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Excercise Induced pulmonary hypertension : Are we neglecting this entity ?

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , on May 8, 2010| Leave a Comment »

 Excercise physiology has been studied most extensively in the last century.The hemodynamic impact of excercise in various disorders of heart has been well established.
Dyspnea on exertion is the commonest symptom in clinical cardiology practice. It is well-known pulmonary stretch receptors located in pulmonary vasculature is one of the  major mechanism of dyspnea.

Excercise increases the cardiac output manyfold.Transporting  up to 10-12 litres of blood every minute across the lungs with a narrow pressure  head (about 10 mmhg ) is not an easy job . It needs lot of lung discipline .

It is surprising to note, there is little data on excercise induced pulmonary hypertension in the evaluation of patients with unexplained dyspnea.

We know, excercise increases the systemic blood pressure ,we  presume it should not raise the PAP (however severe the exertion is 1 )as pulmonary circulation  is a  high compliant low pressure system. 

Is our presumption correct ?

Exercise induced PAH can occur in both   health and disease 

In patients with preexisting disease

  • Stress induced LV dysfunction and resultant raise in LVEDP-PCWP-PAP .This is the most common mechanism in valvular and myocardial  disease.

Apparently healthy population

  • Excercise  induced PAH as a  marker for silent CAD .
  • Transient Hyperkinetic PAH* (Note :Here PCWP is usually normal )

This is similar  to hypertensive response to EST in systemic circulation.Existence  of this entity , is controversial, But this may reflect  reduced pulmonary vascular reserve  or reduced pulmonary nitric oxide secretion.

*The main difference here is the PAH is more often an  isolated systolic PAH. While LV dysfunction induced PAH is  a combined diastolic and systolic PAH .
How to assess excercise induced  PAH ?
It is not an easy job. Invasive catheter derived pressure measurements have been done ,but it is not practical .

The simplest way is to look for the TR /PR jet in echo in both pre and post excercise phase.

Final message

Excercise induced PAH is an inadequately studied entity in cardiology , in spite  it’s great significance .
This phenomenon is observed  in both diseased and normal heart.

The quantum of excercise induced PAH  is  widely variable depending upon the cardiac  status especially  LV function and the  functional integrity of pulmonary microvasculature .

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Why some VSDs close promptly and why some don’t?

Posted in cardiology congenital heart disese, Uncategorized, tagged on May 7, 2010| 2 Comments »

Ventricular septal defect(VSD) is one the commonest congenital heart disease . Right from the days of Gasul , Abbot, and Keith we have analysed the natural history for nearly a century . VSD is an intriguing congenital heart disease where a child can develop a florid cardiac failure within weeks of birth in one end to a totally asymptomatic adult with a benign cardiac acoustics defect (Namely a systolic murmur in the left parasternal area.) But for this murmur , the patient would be labeled absolutely healthy.

 In between these two spectra is the huge population of VSD that gets closed spontaneously. A rough estimate says 60 % of all small VSDs get closed by age 10 .

So ,what we are supposed to do once a child is diagnosed of VSD ?

Should we close or should we wait ?

The indication for closing a VSD is discussed elsewhere ( Read this link )

 What are the factors that determine VSD closure ?

  • The size
  • The site
  • Age of the child
  • The Rim morphology
  • Associated lesions*
  • Hemodynamic stress
  • Inherent tissue factors
  • Infection **

* Associated defects like PDA, RVOT obstruction are strong deerrants against spontaneous closure

General rules of VSD closure

 Size

VSDs <5mm have great chance of closing Large VSD > 1cm is rarely get closed .

Supracristal VSDs located sub arterially are immune to spontaneous closure however small the size is .

Location & Site

 VSDs that are located exclusively within the membranous septum rarely close . VSDs which are located in the perimembranous area (With at least 50% circumference is fenced by muscular or trabecular septum has the greatest potential to close by natural forces.)

Isolated muscular VSD if large can not get closed . Inlet VSD has anatomical difficulty to get closed.

Rim Morphology

 Small muscular VSDs have a potential to close , but it is believed differential cellular lining of VSD rims (Eg : A combination of muscle, membrane , is more likely to close .)

 Process of tissue growth As the child grows the it is expected the heart will outgrow the lesion . This is thought to be the commonest mode of VSD closure. As the IVS mass increases as he child grows it brings he rims together . But logic would suggest unless some degree of neocardiac proliferation occur a VSD may never get closed completely .

Some times even large VSDs try to close with the help of the neighboring structures like septal tricuspid valve leaflet . Indeed this can be the dominate mode of closure in many. This can induce a tricuspid regurgitation .

**Role of infection

Paradoxically an episode of infective endocaditis in the edges of VSD accelerate the process of approximation of tissue plane and healing .

 Relation with Pulmonary arterial hypertension (PAH)

 Once PAH sets in the VSD never gets closed spontaneously , This may be due to all VSDs that result in PAH has to be significantly large

 Can a VSD get larger progressively?

In physics and hydraulics a hole under hemodynamic stress is destined to progress In human biology this is thought to be rare .Post MI VSRs can behave in an unpredictable manner as he edges of the defect a often softened and prone for tissue plane dissection and extension .

Why some VSDs never close ?

It is clear , size and location matters the most , but there are other issues some of them may be unique tissue properties .

Why is it important to know the biology of VSD closure ?

In this era of interventional cardiology we are using mechanical devices to close VSDs and ASDs .It is fraught with many technical issues. If there is a biological glue or membrane that can be delivered by catheter to close small VSDs or ASDs .

 So for no therapeutic approach to hasten the natural closure of these defects has been practiced .Further research is required to explore the cellular adhesiveness and help accelerate closure of these defects.

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Arabian magic in cath lab !

Posted in Cardiology -Interventional -PCI, Uncategorized, tagged , , , , on May 5, 2010| Leave a Comment »

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

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

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

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

Reference

 http://www.ncbi.nlm.nih.gov/pubmed/20088015

http://www3.interscience.wiley.com/journal/122619470/abstract

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The most important article ever to be published about wide qrs tachycardia !

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology-ethics, Uncategorized, tagged , , , , on April 30, 2010| Leave a Comment »

Wide qrs tachycardia often  evoke a   OCD like reaction  among  many  cardiologists (Obsessive compulsive disorder).  Whenever we are given a strip of wide qrs tachycardia  we are compelled to initiate a  conscious or  subconscious debate , whether it is VT  or SVT . Tens of thousands of articles, seminars, CMEs , have been conducted for over 30 years  for  decoding  wide qrs tachycardias  . The fact that the confusion  is still widely prevalent indicate only two things

  1. Either , it is not possible to arrive at a simple fool proof  bed side modality  to confirm either VT or SVT
  2. Or it is a too trivial  electrophysiological   issue  that   need  not be worried about  as we have broad spectrum antiarrhythmics (Like antibiotics ! , where we  rarely  bother about identity of the culprit  bacteria  )

The power of statistics and commonsense have never been applied  in the management this vital cardiac entity  .While a  75% sensitive  exercise  stress test (EST) has a huge following in clinical cardiology , a   99 % sensitive   clinical criteria*  for diagnosing VT is  not respected .

*All wide QRS  tachycardia  in patients with   with history of   CAD/STEMI would be VT

If only we had applied our mind to this article published in 1988 we will never ever have the need to split our hairs for decades.(That too without success !)

In  pursuit of  knowledge , are we often  chasing  an imaginary  issue ?

The cardinal  principle of medicine says

“Diagnosis should precede treatment  whenever possible ”

But there need to be a correction  in the above statement .  Time , effort , cost involved in arriving at a  diagnosis  should be meaningful .( Needless to say  . . . it should  a correct diagnosis  too ) And if the power of statistics far exceeds the  frivolous scientific data  , street sense can be applied  liberally even though current generation may call it un scientific .

The issue here is  not being  scientific or unscientific , but whether you are right or wrong  . The article  which is quoted here  has a great insight  about the philosophy of VT diagnosis.

The message form this article goes something like this . . .

In the diagnosis of  wide qrs tachycardia , If we apply  the so called scientific principles   the chances  for missing   a real VT is extraordinarily high , while  if you blindly apply common sense and logic you are going to be 90% right .

What a powerful  statement this !  even though it appears  absurd ,  it is absolutely true !

A young physician  should realize the importance of this . Scientific  decoding of arrhythmia  may be an academic  pursuit but in a given patient at bedside  diagnosing by experience and common  logic are  far more productive and accurate. Miss diagnosis of VT was not common prior to 1980s .  It has become a recent phenomenon .

Probably too much of electrophysiology haS  made a simple diagnostic pathway a complex one. When we relied only on commonsense the errors were less . I  have  often observed  fellows  making mistakes quite frequently  while  nurses  were too confident  to call a wide qrs tachycardia   as VT .

Final message

Medical decision making is an art , in fact it is  a “fine art ”   We keep saying this for centuries , still medicine as a  science  easily overtakes medicine as an art. Here comes the problem . Some times (or is it many times ! ) too much of inquisitiveness in the   name of  science  make practice of medicine  complicated and the victims are often the patients !

Let us simplify medicine  . . . let us accept an occasional  bad outcome  . . . for not being 100 % scientific  ! After all  , a million mistakes happen every day in the  pure  scientific  pathway .

Reference

http://www.amjmed.com/article/0002-9343(88)90008-3/abstract

Also read Knowledge disease

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How do you locate the level of the lesion in Right bundle branch block ?

Posted in Cardiology - Clinical, cardiology -ECG, Uncategorized, tagged , , , , , , , , , , , , , , , on April 25, 2010| 1 Comment »

Like in neurological disease, one can locate the site of block in bundle branch blocks. Though it has never been thought ,  to be clinically important to localise a BBB . (Unlike coronary lesions)

Generally ,  RBBB can be proximal  or  distal peripheral type.The commonest site could be the distal  type.

It should be realised , for over 100 years in  electrocardiology , we have been using some inaccurate terminologies just because it is easy to understand or being traditional .It is difficult  to assimilate a fact , even today that   “An electrical delay in conduction and block are one and the same ”

In fact,  bulk  of  the RBBB is nothing but delayed conduction over this bundle. So whenever we say RBBB  , we imply an incomplete block  ie conduction still occurring   over the  so called blocked bundle.(This dogma applies for LBBB and AV blocks also to a lesser  extent)

Examples of delayed  RV /RVOT conduction

  • Any disease where  RVOT dilatation  occur can cause a RBBB
  • Atrial septal defect
  • Many cases of RVH
  • Pulmonary arterial hypertension

What is the benign rSr’ pattern in V1 ?

This is nothing but a relatively late depolarisation of  RV outflow or conus that produce a terminal RV activity .

Many of the ostium secundum ASD may show just this rSr’ pattern   confirming there is no organic damage to RBB in ASD .

Calling rSr’ pattern as incomplete RBBB is not advisable (As many ECG books may suggest ) .This is because , even full blown RBBB pattern may actually be an incomplete one .Further , the degree of terminal r’ in V1 or s in lead 1  does  not always   determine the completeness of RBBB.

Is there a totally blocked right bundle branch block ?

Yes , it is not common .

  • It can occur in extensive anterior MI .
  • Some cases of Ebstein anomaly.

It can be an working rule , complete RBBBs  locate the lesion proximally and incomplete  ones distally .

What is the other evidence for RBBB in ASD  is  only a simple   delay  in conduction ?

After ASD closure  in many of the patients the RBBB pattern may disappear.This indicate RVOT regression .

Can you clinically differentiate the proximal from  distal RBBB ?

Ironically ,what is difficult in ECG may some times be possible clinically.The classical description of wide splitting S2 occur often in peripheral RBBB.

It represents a delay in the closure of pulmonary valve due to delayed electrical activation or increased hangout interval as in ASD .Logically S1 should also be split in RBBB. But this is not often discussed.

This is because , the split in S1 is lesser in magnitude and is not influenced by the hangout interval .(Hang out interval is the time taken for the blood ejected from RV to fill the pulmonary circulation. Due to the low impedence of pulmonary circulation the the blood that is ejected into the MPA continue  to run off for about 100milli seconds even after the RV/PA pressure crossover .)

S1(T 1) occurs  immediately with the onset  of RV contraction . Similarly M1 occur with LV contraction.It should be recalled it requires hardly 5mmhg of RV pressure to close the tricuspid valve and about 10mmhg for LV to close the mitral valve.

If for some reason if  there is a delay  in RV contraction , as in very proximal RBBB the T1 is delayed and hence S 1 split.

Note in most of the peripheral or distal RBBB the bulk of the RV free wall contraction is not interfered with . So , in distal RBBB it is highly unlikely the S1 will be delayed or split while S2 will be delayed.

What happens to S2 in proximal RBBB ?

Logic would dictate both S1 and S2 should be wide split.

Final message

There is a simple way (Some would call this an futile  academic  excercise  !)to  differntiate proximal from distal RBBB.If the first heart sound is split wide , it fixes the lesion proximally. This may  indicate a more adverse outcome than a simple peripheral delay in conduction.

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Can you localise accessory pathway with the help of echocardiography ?

Posted in cardiology -ECG, Cardiology -unresolved questions, Uncategorized, tagged , , , , , , , , , , , on April 24, 2010| Leave a Comment »

Echocardiography is an imaging tool . Can it  be used as a non invasive  EP lab ?

Heart is an  electromechanical organ . For every mechanical activity there must be a electrical event preceding it . So, when we analyse the cardiac contraction and relaxation it indirectly provide us clues how the electrical activity spreads across the heart.

The concept of using echocardiography for diagnosing cardiac arrhythmias have never been popular for the simple reason we have a cheap and best modality : The ECG.  But, it  does not give us the temporal relationship with the cardiac contraction. When these two are combined it can be a really powerful tool to analyse many cardiac arrhythmia.

  • In fact ,  for every brady and tachyarrhythmia there has to be an unique pattern of IVS motion and mitral , tricuspid valve movement.
  • Almost all bradycadias can be diagnosed with echocardiogram by virtue of analysing the timing of  atrial vs  ventricular  contraction.
  • We know echocardiogaphy is the only modality available to diagnose fetal cadiac arrhythmias.* (How can  this modality becomes useless when the baby comes out of the mother’s womb  !)
  • Apart from this there is an  unique use for echocardiography to locate accessory pathway in WPW syndrome

The premature contraction of LV can be seen in few as  an early systolic dip in IVS movement -Type B WPW.

Image courtesy :  Helmut F. Kuecherer Circulation 1992;85:130-142

Abnormal jerky movement of LVPW indicate left accessory pathway -Type A WPW

Newer modes of echo like tissue doppler will improve the phase analysis of tissue motion and may provide us accurate information about preexcitation

Final message

The future looks bright . Time is not  far off . . .  where ,  we shall  use ultrasound as an adjunct  EP  study .

Reference

*Fetal Echo  =  to  Fetal electro cardiogram

WPW syndrome

http://circ.ahajournals.org/cgi/reprint/85/1/130.pdf

http://content.onlinejacc.org/cgi/content/full/33/3/782

http://www.heartjnl.com/cgi/content/full/82/6/731

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Sinusoidal coronary stent : A new innovation from Medtronic !

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Uncategorized, tagged , , , on April 24, 2010| Leave a Comment »

When every one is thinking bare metal stents are dead ,here comes  an ace  from Medtronic !

A breakthrough technology that make stent navigation into complex lesion as smooth as “knife in butter”

“If only you feel it ”  says the Medtronic ad

The smooth flowing metal inside the coronary artery

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Extramarital sex : A coronary risk factor ?

Posted in Uncategorized, tagged , , , , on April 22, 2010| Leave a Comment »

It is well-known sexual arousal and activity is a powerful hemodynamic stress .In the healthy persons it is never an issue .In fact there is data to suggest sexually active men and women live longer.

But , in patients with cardiac risk factors or an established coronary event unrestricted  sex can be a risk factor for CAD.

There needs to be a distinction  between a coronary risk factor and a coronary  trigger .Trigger is an  immediate switch  for a coronary event in a  patient with  baseline risk profile .It is highly unlikely triggers alone can  cause an ACS .There need to be risky substrate.

Extra marital sex could be such a trigger in some .(Both male and female)

  • The sexual activity performed with guilt  has  more powerful risk.
  • First time offenders
  • New  partners
  • New environment

All of the above are  supposed to increase  the risk .

The mechanism  attributable is  a   sudden adrenergic  surge  which inappropriately high when compared to marital sex . In conservative societies , the effort taken to hide the illicit relationship   is much more stressful than the event itself. And hence these men and women carry on their new-found coronary risk for longer periods.

Reference

http://www.ncbi.nlm.nih.gov/pubmed/20382352

http://drwes.blogspot.com/2010/04/extramarital-affairs-and-heart.html

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An unusual form of constrictive pericarditis : Annular constriction

Posted in cardiology-Anatomy, echocardiography, Uncategorized, tagged , , , on April 22, 2010| Leave a Comment »

Constrictive pericarditis(CP)  has been a fascinating disease   for the cardiologists  for many decades .  (Of course , not  so fascinating for  our  patients!) The reason why clinicians were thrilled to diagnose this entity is due to the unique clinical and echocardiographic and hemodynamic features. Further , it is  one of the few  curable forms of cardiac failure.
It is also about the  philosophy  , pericardium an inert  membrane  which is supposed to protect the heart , becomes a  villain  . When this innocuous layer  is insulted by  chronic   infection (Tuberculosis most common) , radiation injury or post cardiac surgery  it takes a dangerous avatar and  start invading   the organ which  it  guards .
The pericardium becomes thickened , (often > 5mm -2cm) calcified , behaves like a “shell of tortoise‘ and begin to constrict the heart . Once the process of constriction sets in it becomes relentless . It only   requires   , a 10 -15mmhg of constrictive  pressure to make  the poor heart  struggle to relax .(The maximum intracardiac  diastolic pressure ,12mmhg(LV)   .For the right side of the heart it is very low (0-5mmhg) .
So it is obvious the right side of the heart RA, RV gets compressed first .This is why the classical features of constriction with edema , ascites elevated JVP occur.The associated hepatomegaly some times mimic a chronic liver disease.  Of course  relying only  on the  classical findings to diagnose CP would be a crime now .
There are many atypical varieties of CP
  • Localised constriction
  • LV>RV constriction
  • RV>LV constriction
  • Transient constriction
  • Effusive constrictive

* Rarely  constriction is confined to AV groove .  This article  is about this entity.

It is difficult to imagine how a pericardium constrict a rigid fibrous skeleton of the heart namely the AV groove.
But what happens is ,  there  are some gaps in the ring  . The  posterior mitral annulus which  has a deficient  rim  and forms  the most vulnerable  zone for pericardial constriction
Further , AV groove  is located  in a relatively  gravity dependant portion  of the heart  . It facilitates  stasis of inflammatory exudate  in this groove .This may be  the reason  why the  AV groove  shows high incidence of   calcification.
Clinical features of AV groove constriction
It mimics  a presentation of valvular heart disease.
A mid diastolic murmur across mitral valve may occur mimicking valvular MS.
Synonym : Mounsey’s pericarditis
This type of pericarditis should ideally  be called as Mounsey’s constrictive pericarditis   for his
elegant description of this entity 5o yearts ago  even before    Echocardiography was invented.
(These are the days , we struggle to diagnose Mitral stenosis without echo is a different story !)

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Why hypotension is more common in infero posterior STEMI ?

Posted in cardiology- coronary care, Uncategorized, tagged , , , on April 14, 2010| Leave a Comment »

Human heart is a vital bundle of muscle  weighing  about 300-400 grams. The blood  supply of this muscle  mass  is highly variable . Some areas are abundantly  vascularised(  eg -IVS.) Some areas have a balanced blood supply with  twin blood supply (Often the  LCX and RCA in the  crux of the heart ). Certain areas have a precarious blood supply . They are  some time called as water shed areas or  vulnerable   Bermuda triangle of the heart – the  overlapping zone of   LV apex,  free wall and  the anterior surface.

When the blood supply is so  heterogeneous , it is  not surprising  to find  the neural innervation of the heart to have a  unique pattern as well .The cardiac  autonomic nervous system   is  mediated by the  cardiac plexus  . It  has a  dominant adrenergic  innervation in the anterior   aspect of the heart   that is  rich in catecholamines , while the infero posterior  aspect  of heart has a high density of  vagal fibres .

So , it becomes easy to understand , why  ischemia of inferoposterior regions often trigger  a vagal response and an adrenergic response  in  anterior ischemia  .Of course , overlap can occur especially in multivessel CAD with collateral dependent circulation.

The inferoposterior MI ,  generally  have  a better outcome as it imitates  naturally beta blocked heart . (Less heart  rate , less MVO2  more salvage ) Still  hypotension  can be  a worrisome complication in inferoposterior MI .

The following  factors contribute to hypotension in infero posterior STEMI

  • Heightened  vagal tone  due to Bezold  jarish reflex
  • Involvement of RV is known to occur up to 40% of all  inferoposterior MI. Loss of RV pumping action is the classical explanation of hypotension
  • Recently recognised  fact  : Infero posterior MI often have subclinical and subelectrical atrial involvement. This is a powerful trigger for  the atrial  naturetic peptide secretion. ANP  a water losing hormone explains much of hypotension in this situation. .It should also be noted atrial necrosis is not necessary for ANP release. Simple atrial stretch  or even RV stretch can be a stimulus for ANP .
  • Variable degree of LV involvement is  common in infero posterior  MI .This can have detrimental effect on LV pump function . It  can  be a independent  factor for  the hypotension.
  • Excess sedation with morphine may aggravate or precipitate hypotension.(Vagal  action of morphine )
  • Finally , and most importantly a common cause  is  hypovolemic  hypotension (Applicable for any STEMI – Severe sweating  and sometimes vomiting can  loose  up to  10 liters of body water )

How to manage ?

  • Correct hypovolemia
  • Water challenge in RVMI is a popular (Often abused) concept . Rule of thumb is , if 1000ml  of  rapid infusion  fails to correct the hypo it is  highly unlikely  it will  do it at 5 liters  ! Cases of fluid overload and dilutional hyponatremia have been reported.
  • Atropine (This is one of the rare situations  where vagal blockade increases the BP ) .Dopamine may be useful but logically we need to  reduce the high vagal tone  and bring autonomic parity  . (Increasing adrenergic tone to that of high vagal levels  for autonomic parity  is  a lesser logic !)
  • Temporary pacing may be needed if  blood pressure fail to raise because of  troublesome bradycardia.
  • And  of course  , rapid PCI and revascularisation  when Indicated

Final message

Hypotension in inferoposterior MI is often  considered innocuous. But , it can be dangerous in some , especially in the  elderly and comorbid individuals . It has  varied mechanisms  , that are distinctly different from anterior STEMI.  Recognising the underlying mechanism  hypotension  will aid us to correct it  rapidly.

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