , capture beats are  the common features that help us diagnose AV dissociation. Unfortunately these  occur only in about  40 % of patients  with VT.(Fusion beats in VT are also  called as Dressler’s beat)

For clinical features of AV dissociation follow this link

What is the normal AV association ?

In  normal physiology ,  even though atria are passive , powerless chambers  in terms of mechanical activity  ,  it reigns  supreme control over ventricle and   dominates   electrically  . In fact , the atrium  and the AV node together ,    dictates when the ventricle has to contract and at what rate  .  So,  in normal human  beings in  sinus rhythm ,  there is a complete AV  association   where both chambers live in a perfect harmony.

What is VA association ?

The atrium and ventricles are  not only related   antegradelyy it  also  has a concealed  retrograde  relationship , (which is often pure electrical ! ) called VA conduction .The conduction velocity and the refractory period of VA  junction is  variable .The AV junctional refractory period is determined by the penetrating power of both atrial and ventricular impulses .

What is complete AV dissociation ?

For complete AV dissociation to occur there should be no physiologically or electrically  linked relationship between the atria and ventricle.For it  to occur the atrial impulse has to get  blocked  in AV junction .

This block can   either be functional  or organic,   partial or total , persistent  or intermittent

This occurs in   primarily in   AV junctional pathology like CHB  etc, that result  in complete AV dissociation . The next major cause for AV dissociation , is   by an  interference from  an accelerated lower pacemaker as in ventricular tachycardia or accelerated idioventricular rhythm .

What does the atria do when the ventricle  starts  contracting rapidly and  independently as in ventricular tachycardia ?

When the ventricle , starts firing independently at a rate of > 200 each of the impulse and  tries to  traverse  the AV junction retrograde . At the same time , the sinus impulse which does it’s normal routine job  by beating around 70/beat ,   faces an  unusual interference on its normal downward journey by  the pathological bombardment  from  the upcoming  ventricular impulse .What happens when both these wave fronts  meet head on . (The hither to perfect harmonical  relationship becomes  a rivalry for the electrical control of heart.)

Sadly , the ventricle mostly succeeds  in the race and  most of the   ventricular impulses    retrogradely  enter  the AV  junction and colludes with  the incoming atrial impulses. When this happens , the AV dissociation is said  to occur. The important point here is,  many times if the retrograde VA conduction is fast and optimally timed , it can cross the AV node without difficulty  and reach the atria  and  subsequently  even    depolarise  the SA node   and  reset  it  . If the VT is persistently conducting  retrograde  it can suppress the SA node as long as the VT is there. This makes a P wave becoming totally absent.  (Note of caution : If you say VT as one of the causes of absent P wave you may be failed in your cardiology board , but this remains a fact !)

So the atrial  depolarisation  and contraction During VT is a complex one. It depends  mainly on the  intensity of the  upcoming    electrical wave front   from the ventricle  . The distance traveled by this wave front  determines  the location of  p waves .It may be in one of the following ways .

  • P waves can be totally absent
  • P wave may occur antegrade
  • On the QRS
  • Over the T wave

In effect the P wave can  literally be any where   in the given strip of  VT

When does a fusion  beat occur ?  When does a capture occur ?

This again is determined by the AV  junctional refractory period. If it permits ,  an   occasional atrial impulse may sneak through the AV junction and capture the ventricle . This is capture beat. Capture beats   are usually narrow qrs  . So in a wide qrs tachycardia  if we note  an occasional narrow or relatively narrow  qrs complex it could denote a VT.

If the atrial impulse after crossing the AV junction   collides with the   upcoming ventricular  impulse  the surface ECG inscribes  a fusion beat. An incomplete capture beat is a fusion beat. It is a combination of two qrs complex one activated from above , one from below .The width of the fusion beat may be wide , narrow or intermediate.

So the evidence for AV dissociation  in surface ECG  is rarely  manifested  if the VT is successfully  traverse  the AV junction and   reset  the SA node  or keep it in a semi depolarised state  .This could be clinically important  some times , the SA node takes time to recover following  A DC shock especially in elderly

An episode of VT can unmask  a hidden sinus node dysfunction , as VT is technically similar to an atrial override pacing   of course  from  below .

Final message

During VT , electrophysiologically  there must be a dissociation between  the atrial  and ventricular contraction.But the evidence  for which is not manifested in surface ECG in the majorty.The primary reason for this,  due to  the  intact  VA  conduction  that    result in  retrograde VA  association.This  makes the  classical findings of   AV dissociation a redundant or invisible  one .

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Can you diagnose AV dissociation without looking at ECG ?

September 9, 2009 by dr s venkatesan

AV dissociation is  common clinical situation that can occur  during both    bradyarrhythmias  and tachyarrhythmias .

Bradycardias

  • Complete heart block
  • During pacemaker rhythms

Tachycardias

  • Accelerated junctional  rhythm
  • Idioventricular  rhythm
  • Ventricular  tachycardia

AV dissociation is essentially an  ECG diagnosis. But it is associated with some  clinical  signs   ,which can be detected by an astute physician in the bedside. At rapid heart rates  it may be really difficult at times to recognise theses findings, but a  cardiology fellow should look for these whenever they encounter AV dissociation  in ECG.

  1. Varying pulse volume
  2. Varying korotkoff  sounds during BP measurement.
  3. Cannon a waves in JVP
  4. Varying intensity of first heart sound on auscultation
  5. Mitral regurtitant murmur may be heard
  6. Hypotension in compromised hearts

What is the mechanism of clinical signs of AV dissociation ?

During AV dissociation , the atrial and ventricular contractions occur  out of phase  and the sequential contraction  is lost. So atrial contractions  might  occur with a closed AV valves .  This result in reflux of blood into the neck resulting in cannon waves . It may be visible only in few beats as the retrograde conduction VA conduction , is highly variable.

Further , only some atrial beats contribute for ventricular filling some do not.This results  in varying LV volumes and this  could result in changing pulse volume.Occasionally the ventricular and atrial   contraction occur simultaneously  .When this happens ,  some amount of blood  reguritates through the open tricuspid valve and mitral valve  which result in MR or TR .

Clinical utility

This could be important , in differentiating  the perennial  issue   of decoding the   wide qrs  VT from  SVT with  aberrancy .A rapid clinical assessment  here could  aid in the diagnosis  of VT  by  identifying  AV dissociation  . An experienced cardiologists will realise even in a given  ECG  with VT  identifying or ruling out  AV dissociation is not always a  pleasant excercise !

In this era of  high tech gadget  oriented cardiology is it not too much  to call for clinical   recognition of  this  entity ?

Definitely not , if  we know Wencke bach  recognised  the classical type 1 2nd degree  AV block in late 19th century even before the ECG machine was  invented ,

Simply by looking at the neck , by carefully observing progressive prolongation of  distance between a and c waves and subsequent dropping of c waves . Amazing isn’t it ?

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