Archive for April, 2010

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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It is  over a century old dictum , that  edema legs and elevated JVP is the hallmark of cardiac failure.In fact , these two  constitute  major criteria of Framingham  cardiac failure score.When these criterias were formulated the concept of diastolic heart failure was not in vogue. So we  do not know whether the same would apply for diastolic heart failure also.

In all probability these  conventional criteria may not apply to diastolic heart failure  .

But why not ?

We know diastolic heart failure  of the left ventricle  is less likely raise the  systemic  venous pressure  to cause the edema and raised JVP. But still ,  isolated LV diastolic dysfunction can increase the PCWP and PAP and RVP . Remember diastolic  septal dysfunction , may compromise RV relaxation also.(Reverend Bernheim like  effect)

We should  also realise , raised  venous pressure is not the only mechanism for edema legs.

Diastolic dysfunction can trigger  ACE genes  .IT can get activated and hence renal conservation of sodium.This neurohormonal activation can be dominant  mechanism of edema in few. This  prevails over  the hydrostatic forces. And  hence edema can result in isolated diastolic dysfunction.

What about RV diastolic dysfunction as a cause for right sided failure ?

This is a poorly  understood entity.Logic suggests  it may have clinical significance. Since  morphologically and developmentally LV  and RV share a common  sheet of muscle  , LV diastolic dysfunction can have it’s impact t on the RV as well.

Final message

Edema legs and raised JVP is a hall-mark of  isolated  systolic heart failure or combined systolic and diastolic failure   .It is not rare to find an occasional patient isolated diastolic dysfunction*  to present  symptoms of  systemic congestion .

*Of course ,  in this era of hi tech cardiology practice  it may be  inappropriate  to  depend on these  primitive clincal criterias  to diagnose CHF . (These  manifest very late in the course of CHF!)

Read also

Why  some patients with cardiac failure never develop edema ?

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LBBB is probably the most important  conduction defect of the heart .When we say LBBB , we visualize a  strikingly  wide bizarre qrs complex .

Left bundle even though is considered  a discrete structure , the fascicles  make it a diffusely spread structure. Many varieties of LBBB with various degrees of involvement occur.

Talking about the basics of  LBBB  electrophysiology  is out of place for the current generation cardiologists,  who  have little spare time as  they sweat it out inside the cathlabs.

In early 1960s and 70s great articles came from pioneers regarding these defects. If we want get a good insight  read  this  articles from  Sodi palleres .Who  says LBBB is a dynamic process, where it can occur from mild functional  delay to a total block .

The conduction  properties of left bundle is very much influenced by heart rate.

Law of statistics would  suggest  for every complete LBBB  at least three to 4 times incidence of incomplete  LBBB

Then . . .

Why we are not diagnosing ILBBB often ?

  • We miss it
  • Mistake it with LVH
  • We know it  is there , but we do not  want  to diagnose it .

How to diagnose ILBBB?

See  Sodi palleres criteria*

What is the relationship between qrs width and completeness of LBBB ?

Surprisingly and contrary to the belief , the width of the qrs has no linear correlation between severity of LBBB. In fact incomplete  LBBB can occur with even 150ms qrs !

Then ,  what  exactly determine the completeness of LBBB ?

What  matters is , whether the down coming impulse gets blocked  and split in the  left side of the IVS or not ? This causes the  the septal vector to  change  it’s direction ( ie  right to left instead of the normal left to right) It  removes the initial small r wave in v1  and q in v6  in complete LBBB. In  incomplete LBBB these  r and q are  often retained .

What is the differential diagnosis of ILBBB ?

Type B WPW may mimic LBBB and vice versa.

LV hypertrophy .

Differences : See table in  the Barold’s article  linked above .

Unanswered questions

  1. How common is ILBBB in STEMI ?
  2. How often ILBBB progress to LBBB ?
  3. ILBBB in dilated cardiomyopathy : Is desynchrony an issue ? (Normal QRS CHF !)
  4. Is functional  rate dependent  LBBB in cornary care units  same as transient  ischemic LBBB ?
  5. Intermittent LBBB and Incomplete LBBB  aren’t they  synonymous ?

Final message

ILBBB is not that uncommon as one would  tend to perceive.


My humble tributes to  Barold, Sodi -palleres , and Leo  Schamroth . Probably  one of the best  article on ILBBB is linked below. Reviewed    in 1963 !  Not much data has been added  in the next 47 years as on 2010

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ERS -Early repolarisation syndrome  is known as a   benign ECG finding  for  many decades  .Now it  is beginning to look dangerous as evidence is accumulating  it may have a link with ventricular arrhythmias.

ERS represents complex changes in  ionic movements during  cardiac repolarisation . (To be specific , it is due to a functional gain of  K + ionic channels during phase 3 of action potential).Generally this is a very benign condition. But , what concern us is ,  it can predispose to ventricular arrhythmias when these patients are confronted with ischemia .

When repolarisation occur early it indirectly shorts the QT interval .We know QT interval is a notorious period in human ECG as both a short and long (<320ms, > 460ms)  can be dangerous.

Is ERS a marker for potential cause for primary VF ?

Read this article from NEJM 2009

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There are thousands of medical journal published worldover. Dozens are available in the field of cardiology .Only a few  are dedicated for pediatric cardiology.  Annals of pediatric cardiology is one .

It is all the more  creditable , as it comes from India , A country which is lesser known for scientific infrastructure  .  Full credit to the  pediatric cardiologist associataion of India and the medknow publishers for  bringing  this  highly specialised scientific content in this part of the world .

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Association of pediatrics of India  has done a wonderful job .This may the first of it’s kind to formulate a excellent guidelines for managing CHD in India . This was made possible by the consensus conference on CHD held in AIIMS in 2007.

A must read for every physician, pediatrician and  cardiologist

It is recommended , this  guideline should be incorporated in every undergraduate curriculum of  medicine .This article which was published three years ago ,  should  have been published in the Indian  heart journal also.

Thanks to Indian association of pediatrics for providing this article  free

Link to article.2007 consenus conference on CHD Newdelhi

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