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What are the mechanisms of “Pulmonary Arterial Hypertension” in Dilated cardiomyopathy ?

February 18, 2012 by dr s venkatesan

Pulmonary  arterial hypertension (PAH ) is  an uncommon manifestation of dilated cardiomyopathy .While pulmonary venous hypertension of some degree is expected in most patients with DCM,  it is rare for these patients to go for severe arterial hypertension.

The reason for this may be the  natural history of DCM do not allow these patients to live that longer to manifest severe PAH.  Still ,  we encounter this problem  atleast in tertiary hospitals. Presence of moderate to severe PAH (> 50mm peak PAP) is a sinister sign in  DCM. They not only do badly , they also make  the transplant outcome dismal .

What causes this severe   PAH in DCM ?  The following observations are made in our institute .

Now we know , isolated  systolic dysfunction is  rarely associated with PAH  .It is the presence of  LV diastolic dysfunction (Often restrictive )  that raises the pulmonary pressures.  PAH of DCM is rarely progressive.

One important suggestion is the DCMs  which are associated with  severe  PAH may indeed represent  late stages of RCM , when the LV begin to dilate.

Associated mitral regurgitation   contributes  to PAH

Atrial fibrillation has a significant impact on elevating  pulmonary  venous and arterial  pressures in DCM.

Hypoxic PAH can occur in any medical situation  in susceptible population . DCM is no exception

For some reason  idiopathic DCM is more often result in PAH than ischemic DCM . (Is that possibel , some form of  idiopathic   PAH and DCM are etiologically  related ?)

Further , the positive inotropic agents when liberally used will worsen the diastolic  properties of LV.

Finally involvement of  right ventricle  in the cardiomyopathy  process can have an ameliorating effect on PAH.  A good RV function is essential to lift the PA systolic pressure. If RV failure is causing a low PAP , do not be happy .It simply means RV is going to  say  good bye  . . .  for the final  time !

How to manage PAH in DCM ?

There is no specific management strategy .

We do not know yet  whether Sildenafil ,  Bosentan, and Epoprostenol  have any role in this  form of  PAH. These are all basically vasodilators. It’s use in DCM is vested with a risk of  catastrophic hypotension . Of course ,  we do have a role for balanced vasodilators in cardiac failure .(As most of these patients would be already on adequate ACEI )

Presence of PAH should be considered as an independent indication for anticoagulants as in situ  pulmonary thrombus is common.

The effect of  cardiac resynchronisation therapy in reducing the PAH of DCM is not convincing.

Final message

PAH  in DCM is an unwelcome development. It makes the situation  tough .  The mechanisms are diverse  .Understanding the mechanism would help us deal  this problem better .  Conventional anti failure treatment may help  ,but  it is wiser to try  reserve drugs.

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease | Tagged , , , , , | 1 Comment »

Tough calls in cardiology : How will you manage ventricular tachycardia with a mobile LV clot ?

February 16, 2012 by dr s venkatesan

Clinical cardiac  problems can be very demanding at  times. Here  is a  situation even the toughest will struggle.

A 52 year old man comes with a wide qrs tachycardia  with a blood pressure of 90 /70 with class 4 dyspnea .He was restless , trying to sit up because of  orthopnea. The ECG showed  a definitive ventricular tachycardia  with LBBB morphology.The patient was   connected  the   oxygen line ,  cardiac monitor, oximetery, etc

The consultant  on call instructed   immediate DC shock   and  he  warned  about  impending ventricular fibrillation .He  casually told the fellow to  do a echocardiogram also and rule out any structural heart disease. Even as  the staff was  arranging the defibrillator , the fellow did   a  rapid bed side echocardiogram . He was  shocked to find a  large mobile LV clot   with a  dilated ,  severely dysfunctional left ventricle  having an  EF  of  25 % .

Now comes  the critical time . Should we shock this man with VT and LV clot?

What will be your option now ?

  1. I will not mind the LV clot  ,  will go ahead with DC  Shock . Let him dislodge his LV clot . If It is his fate  let it be !
  2. Defer the   DC shock . Fall back on medical cardioversion like  Bretyllium, Amiodarone or magnesium  . After all . . .  it is not a pulse less VT. He is not in cardiac arrest . He can afford to wait .We can’t risk a stroke .
  3. Give a low energy  shock  25 joules  with paddles  avoiding the LV apex.  .It may not dislodge the apical clot , still  VT may be terminated.
  4. Try overdrive  pacing instead of DC shock
  5. Refer the patient for emergency surgical removal of LV clot
  6.  Suck out the LV clot with a   LV suction catheter and plan elective DC version*
  7. Insert a temporary Aortic filter and shock the patient **

*  Such catheters are in preliminary stage of development . Is  that true ?  ( If  no I  should get the royalty for the idea  ! )

(Read the related article in my blog )

** A loud imagination . Such filters do not exist.( If  IVC  can be filtered   why not  Aorta ? )

What was finally done ?

After analysing each  of the above  , we decided   option one (  “Prey the  God  and shock the heart” ) After all if it is  a VF ,  this  issue becomes null and void !  . Luckily God was with us.  The  patient  was  reverted to sinus  rhythm with 50joules   and  had  no  untoward events . He was subsequently anti-coagulated .  He is being planned for CRT/ICD therapy

Final message

Critical care  medicine is all about risk taking .Many times , therapeutic maneuvers  confer a  significant   risk  to life  comparable  to the   index problem.  But that  should not be a deterrent .  A careful learned decision  is warranted.

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology | Tagged , , , , | Leave a Comment »

Arruda scheme for rapid localisation of WPW syndrome

February 14, 2012 by dr s venkatesan

Localising  WPW syndrome is a favorite  time pass  for cardiologists in spite of  serious  limitations of surface ECG .Still , it is vital to generate a rough idea about the location of  these pathways ,  so that we can focus  our efforts  on  some sort of ablation procedure .

Arruda algorithm is probably a simple and fairly useful technique to remember. It asks us to climb 4 steps   and pause at each  step and look sideways   for the accessory  pathways !

Step 1 (Left free wall step )

Initially one need to look only two leads .

Look at lead 1  and  V1 for   delta wave and R/S ratio .After Identifying delta wave look for the polarity of delta wave (This can sometimes be really difficult ) .If there is iso-electric or negative delta it immediately  fixes the pathway  in left free wall . Similarly if V1 R >  S it also fixes in left free wall. To locate more precisely in left free wall  look  for  delta  wave polarity in  AVF  and proceed down*

If none of these finding are present then  Go to step 2 .

Step 2 (Coronary sinus step )

It is the most simple step . If negative delta  located in lead 2 (often mimic inferior MI)

Here the pathway is often located in coronary sinus /middle cardiac vein often as diverticulum.

After excluding left free wall and coronary sinus origin one has to look at possible septal  pathway  .

For this  go to step 3

Step 3  (Septal step ) And  again v1 lead  becomes important if v1 shows negative or iso-electric  go down  to septal  pathway decoding

After ruling out septal origin the scheme takes us to right free wall by default.

Step 4  (Right free wall step)  If the delta wave does not fit in  any   of the above three steps (Including  positive  delta in V 1 )  it  fixes  the right free wall  pathway

Arruda scheme summary

Arruda scheme  guides  us  to scan  systematically  for pathway from left free wall  to  septum and lastly  the right free  wall  (The key  to  locate  the APs is  to look at  delta waves in lead  1, 2  AVF and R/S ratio In V1 )

Here is a  simplified version for basic localization

Reference

  1. Arruda MS, McClelland JH and Wang X , et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol 1998;9:2–12.

Posted in cardaic physiology, cardiac physiology, Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias | Tagged , , , | 1 Comment »

A forbidden book for doctors !

February 11, 2012 by dr s venkatesan

Doctors would simply hate  this book   because  it tries to  expose them !

I would n’t agree with  the tone and conclusion of  this book . But one should soul search  , why such books are written  in the first place ?

The medical professionals  definitely  need to ponder over this  issue .

I stumbled upon this book  in Amazon book store

 

http://www.amazon.com/Medical-Blunders-Amazing-Stories-Dangerous

How  frequently doctors make blunders  ?   What  is your take ?

Would you like to vote in this poll  ?

Posted in bio ethics, cardiology-ethics | Tagged , , | Leave a Comment »

Basic lessons in STEMI :Does dying myocytes release potassium into the circulation ?

February 10, 2012 by dr s venkatesan

Human life is a bundle of energy orchestrated by ions coming  in and  going out  of  every cell . Potassium is the life sustaining ion which  determines the  resting membrane potential  of our cells.

When the  heart  suffers a massive necrotic attack  what  would  happen to the potassium dynamics  inside the  myocytes ?

K  + is the dominant  intracellular cation  ,  when  about  100 million myocytes   die  suddenly ,  a chaos in the  potassium  metabolism  is expected  is it not ? .

When skeletal  muscles dies  it  releases  potassium  . We  know   this  from typical crush injuries and rabdomyolyis.

It is  more of a  common sense  to expect this   . . . from myocardium as well .


Which ion is responsible for the current of injury ?

We know a  strong and continuous  negative current that  emanates from the necrotic zone after STEMI  .  (It is so powerful it  shifts the baseline  itself  !), We do not know yet what exactly  is causing this current of injury .  It goes without saying sodium should sustain the depolarisation wave but  potassium will  also have a major role in the  propagation  of this injury current.

Do dying myocytes   excrete the potassium into the circulation   ?

Is    k+  a marker of extent of MI  ?

What is the mechanism of hyper acute tall T waves in  MI ?

Questions  galore  . . . Answers struggle !

When a  large  area of  cardiac muscle goes for necrosis  it  leads to  leaking   of   K +    . If it is true  , it  is expected to be a marker for extent of  infarct. In reality it is not . Why ?  This is because cardiac  potassium pool is much  small . A  leak from  an organ which weighs   400 grams   do not elevate the ECF  potassium .  Still , there is ample evidence  for   K + to accumulate  in the local  intracellular milieu. (Myocardial hyper-kalemia ) In fact ,  one of  the mechanisms  suggested  for tall T waves in  hyper-acute MI phase   potassium excess .

Image courtesey hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

http://hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

Potassium levels and incidence of  ventricular tachycardia.

Many of the primary ventricular arrhythmias  are  due to acute ischemia .  We  have conflicting evidence  for  the effect of ischemia on QT interval. How does ischemia trigger VT  ?
The answer to this question  remain as a missing link !  . Grossly simplifying ,  one could suggest it is  due to   ischemic cell membrane damage that alters the ion channel function  , resulting  in intracellular accumulation of calcium and triggered  activity  .

What is the effect of potassium  on cardiac contractility  ?

Myocardial paralysis.  (Please note  it is the  hypokalemia  that primarily  causes paralysis in skeletal muscles !)

It causes  myocardial  stunning  a manifestation of local potassium  leak ! A temporary myocardial paralysis.

What does the current guidelines of ACC/AHA state about potassium hemostasis  in STEMI ?

It suggests   a fairly aggressive  maintenance of potassium levels  to  upper normal levels. Traditionally we are worried more about hypokalemia than the hyper. It is  surprising   we had the facts wrong . . .  for so long !

What is new in the regulation of potassium level during STEMI ?

This landmark paper from JAMA seeks  to set right the misconceptions about potassium during STEMI. It suggests  K + levels  has a U shaped  morbidity curve in STEMI . One need to be cautious in  correcting borderline hypokalemia .  Serum   K +   is   absolutely useless  surrogate marker for myocardial K +   . We do not know how  K  +  behaves in the vicinity of MI  zone . So  extreme caution is required  when giving IV  K +  supplements in coronary care units .

Watch out :  Beta blockers /ACEI   may worsen  hyperkalemia

Early introduction of ACEI and ARBs   is a strong risk factor for systemic as well as myocardial  hyperkalemia . This  is  especially true  in diabetic individuals  who have  low rennin  levels due to diabetic micro circulation defect in kidneys .(Hypo-reninic  hypo-aldosternosim )

Beta blockers are also known to raise potassium by two mechanism

1.Blocking rennin

2.Reduced uptake of K + in to  the cells.

http://medicineforresidents.blogspot.in/2010/09/hyperkalemia-with-beta-blockers.html

Final message

In the management of STEMI  ,   revascularization  of  the myocardium    is  considered as  the only  therapeutic aim . We  need to realise it   is  much more than that .  There are some subtle but important ways of resuscitating and  protecting  myocardium .  Over  indulgence in electrolytic management  in coronary care  is to be avoided.

Reference

Importance of sympathetic drive and  potassium levels

http://www.nejm.org/doi/full/10.1056/NEJM198002213020803

http://ccn.aacnjournals.org/content/23/6/14.full.pdf+html

Posted in cardaic physiology, cardiac physiology, cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged , , , , , , , , , | Leave a Comment »

Great men in medicine : Virchow is much . . . much greater than his “Lymph node and the Triad” he is known for !

February 8, 2012 by dr s venkatesan

Some scientists are  known for their discovery ,  few are known for their vision  few for their character .Here was a man who  had  all of them  can be termed as father of modern medicine .

Rudolf Virchow - German pathologist( 1821-1902)

Unfortunately the current generation knows him for his concept and theory of blood clotting  or  lymph  node in the neck .

Here is a  reviews about this man who single handedly   taught  the world

He  insisted  , caring  the sick and treating illness  is  more of a social science than medical one

We  have probably  not  learnt  a single lesson yet , from this master  teacher is a different story !

Avid listeners to Virchow in Berlin university

My  Virchowian thoughts

This man’s understanding of medicine was much . . .  much sharper than us –  100 years ago  , when  cardiology was practiced  with out  even an  ECG and   X-ray chest  . ( Is itn’t  true   today  we struggle with  loads of  3 dimensinal  gadolinium enhanced  cardiac MRI ! images )

Virchow’s  concepts  are most relevant in today’s world  , where the corporate and capitalist  culture  has  hijacked the  noble profession . Inhabitants of this planet are  threatened with eccentrically blown up  healthcare  system   where  the  development of   modern medical   modalities is completely out phase of with what  is required for the people .

We will pay a heavy penalty  if  this world  continues to witness   people die  for as  flimsy  reasons  like lack of oral re-hydration fluids   , while the other section of society is  marketing an exotic  mitochondrial DNA  slicers  for prolonging a  cancer victim  life by few months .

In a global society  where  social , economic  and environmental  responsibilities  and liabilities  are shared ,  it would be disastrous if  one country is simply not bothered about what is happening in other country.


WHO the world health organization came into being exactly for this reason .

We know  .  . . how it functions .  It is the  most abused united nation body . It has  neither the required  power nor the will to  tell the world  and insist them the  righteous  route for human health !

If the rich  are  not bothered about poor ,  it is certain  the rich will  also be eliminated  from the planet  for the same reasons  . . . it’s  just  a matter of time   !

Reference

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1305179/pdf/westjmed00323-0041.pdf

http://en.wikipedia.org/wiki/Rudolf_Virchow

Posted in general medicine, Great websites in cardiology, history of cardiology | Tagged , , | 1 Comment »

What is the mechanism of deep q waves in volume over-load of left ventricle ?

February 5, 2012 by dr s venkatesan

Here is an X -Ray and ECG  of a patient who came with  palpitation ,  which he  said  descriptively

“I  could feel  it   with  my hands over chest “

He also had class 3 dyspnea  and nocturnal chest pain . (Read here :  What is the mechanism of nocturnal angina in AR ? )

Clinically  it was classical  severe aortic regurgitation .

His x – ray and ECG showed

  1. q  represents  LV end diastole  . The  maximum diastolic  stress  point.
  2. q  indicate septal forces . When  LV is dilated  q  also  reflect cavity potential . Both gets  summed up inscribing  a classical deep q
  3. In severe volume overload   LV  is not only  dilated , it’s  mass increases  and is brought near  the chest wall . Since the leas V 5 and V6 are the most proximal to LV  both  R and q  increase correspondingly (Shall we call as  reversed Brody effect ?  )

Other findings of volume overload of LV are

While deep q  is  very valuable in LV diastolic volume over load there are other useful ECG signs.

  • Increased  qrs  amplitude (May be equally important like deep q . Both always go together )
  • Absence of  typical ST/T changes (Systole is stress free !in pure AR/MR) . Still ,  ST/T changes  can occur if   there is associated  LV dysfunction.
  • Left axis deviation.
  • Left atrial enlargement (In case of MR/ Large L-R shunts / or late stages of AR )
  • Rarely  U waves are reported in LV volume overload*

Can we  dignose volume overload without q waves in V 5 , V 6 ?

Most times no, but if there is associated incomplete LBBB q wave disappears.

Which  is rare in pure volume over-load. In fact absence of q in isolated systolic overload of LV is attributed to the presence of incomplete  LBBB by the ECG legend  Shamroth !

Reference

* http://www.ccjm.org/content/78/8/505.full

Posted in Cardiology - Clinical, cardiology -ECG | Tagged , , , , , , , , , | Leave a Comment »

What are the mechanisms of “Nocturnal” Angina ?

February 2, 2012 by dr s venkatesan

Angina occurring at night is relatively uncommon . It is  still  more rare  for angina to occur exclusively at night (With a possible exclusion of  syphilitic aortits with AR !) The underlying conditions and mechanism  of nocturnal angina  are largely unexplored. In most clinical situations nocturnal angina  is  associated with day time angina as well .

Various mechanisms are proposed

  • It is primarily due to  increased demand  (Holter monitoring has documented  brief bursts  of  HR acceleration  just before  nocturnal angina with  manifest  ST depression )
  • Increased demand  during  REM sleep .
  • Dreams  related adrenergic surge has been implicated.
  • Rarely it is due to supply side defect .
  • Coronary vaso-spasm ( Mostly  in a pre-exisiting lesion )
  • It could  simply  represent  paroxysmal nocturnal dyspnea (pnd)
  • Sleep apnea can precipitate angina  ( Ironically angina occur during   re-breathing  phase )
  • Altered hemo-rheology
  • Nocturnal gap in anti anginal medication *

* May be more  common than we realise.

Cardio vascular hemo-dynamics  at night

If we  believe , sleep is  the great relaxation , and the heart   would enjoy the   “night time”   we  are absolutely wrong . Even in sleep ,  heart has to pump the same 250 ml of blood every minute. Of course , the sleeping heart rate slows down considerably , still  it is interspersed with spikes of activity.  When the heart  rate  slows down  , diastole is prolonged , coronary blood flow  is expected to be copious  unless there is critical CAD.

                                      We  know , sleep is not a passive process  , even as the  autonomic nervous system takes complete control over the  somatic  system .The true colors of  our delicate autonomic system will come to light only during sleep.The muscle tone ,  the sympathetic drive fluctuates according  a pre-set degree . Dreams and REM sleep disturbance can have considerable impact on the sympathetic nerve terminals which ooze  catecholanines  .

Sudden awakening  from  early sleep  is vested with a risk of dangerous   spikes of adrenaline release  .This becomes especially  important in compromised coronary circulation .In fact , this is commonest  sleep -awake  sequence  in patients with nocturnal angina.

Silent ischemia at night

It is curious to note 24 hour Holter  monitoring  reveals  most episodes of ST depression at night are silent. There must be a  specific pain threshold above which a patient awakens  with angina.   The  available  studies   do not  answer this issue   and are not perfect  . We have no way to find  true   silent ischemia  during  sleep.(PET scan in thalamus ?)

Nocturnal angina  in  Aortic regurgitation

Aortic regurgitation  has special relationship with dusk  .For angina to occur AR must be severe and usually isolated .

  • Prolonged diastole at night   -Regurgitation time is prolonged .
  • Dilated LV . Increased  LV mass .Increased demand.
  • Raised LVEDP due high wall stress.
  • Diastolic coronary stealing . Venturi  effect of AR jet

Nocturnal Angina : Is it stable or unstable ?

Most  consider it   as a type of stable angina .Now ,we have reasons to suspect  it could a  marker of unstable angina as it is an  expression of rest angina .

Nocturnal angina vs nocturnal STEMI

How often an episode of nocturnal angina end up in STEMI ?

STEMI is more  common in the early hours of the day and is more related to the hemo-rheological factors  . Please  note ,  STEMI is  a supply side defect  while most episodes of nocturnal angina is due to  demand ischemia . However  it is possible   nocturnal angina episode can precipitate STEMI if  vasospasm is  the underlying mechanism  and if  it is prolonged can trigger thrombosis.

We do not know the answer as yet.

Nocturnal  Angina : Can  it  be PND equivalent ?

Paroxysmal nocturnal dyspnea (PND)  is a classic manifestation of  episodic LVF.  We  know dyspnea can be an anginal  equivalent.  What prevents angina  to  become a  dyspnea  equivalent ! ( Especially the nocturnal ones ,   since the  mechanism  of generation of PND   are very similar  to the  genesis of  angina ). It is distinctly possible  one  may  be mistaken for the  other .  Both occur when  sudden hyper-adrenergic  state  is evoked  which demands   high MVO2 .  An  ischemic heart has every reason to  respond with  angina  .

It is well known  ischemia can result in transient diastolic dysfunction and  elevate the PCWP simultaneously  and PND  would be  the sequel .  When we analysed the  nocturnal calls (  Our fellows ,  do get lots of  such calls from   general wards  at night ),  many  patients with LV dysfunction  who complained  of  classic  chest pain  had  some degree of  dyspnea  and few crackles over lung base as well  .

Nocturnal angina and obstructive sleep apnea

The incidence of nocturnal angina is more common in obese population with obstructive sleep apnea.

The reason is two-fold

1 .Hypoxia mediated

2. Inappropriate tachycardia during recovery phase

Is there any  specific management strategies  to control nocturnal  angina ?

  • General  principles apply .
  • The timing of  anti anginal medication can be adjusted . Long acting preparations taken  in  morning hours to be avoided as they do not cover night time.
  • A calcium   channel blocker   (with optional  beta blocker )  at night may be the best bet to prevent nocturnal ischemia.
  • Dinner to sleep time to be widened.
  • Heavy diet at night to be avoided.
  • Sedatives role is not clear. (Can Diazepam suppress nocturnal angina ?  If so . . .  we  can call it as anti anginal drug  . . .  is isn’t )

References

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2884%2991693-3/abstract

http://www.ncbi.nlm.nih.gov/pubmed/8419815

http://www.nejm.org/doi/pdf/10.1056/NEJM199302043280502

  Obstructive Sleep apnea  and  Angina 1  : http://www.ncbi.nlm.nih.gov/pubmed/7715342

 Obstructive sleep apnea and Angina 2 http://content.onlinejacc.org/cgi/reprint/34/6/1744.pdf

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease | Tagged , , , | Leave a Comment »

Do not undermine the Importance of “Poster presentations” in scientific conferences !

January 30, 2012 by dr s venkatesan

We do come  across ,  even  senior  cardiologists , who  tend to undermine  the importance  of  poster  presentations in scientific  conferences   (I know a  few ,  who  ridicule it as well  ? ) .

                      Is  it not a meanly  job   for  a  cardiologist  to paste a  poster  and stand  beside  it  for hours  , waiting for scientifically motivated audience !

But , what really matter is the thoughts ,  concepts  and often the hard work   that brings  these  posters to  big league  conferences .

Please remember   abstract posters  must cross the hurdle of  the conference peer review  committee’s scrutiny . Often times   the poster arenas   has  launched  some crazy ideas  ,  transform  them to  great  discoveries.

If   only  , Gruentzig had shied  away from the poster  he famously  pasted on lawns of   ACC  , Annual scientific sessions ,Florida

1975     .  .  .  the    revolutionary  concept  of  PTCA   would still be  in utero  !

Final message

I argue the young  fellows in cardiology to send as many  scientific  abstracts as  possible   in their  national or international  meets  . This is  where the  the future of cardiology lies ! Simply don’t  bother about the critics  .

Posted in Cardiology -Interventional -PCI, history of cardiology | Tagged , , , , , , , , , | 2 Comments »

Iam sure . . . 9 out of 10 times , this ECG will mislead you !

January 23, 2012 by dr s venkatesan

This  is the ECG  of  a  45 year old man with  H/O hypertension  and  chest pain .The general practitioner who first saw him alerted this  patient about a possible  heart  attack  asked to meet a cardiologist immediately. The cardiologist who  saw  this ECG   tended to confirm  the diagnosis  and advised admission in  a coronary  care unit .

The patient   defied  both  and  somehow landed in my echo lab  .  Looking at the ECG   I also  expected  it to be a  STEMI  evolving into a  Non Q  MI .

I was surprised  to find  only LVH with absolutely no wall motion defect  . There was no evidence of ASH,  HOCM or apical cardiomyoapthy as one of my fellows initially  suspected . His  EF was 70 %.   Cardiac enzymes were sent by then. When  I spent few minutes  with him ,  listening the history , it was very clear  what  he had was  non cardiac pain . In the anxiety ,  no one  got it right  about the character of pain ,which  was localised , lasted  for few seconds and  least suggesed angina.

The moral of the story is   listen to the patient  however dramatic the ECG may look !

What is special in this ECG ?

It is common for LVH with ST depression to be  mistaken for  ACS/NSTEMI

Here , there were  other  observations that  added  more  complexity .

  • Presence  of  ST/T changes in inferior leads(ST elevation in lead 3)
  • Bi-phasic  T wave in v1 to v3
  • ST elevation  in precardial leads

In LVH  it is usual  to note  ST depresion , how do you explain ST elevation in LVH ?

ST elevation in LVH   may occur in  leads  v1 to v3   . It is very rare  for LVH to inscribe  ST  elevation in   v4 v5 v6  .   Why certain  leads elevate the ST segment while others depress  in LVH  is not clear. It may represent  incomplete LBBB pattern where the ST segment deviates opposite to the  dominant QRS  complex. Septal  hypertrophy often elevate  while free  wall  hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads  record  classical  ST depression .

Importance of Bi-Phasic T waves

Please remember  Bi phasic T waves are notorious for it’s  unpredictability. An  innocuous looking bi-phasic T waves  (especially  with dynamic behavior )   is a  harbinger of proximal  LAD or even left main disease.

Finally , what will be ECG  changes if a patient with classical  LVH  who  develops a  real  STEMI ?

  • LV strain  pattern normalises ?
  • Further ST depression  occurs ?
  • No great changes . ECG  Looks near normal ?

Answer : ?

What is the significance  of   Bi-phasic T  waves : A  link to  a related post

Posted in Cardiology - Clinical, cardiology -ECG, cardiology- coronary care, Cardiology-Coronary artery disese, critical care ccu | Tagged , , , , , , | 1 Comment »

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