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Unusual arrhythmias during Excercise stress testing

February 29, 2012 by dr s venkatesan

A young  man  fell  off the tread mill  soon  after complaining of chest pain in the immediate recovery  phase.

He had just completed 8 minutes of standard Bruce without any difficulty .

Even as the defibrillator was being  moved near him , he was  successfully   shocked with hands  of a hefty nurse !  ( 25 joules ? )   . He  got into this rhythm !

Note the ECG shows diffuse ST elevation .  The ECG soon settled and a diagnosis of  variant angina was  presumed.

He was shifted to CCU. There was no elevation of enzymes , though he showed a transient wall motion defect lasting up to 48 hours.

The subsequent elective  angiogram did not reveal any critical CAD favoring  Prinzmetal angina.

Provocative tests for vaso spasm is not practiced in our part of the world  (I wonder  whether it is still in vogue at all !)

* The classical  angina of prinzmetal is not related to exertion .  Can we call this as a variant of the variant angina ?

Final message

  • VTs are rare arrhythmias  during EST. However , there are important link between exertion ,  VPDs and VT .
  • Exercise induced RVOT  VTs are  supposed  to  more  common. However , ischemic VT during exercise has to be ruled out in every patient.
  • Non sustained VTs in patients who have baseline VPDs are usually benign .
  • Paradoxically VPDs disappear in many  during exertion indicating overdrive suppression by sinus rate .This again can be ignored.
  • Mono morphic VTs  would suggest structural defects.
  • Polymorphic VTs during exercise indicate either ischemia or electrolytic origin

Also read

Wrong concepts in coronary spasm

Acknowledgement

ECG Courtesy:  Dr G.Gnanvelu MD,DM  Professor of cardiology . Madras medical college

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Clinical cardiology | Tagged , , , | 4 Comments »

How accurate is the TR jet derived Pulmonary artery systolic pressure ?

February 21, 2012 by dr s venkatesan

Measuring TR peak velocity is the most popular  method to assess pulmonary arterial  pressure.It is  universally  believed  TR jet predicts the systolic PA pressure fairly accurately. By all means it is  a wrong perception.

At best ,  it has only 40% correlation with cath  derived PAP  . In other words cardiologist are fooled by TR jet more often than not ! Here is an  elegantly done study  from American  Journal of  Respiratoty and critical care medicine  in  patients  who had undergone lung transplantation . It compared  systolic PAP derived from  Doppler vs cardiac  cath.

”

Source : http://ajrccm.atsjournals.org/content/167/5/735.full.pdf+html

Important observations about TR jet derived PAP

  • Over estimation is the key error.
  • Error of  under -estimation  less common .
  • Over estimation often occur in normal persons
  • Under estimation more frequent in patients with PAH.

(The above study documents  over estimation of 10mmhg  in systolic PAP in 50 out of  100 patients )

Final message

Nothing is perfect in science ,  especially in medical science.  In spite of the limitations  of  TR  jet  , it   will remain the corner stone in the hemodynamic evaluation of right heart pressures . (Forget for the moment . . . the umpteen variables  in  the modified Bernolui equation  , flow acceleration , viscous friction etc )

It is prudent ,  cardiologists  are expected to be aware of this harsh  fact  and  should be meticulous in tracing TR jet and  reduce the error.

One controversial  but logical  suggestion  would be  to drop the ritual of adding  empirical  RA pressure   5- 10mmhg  over the TR  jet  while  calculating PAP , as there is   60 %  error  of  over-estimation  that naturally occur with TR jet. 

Reference

http://www.registroep.org/documenti/IPERTENSIONE%20P.%20CRONICA%20TE/06_Sciomer%20ECO.pdf

 http://ajrccm.atsjournals.org/content/167/5/735.full.pdf+html

Posted in Clinical cardiology, echocardiography | Tagged , , , | Leave a Comment »

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 »

Importance of recognising type C RVH in clinical cardiology !

February 5, 2012 by dr s venkatesan

RVH is  traditionally  categorized into three types . With  the  advent of echocardiography  diagnosing  RVH by ECG would  appear  redundant. Still , it gives vital information about the electro-physiologcal basis  of RVH. Knowing different mechanisms of RVH helps us decode  regional variations in RVH.

Type A , Type B  are easy to diagnose as they fulfill the conventional criteria of tall R in lead V1

Type A  RVH occur in severe  pulmonary hypertension and critical valvular pulmonary stenosis.

Type B  RVH occur in  volume overload states like ASD and moderate  forms of mitral stenosis.

( Severe  MS may cause Type A pattern  if RV pressure exceed systemic pressure)

Type C  RVH    has  no classical signs of RVH. Here  RVH  is diagnosed by proxy . Look for RAE  and a  vertical QRS axis . ( For all practical purposes RAE will indicate  RVH  except in isolated tricuspid stenosis.

Type C RVH occurs classically in COPD and in some cases  of acute pulmonary embolism .In other- words type C  RVH  reflects  predominantly  RV dilatation rather than  hypertrophy.

Why Type C  RVH is important ?

It is important  for two  reasons

  • It  is  basically a  masked   RVH .
  • It mimics Anterior MI

Missing the first  one and erring  in  later  both  can have major  implications  in clinical cardiology  especially during emergencies.

What is  the mechanism of poor  R wave in precardial leads in  Type C RVH of COPD ?

The fact that  poor  R wave  in precardial  leads occur in  most  cases of  COPD  (whether or not RVH is present or not)   convey an important message.

The  lack of  R wave  progression   is probably  less to  do  with   rotation of  RV  than  the insulation effect  lung  . Further, the  elongated lungs   drags   the heart down , and  make it more vertical and in spite of RVH tall  R  is not picked up by v1 v2 .

Unlike primary PAH and critical MS where the RVH  can dominate the LV  ,  the  quantum of  RVH is never huge in pure COPD . However , presence of RBBB  could  alter  the R wave amplitude .

ECG in acute pulmonary embolism

This resembles the type  C  RVH . The  R  waves in V 1  and  V 2 can not gain the voltage acutely.

The S 1 . Q 3 , T 3  pattern if present indicate the  acute RV strain and  the resultant  RV wall motion defect.

.

Clinical scenario : Practical utility of  decoding    RVH   by ECG ?

A  middle aged female came  to our CCU  with acute  dyspnea with tachycardia .

Echo revealed a dilated  RA and RV . She had  mild TR and moderate to severe PAH (The TR jet measured 3.8m/sec)

The MPA showed a hazy shadow suspicious of thrombus . The patient  had no evidence for DVT .

The fellows  arrived at  a conclusion about a  severe  PAH  but , the etiology was debated.

One is chronic thrombo-embolic PAH . Other groups argued for acute massive pulmonary embolism and resultant PAH.

This raised an  important    therapeutic   issue  as one of them wanted to lyse the thrombus  ,  the  other argued for simple heparin .The  argument continued as the first fellow reminded ,  presence of RA, RV dilatation is a sign of acute RV strain  . The other countered the  same  as  it could be  a  chronic response  to pre existing PAH.

How do you know  in an emergency ,  whether the RA, RV dilatation is new onset  or a chronic one ?

In spite of  good   echocardiogram  we were confused .  Then it struck  to us ,  ECG would solve our problem . It indeed helped us. She had a tall  monophasic  R  in  V1  indicating   Type A RVH , which suggested chronic PAH   and  the thrombus in MPA  in all likely hood  was a sequel  to PAH  and  not vice versa . A type C RVH  would have voted  in favor of  acute pulmonary embolism.

Meanwhile a  CT pulmonary angiogram  report was available   . It showed a small  thrombus in MPA and LPA with no clearcut perfusion defects ruling out acute pulmoanry embolism . The thrombus was probably  de-nova in- situ thrombus due to PAH.

 

 

Final message

It may  appear  funny for the  present day cardiologists to waste so much time  to analyze  the  RVH  by surface ECG . But please remember ECG remain the only simple and cheap  investigation that transmit live data from the heart instantly  .Most importantly unlike other imaging  modalities  ECG data do not vary with person who records it !

Reference

A very good referen from   Basic and Bedside Electrocardiography   By Romulo F. Baltazar

Posted in Uncategorized | Tagged , , , , | 3 Comments »

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