Archive for August, 2010

Welcome to the new era of “medical avatar “

Cardiologist’s ultimate dream  of  monitoring  their patients

Live ECG feed in your cell phone  !

Thanks to the American “scientific  pursuit” and the mankind  will be  the beneficiary !

Courtesy :

Airstrip technologies

What’s next ?

Remote DC shock and pacing  .

Watch out  . . . it is going to happen in next 5-10 years !

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These simple questions were asked once upon a time  when cardiologists were not known as interventionists.Now many of them  have neither time  nor interest  to ask such questions .! An article   which came in Circulation 1974 addresses this question lucidly.

It is known, HV interval represents infra hisian conduction . And LBBB is  just that ! Then , why it is not prolonging it ?

The answer is ,  it does prolong  the HV interval  by 20 -40 ms , but , it is not manifested in surface ECG .  A 20 ms increment in PR interval (Say 160 to 180 ms ) is not a big issue generally.

* Then the concept of incomplete and complete LBBB is always there to confront us !

Many believe , the intraventricular conduction delay in LBBB may simply represent  the  “unmaking effect”  of   LBBB   which  re-routes  the conduction  in the slightly delayed  , circuitous   right bundle  highway   . But it is only a   assumption.Many things can happen in a  ischemic , degenerative, dysfunctional heart.

When does the HV interval prolong pathologically in LBBB ?

Acute LBBB (Note Left bundle  has two fascicles , technically  equivalent to bifasicular  block )  A 40ms  increment in HV interval (Hence in  PR interval also)   can be a dangerous delay in LBBB .

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The commonest cause of syncope is the neuro-cardiogenic or vasovagal syncope .

The following is  the possible neural  circuit  of this syncope . In fact . it is a  “Neuro -vascular circuit”

The afferent* (Two components  are present  -Both trigger sympathetic signal )

  1. Sympathetic (Prodrome /Anxiety /fear )
  2. Cardiac mechano /stetch receptors  located mainly in LV .(Can be in Aorta/Carotid )

* In some cases sensors  and afferent can be same entities.

The centre – Medullary Nucleus ambiguous /Tractus solitarius

The efferent -Strong parasympathetic overshoot and sympathetic withdrawal

Parasympathetic excess lead to bradycardia primarily, while sympathetic  withdrawal lead to


Syncope recovery

As patient recumbent posture ; LV gets filled and  LV mechanoreceptors are passified .

Final message

The exact pathophysiologic basis of this syncope  still  not elucidated.But one thing is clear , the syncope is due to sympatho- parasympatho signal mismatch( and sort of a rivalry reaction)  !In this neural game , heart’s behavior is all the more funny , it initiates the reflex  while  the brain stem  “Boomerangs” it back to heart and vascular system ,  with a vagal onslaught .

To call this  simply as vasovagal  is not proper , that is why neuro -cardiogenic syncope was used.

Ideal terminology  would be  to call it as  cardio -neuro -cardiac syncope   as the cardiac component form the afferent limb as well as the efferent (target organ )


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Pericardium is a  fine  biological sensor. It   makes   noise when the kidney is in distress .

We call   this as uremic pericardial  rub .  This is not a universal phenomenon in renal failure.

Occurs in about 10% of renal failure .


  • Chemical pericarditis . Uremic middle molecules ?
  • Dialysis related pericarditis
  • Associated infection

Two  themes can occur .

  • Pericarditis without effusion .
  • Effusion without pericarditis

The later is more common .

Is it a exudate or transudate ?

Usually a transudate. Protein accumulation may occur .

Hemorrhagic or non hemorrhagic effusion ?

Again both can occur. Platelet dysfunction is well known feature of renal failure .Bleeding into pericardial space  even a few cc of blood is suffice ,  to color the entire effusion  red  .

ECG features of uremic pericarditis , how is it different ?

The uremic pericarditis  less often results  in classical ST elevation  (concavity upwards)  instead the hyperkalemia features dominate , if present.

The reason for less conspicuous ST  elevation is due to the relative lack of  epicardial electrical injury . Further , the pericardial fluid  is enriched with  oppositely charged uremic molecules  which neutralise’s the

electrical gradient .

Relationship  of pericarditis  with acuteness of renal failure

Though it can occur in any form of uremia.It is more often observed in rapidly worsening renal failure

Relationship to dialysis

  • Presence of  pericardial rub is a classical indication for dialysis .(But not presence of effusion per se  )
  • While pericardial rub disappears in many ,  a  pericardial  rub that is  exclusively  observed  for the first time  after dialysis is well known .
  • The exact mechanism is not  clear . One explanation could be  the pericardial   surfaces gets approximated once pericardial fluid is filtered by dialysis.


Tamponade is common .Usually tolerated well till late stages as  LVH  and mild PAH are common which resists fluid compression.

Constriction can rarely occur. Tuberculosis can co exist.


  • Indomethacin /Other NSAIDS
  • Steroids
  • Pericardiocenetesis
  • Surgery may be needed if recurrent pericarditis occur

Patients with pericardial rub should be dialysed heparin free .


Review article



Surgical management


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Detection of  pericardial effusion was  the earliest  clinical application of echocardiography. Diagnosing  large effusions is a non issue .Assessing  minimal effusions (Systolic vs diastolic echo free space) and associated  thickened pericardium is tough even after 50 years of echocardiography.

Mainly , we are limited by the resolution power of echo. Further , lack of echocardiographic landmark for visceral  layer of pericardium (It is same as epicardium !) makes  diagnosis of  thickened pericardium a real tough exercise.It is said , normal pericardium is less than 4mm .

Where to measure it ?  how to measure is still not clear.

Why differentiating  minimal  pericardial effusion from  thickened pericardium  is important ?

  • Mild  pericardial effusion is  largely a benign finding in vast majority.
  • But , even a minimally thickened pericardium  due to active inflammation  can be significant.
  • Sticky pericardial effusion predispose to thickening and constriction.
  • Early recognition of this dreaded pericardial pathology is essential to interrupt the inflammatory process.
  • In CRF (With or without dialysis) even a  minimal pericardial  effusion can denote a dismal outcome .

Here is a link to Horowitz classification of mild  pericardial  effusion ...


It could help us understand, How thickened pericardium presents in echo. Of course, CT and MRI now have increased sensitivity for diagnosing  pericardial thickening.

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Cardiologists are often confronted with pregnant women in distress with heart disease. Obstetricians promptly refer them to cardiologists.

There is a tendency among cardiologists,  to make fun of obstetricians who  some times  call them for  frivolous  cardiac problem at odd hours  .(Say a VPD in the monitor or a systolic murmur of anemia etc)

Of course  , this   doesn’t mean in any way ,  cardiologists  belong to a superior  species  ! The fact  is  , many  cardiologists fare poorly in their  knowledge about the hemodynamics of pregnancy (Let them prove this wrong !)

A small quiz . . . for all cardiologists

  1. How much of  blood enter the maternal circulation after each uterine contraction during active labor ?
  2. Is the stress of normal delivery is   greater than that of  cesarean section under epidural anesthesia ?
  3. What anesthetic agent is ideal in patients with pulmonary hypertension ?
  4. How safe is  general anesthesia in a hypotensive  , heart disease patient ?
  5. What is the clinical significance of administering IV anesthetic vs inhaled anesthetic in a patient with right left shunt lesions ?

If a cardiologist is able to answer all  these 5 questions correctly without guessing , probably  they have  the right to make fun of obstetricians  or else  they have  to  quietly buy this book and read !

Final message

Every responsible cardiologist  must have good awareness about hemodynamic  stress of pregnancy and the intricacies of obstetrical anesthesia

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It sounds  to be a  simple question . But, cardiology literature is sparse  on the subject.

RV mimics a three dimensional triangular chamber .The inflow, body and outflow align themselves in complex planes .This makes measurement difficult.

What  are the measurements to be made  ?

  • RV inflow tract (RVIT)
  • RV body
  • RV outflow tract (RVOT)
  • RV Free wall thickness

How to measure RV size ?

  • Inflow diameter is assessed in inflow view ( Para sternal long axis,probe  tilted down towards lower  sternal edge (cool . . .That is were tricuspid valve is located !)
  • RV body can be assessed in long axis or 4 chamber view
  • RVOT in short axis view.

What is the normal range ?

RV Body

< 3 cm in parasternal long axis view

<8 cm Long axis ( RV apex to mid point of TV )

RV inflow(RVOT)

<  3- 4cm

RV outflow (RVOT)

1.8 to 3 cm

Note :

  • All measurements are taken in end diastole .
  • The largest diameter of RV is at its inflow(it is roughly equivalent to tricuspid annulus)
  • RVOT size can vary  , generally tapers as it reaches near the pulmonary valve .

How common is the  differential RV enlargement*?

The complex shape and architecture of RV  make  the  direction , sequence  and magnitude of  RV enlargement less predictable .

  • Diastolic loading of RV generally have more uniform enlargement of RV .(Inflow, body, outflow )
  • In dilated cardiomyopathy RV enlargement  common in short axis > long axis
  • Pressure over  loading may not result in uniform enlargement as the pressure points on RV surface is not homogeneous.
  • In congenital heart disease , RV shape and size  depend more on the morphology(location of VSD, infundibular  anatomy, muscle bundles, extent of trabeculations etc)
  • In arrhythmogenic  RV dysplasia (ARVD) outflow  tract enlargement is more dominant.

* The fact that ,  RV can enlarge  in focal and localised manner make it mandatory to measure RV dimension in multiple views and in all possible diameters.

At what  pressure RV begins to enlarge ?

RV is believed to enlarge at > 60mmhg .Hypertrophy is usually precedes dilatation  .

At what volume overload RV begins to enlarge ?

Our experience with ASD indicate when the pulmonary  blood flow  is twice that of systemic blood flow RV is distinctly enlarged. May be it begins to enlarge at>  1.5: 1 shunt

RV begins to enlarge horizontally or longitudinally ?

this aspect is not studied much.  Generally volume overload causes more uniform enlargement.

How does acute RV enlargement differ from chronic RV enlargement ?

Dilatation is more conspicuous in acute RVE ( Pulmonary embolism, RV infarct ) associated wall motion defects and thinning favors acute RVE.

Normal or increased thickness is expected in chronic RV enlargement

Here is a  five-star rated  article on RV dimension

Published in 1986 , still considered a  land mark paper  . . .

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