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Tubular heart : A case of Hypo-cardiomegaly of heart

Posted in Uncategorized, tagged , , , , on October 26, 2010| Leave a Comment »

It is a great journey , the  heart begins  on the 22nd day of fetal life from  a pair of  tubes. It joins , folds, bends and grows into a 4 chamber power house  and works  like a bull for the next  70-80 years , before retiring.

It is an irony in certain population with chronic obstructive pulmonary disease (COPD)  heart is stretched , elongated and assumes a tubular shape (Memories of  the primitive fetal  heart tube !) .The LV cavity becomes small , RV and LV gets aligned one behind the other  bringing  the CTR further narrow.

Tubular heart

CT ratio will be less than 1/3rd of thorax. (Just more than aorta ! )

Conditions

  • COPD with emphysema
  • Somes cases of hypoadrenalism(Addison) due to chronic volume hypovolemia and underfilling of the  entire vascular  system that includes the heart .

Here is a patient , 50 year old female with severe emphysema and  contracted and elongated heart.

  • Her CT ratio was 30% .Note wide rib spaces and pulling up of both diaphragm by fibrotic lung
  • Note the LV apex conspicuously absent
  • LV diastolic dimension was 30mm and  systolic was 19mm
  • End diastolic volume  was critically low at 40ml .
  • She was complaining of class 3 dyspnea.It was primary attributed to COPD but the contribution of under filled LV and resultant diastolic dysfunction is often overlooked.


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What is the response to oxygen administration in central and peripheral cyanosis ?

Posted in Uncategorized, tagged , , , , , , on October 22, 2010| 1 Comment »

Answer : Peripheral cyanosis  reduces or disappears  , while central cyanosis persist.

This is how , 99% of cardiology fellows answered in one of my  classes ! And they were quoting few  references for it .

Is that correct ? If so , what is the mechanism  of  oxygen response ?

Comments welcome . Discussion will start soon .

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How to recognise reduced pulmonary blood flow clinically in the bed side ?

Posted in Uncategorized, tagged , , , on October 21, 2010| Leave a Comment »

During  clinical examination of cyanotic congenital heart disease(CHD) ,  the major  task is to differentiate conditions with reduced  or increased pulmonary blood flow .

When a child with  CHD  is presented in clinical examinations , students are often asked to arrive at  the diagnosis  from history , physical examination before going in for ECG, X ray  or  echocardiography.

History,  surprisingly can  suggest  the  correct diagnosis in many (Most ?)

Reduced pulmonary blood flow is often associated with

  • Cyanosis   appearing with  /or worsening with   exertion*
  • Hypoxic spells.(Almost always occur in reduced pulmonary  blood flow )
  • History of squatting( Majority in reduced pulmonary flow)

Relief  of dyspnea   by assuming squatting position  convey   important hemodynamic information. It implies  there is significant reduction in pulmonary blood flow in standing posture , that  gets corrected  in the squat position.For squatting to improve pulmonary blood flow there must be a communication between right and left heart .This is most often due to a large VSD, rarely an  ASD .

Related article : How squatting relieves hypoxia in TOF ?

*Note :  Cyanosis  is  not  specific for reduced pulmonary  blood flow. In fact , simple reduction in pulmonary blood flow per se , cannot result in significant cyanosis .There need to be admixture /or right to left to shunt to produce cyanosis .Cyanosis in  pure admixutre states like TGV, Single ventricle , Common AV canal , Common atrium TAPVC,  are less Dependant on the reduction of  pulmonary  flow. In these situations RVOT obstruction if  present  will aggravate the baseline cyanosis.

Examination

Apart  from direct evidence for reduced pulmonary blood flow , lack of evidence for increased pulmonary  flow could  often mean ,  we are  actually  dealing  with  reduced pulmonary blood flow.

The following are the clinical clues to suspect  reduced pulmonary blood flow.

  • A quiet precardium*
  • A inconspicuous pulmonary component of S 2
  • Generally if  S 2 is well split  and both components are well heard it is highly likely the  pulmonary  blood flow is not reduced.
  • Lack of  pulmonary  arterial pulsations
  • Absence of mid diastolic  flow murmurs  in AV valves
  • Presence  of continuous murmur in a patient with cyanotic CHD almost always mean   reduced pulmonary flow and the lungs are perfused by alternate arterial collaterals (MAPCA)

* A silent  heart is the hall mark of Tetrology of Fallot which constitutes 80% of all CHD with reduced pulmonary blood flow.

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C reactive protein : Old wine in “older bottle” !

Posted in Uncategorized, tagged , , , , , , , , , on October 20, 2010| Leave a Comment »

What we know about CRP . . .

  • It is an acute phase reactant.
  • Secreted mainly in liver.
  • It is a marker for systemic inflammation.
  • Hs CRP more than 1 -3 mg is significant

What we think ,  we know . . .

It is a direct marker for increased risk of CAD.

Reducing CRP levels reduce CAD risk  and vice versa .

What we definitely do not know . . .

Does CRP damage the coronary  endothelium ?  Or  Is it secreted  from the inflamed plaque ?

How statins reduce CRP ?

How can you differentiate cardiac origin of CRP from peripheral origin ?

Fibrinogen levels  tend to raise in non cardiac CRP elevation .

What are  the commercial interest in this molecular test   ?

Hs CRP is  being proposed  as a screening test  for  detecting high risk CAD ,   to enable it  for  mass marketing . For drug companies  developing a  drug is huge task as  tight regulations  are vigorously pursued. While getting  clearance for  a   biochemical   investigation   is  a much easier task,  as it does not involve  patient safety or  ethical issues .

So, one of  the major studies  on statins  ,  suggested   a major role ,  for  estimation  of  Hs CRP  to identify high risk subsets among  those with normal LDL levels.  This study  many academicians felt,  was  aimed to promote  this investigation .  Care takers  should be aware  of the motives behind  the so called  global war against CAD . Many such  interventions could be  entirely commercial . This is a dangerous trend  ,  the medical profession  is facing .  It could  be more damaging than the ubiquitous atherosclerosis !

What we should know ?

Final message

  • C reactive protein is  nothing more than a  new generation ESR !
  • It  may  not have any specific value in a given individual to predict / not predict  a cardiac  event  .
  • The only role could be to identify  subset of  population who may be at higher risk of developing inflammatory  CAD.
  • But it  is largely a hype ,  to call it as a landmark  triaging  molecule  for  preventing  CAD is not acceptable to many.
  • The meta analysis  on CRP in Lancet  2010  was published  . I am afraid ,  it has not answered the elusive question  : What is the utility value of Hs CRP in the  clinical cardiology and preventive cardiology  ?

What we need to know is ,

  • Avoiding  junk  food,
  • Good physical activity,
  • Quitting smoke ,
  • And  a relaxed mind  (All of them come free of cost ! The first one , in fact  pays you !)

Is the best way to prevent CAD epidemic !

One need not go behind this fancy molecule  . . .

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Does the right ventricle really dilate in ventricular septal defect ?

Posted in Uncategorized, tagged , , , , , , , on October 20, 2010| 2 Comments »

The following  questions  are asked frequently  in clinical cardiology classes on congenital heart disease.

What are the chambers that dilate in ASD ?

Right atrium and  right ventricle .

What are the chambers that dilate in VSD ?

LA, LV , ± RV,

* Image courtesy Wikipedia

While there is no controversy about ASD, The chambers that enlarge in VSD ,   is  by and large  poorly (or rather wrongly ) understood .  Whenever we  diagnose  VSD , our brain is tuned  to think  this way : Blood  will be  shunted form LV to RV.  RV  would  handle more blood and it  should   enlarge . In reality it does not happen.

The VSD  shunts  the  blood from  LV to RV outflow*   or even directly into  pulmonary artery  .  Hence , VSD even if it is large  , does not dilate  the RV until the onset of  pulmonary hypertension and RV dysfunction sets in . It is surprising to note , even the RVOT ( The entry point of most VSD jets) does not significantly  enlarge

Importance of diastolic shunting in determining RV size in VSD

It is also important to recognise, the VSD shunt predominately occur in systole .(90% ?) In systole , the RV is also contracting along with LV  , so it’s size is diminutive  and hence RV can not be volume overloaded in  most of the VSDs however large it may be. Instead in ASD , there is diastolic overloading   involving  all regions(Inflow, Body, Outflow) of  RV   .This enlarges the RV   in a classical  fashion.

Significance of  anatomical location of VSD and RV enlargement

When VSD shunts blo0d into RA as in Gerbode defect it is bound to enlarge RV (like ASD) as there is diastolic volume over load of RV.

In some large muscular VSD , RV body can be  volume  overloaded. This is because the VSD and RVOT are well separated geographically .The  blood that is coming in from LV can enter the pulmonary artery , only in the next cardiac cycle  . So , RV needs to accommodate the shunted  blood till the next beat. Hence RV enlarges.

What are the situations RV can enlarge significantly in VSD ?

  • Rare VSDs of inflow or large muscular VSDs.
  • Eisenmenger syndrome.
  • Tricuspid regurgitation
  • Pulmonary regurgitation
  • Associated RSOV.

Final message

Right ventricle   does not enlarge  significantly in uncomplicated  VSD .This is in contrary to the  traditional teaching and understanding  for  many years. It enlarges only in specific sub types of VSD  or  after the onset of PAH and cardiac failure .

Coming soon

Katz-Wachtel phenomenon is not  due to  bi -ventricular hypertrophy !

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Artificial valves in unusual location : “Yes” within lungs

Posted in Uncategorized, tagged , , , , , , on October 16, 2010| Leave a Comment »

 Cardiologists  often  think heart is the supreme organ.  As medical  science  advances at a rapid pace we fail  to notice the development  in other  specialities .It is getting more and more difficult  for a  physician  in one field ,  to  understand the  advances  in other  . Often it becomes a  struggle to  decode  non cardiac  case sheets and prescription  filled with latest  generation treatemnt  modalities .

Here is a stunner  at least for  me  !   to find  , artificial  valves  being used   in the human bronchus ,  to regulate the air flow  in patients  with emphysema.

So,  cardiologists be ready  to prescribe  ” lung valves ” for  managing severe cases of cor pulmonale  secondary to emphysema !

 

Reference

http://www.sciencedaily.com/releases/2007/10/071022120150.htm

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

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Why there is wide and fixed split of S2 in ASD ?

Posted in Cardiology - Clinical, Uncategorized, tagged , , , , , , , , on October 13, 2010| 3 Comments »

  • Second heart sound is widely split because the pulmonary hangout interval* is wideFixed because , the RV stroke volume does not show the normal respiratory changes.This is due to dynamic phasic shunting across the IAS ( For example : During inspiration , if RA,RV volume gets augmented by 50ml from IVC inflow , in expiration this IVC augumentation is removed but a 50 ml augmentation from left atrium takes place , this keeps the RV diastolic , as well as systolic volume relatively constant.) This makes the 2nd heart sound fixed .

    * Hangout interval is the gap ( in time ) between the arterial pressure curve and the respective pumping chamber pressure curve (RV, LV) at the level of incisura.

    Incisura is the notch on the descending limb of arterial pressure curve , when the pulmonary or aortic valve closure occurs . When we analyse the simultaneous pressure recordings of RV ,LV/Pulmonary artery/Aorta , the arterial pressure curves faithfully accompanies the chamber pressure curve along the dome of the chamber pressure curve till it descends , where it dissociates , from the chamber pressure curve and hangs out for a certain milliseconds. This time interval is called as hang out interval (Named by Shaver et all )

    What is the normal pulmonary hangout interval and systemic hangout interval /

    Pulmonary hangout interval is 60-80ms

    Aortic hang out interval is 20 ms

    Why does it happen ? What does it signify

    It happens because , even as the chamber pressure falls below the arterial pressure ( Note: Semi lunar valves close at this cross over point ) blood continues to rush forward , with momentum in to the pulmonary and systemic circulation, in spite of the pressure cross over has happened, the semilunar valve doesn’t get closed exactly at the cross over point .It gets closed little later than true cross over point.This gap in time is the hangout interval. This Interval keeps the arterial pressure not only to be sustained little longer but also slightly higher .

    This interval is an indirect( inverse) marker for vascular impedance of the distal draining circulation .The impedance is same as vascular resistance for all practical purposes.Since pulmonary circulation is a low impedance circulation , it has a wide hangout interval and the systemic circulation vice versa.

    How much of S2 widening is contributed by RBBB in ASD ?

    This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often incomplete and peripheral one .( Pesudo RBBB due to RVOT dilatation )

    What happens to S2 when pulmonary arterial hypertension develops in ASD ?
    It is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to behave like systemic , hence the impedance becomes high and the hang out interval is significantly lost and second sound is narrowly split. (But fixity may be maintained.)It also depend upon the RV function and associated RBBB. RV dysfunction and RBBB both tend to widen the split.*Mild PAH usually does not alter the S 2 splitting

    Is there any other cause for wide and fixed splitting of second heart sound ?

    Having known the reasons for widening and fixity it is easy to understand , a patient with right heart failure and RBBB can have a wide and fixed split .

    Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good enough to handle the inspiratory augmentation of RV end diastolic volume.)

    Why in VSD the second heart sound is not wide and fixed split even though hemo- dynamically it fulfills the same hemodynamic scenario ?

  • This is due to dynamic phasic shunting across the IAS ( For example : During inspiration , if RA,RV volume gets augmented by 50ml from IVC inflow , in expiration this IVC augumentation is removed but a 50 ml augmentation from left atrium takes place , this keeps the RV diastolic , as well as systolic volume relatively constant.) This makes the 2nd heart sound fixed .

    * Hangout interval is the gap ( in time ) between the arterial pressure curve and the respective pumping chamber pressure curve (RV, LV) at the level of incisura.

    Incisura is the notch on the descending limb of arterial pressure curve , when the pulmonary or aortic valve closure occurs . When we analyse the simultaneous pressure recordings of RV ,LV/Pulmonary artery/Aorta , the arterial pressure curves faithfully accompanies the chamber pressure curve along the dome of the chamber pressure curve till it descends , where it dissociates , from the chamber pressure curve and hangs out for a certain milliseconds. This time interval is called as hang out interval (Named by Shaver et all )

    What is the normal pulmonary hangout interval and systemic hangout interval /

    Pulmonary hangout interval is 60-80ms

    Aortic hang out interval is 20 ms

    Why does it happen ? What does it signify

    It happens because , even as the chamber pressure falls below the arterial pressure ( Note: Semi lunar valves close at this cross over point ) blood continues to rush forward , with momentum in to the pulmonary and systemic circulation, in spite of the pressure cross over has happened, the semilunar valve doesn’t get closed exactly at the cross over point .It gets closed little later than true cross over point.This gap in time is the hangout interval. This Interval keeps the arterial pressure not only to be sustained little longer but also slightly higher .

    This interval is an indirect( inverse) marker for vascular impedance of the distal draining circulation .The impedance is same as vascular resistance for all practical purposes.Since pulmonary circulation is a low impedance circulation , it has a wide hangout interval and the systemic circulation vice versa.

    How much of S2 widening is contributed by RBBB in ASD ?

    This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often incomplete and peripheral one .( Pesudo RBBB due to RVOT dilatation )

    What happens to S2 when pulmonary arterial hypertension develops in ASD ?
    It is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to behave like systemic , hence the impedance becomes high and the hang out interval is significantly lost and second sound is narrowly split. (But fixity may be maintained.)It also depend upon the RV function and associated RBBB. RV dysfunction and RBBB both tend to widen the split.*Mild PAH usually does not alter the S 2 splitting

    Is there any other cause for wide and fixed splitting of second heart sound ?

    Having known the reasons for widening and fixity it is easy to understand , a patient with right heart failure and RBBB can have a wide and fixed split .

    Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good enough to handle the inspiratory augmentation of RV end diastolic volume.)

    Why in VSD the second heart sound is not wide and fixed split even though hemo- dynamically it fulfills the same hemodynamic scenario ?

    • Guess the answer .It will be posted soon.

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    Clinical and hemodynamic tips to diagnose VSD and Aortic regurgitation

    Posted in Uncategorized, tagged , , , , , , , , , on October 8, 2010| Leave a Comment »

    Aortic regurgitation complicating VDS  is an important clinical  entity in congenital heart disease.It is  also  a popular case for the cardiology fellows in their  final clinical examinations . AR is a  late manifestation of VSD (usually in early  adolescent  or adult hood) .This develops due to loss of aortic valvular support provided by the inter ventricular   septum.

    In fact ,   IVS can be termed  as a foundation stone  on which  a  part of  aorta (Mainly its anterior part) rests . So, it is not surprising VSD patients  are prone to develop AR especially,  as they grow when aorta tires to outgrow the septal support . Further,  the hemodynamics of VSD has a crucial impact on the AR progression.(See image below)

    Pulse /Blood pressure

    Large volume pulse,  may be collapsing

    Peripheral signs of Aortic run off usually present

    Apical impulse

    Shifted down and out Hyperdynamic

    Murmur

    To and fro murmur (To -Systolic , Fro -Diastolic )

    It is differentiated from continuous murmur by a distinct reduction  in the intensity of murmur towards the end systole and a different murmur  appear  in diastole  . While , a continuous murmur  is  a single murmur  that peaks  around sound  heart sound , overlaps the second  heart sound and spills well into diastole.

    Other useful diagnostic clues

    • Usually the VSD  is  restrictive  .Left to right shunt is often below  2:1
    • With the onset of AR  ,there is  further reduction in the left to right shunt of VSD
    • Hence,progressive pulmonary arterial hypertension is uncommon and Eisenmenger is reaction is very rare in  VSD with AR.
    • Presence of AR makes  LV dilatation disproportionate to VSD  shunt  (LV size  is not useful to assess the  hemodynamic  significance of VSD)
    • LV dilatation invariably means significant AR rather than VSD.  VSD induced LV enlargement  is  usually less conspicuous as it is  represents  physiological flow across mitral  inflow .  While , AR is a high gradient leak  from a non-physiological chamber (Aorta)
    • ECG volume overload of LV   is  evidenced by  more prominent * q waves in  V5 V6

    *Double dose of volume overload (AR +VSD)

    Management

    • If AR is mild ,only VSD closure is advocated *
    • If AR is moderate  , repair of aortic valve is  considered along with VSD closure.
    • For severe AR , Aortic valve replacement or repair with VSD closure mandatory.
    • Device closure of VSD and percutaneous  aortic valve replacement  not feasible at the moment .May be a future possibility.

    * If both  VSD and AR are very small ,  simple follow up , and observation (Leaving the patient happy!)  could be a distinct option !

    Pathogenesis of AR in VSD : The landmark article from Japan in 1973 by Tatsuno  and Sakakibara

    http://circ.ahajournals.org/cgi/content/short/48/5/1028

    Thanks to circulation .Such articles are made available .

    http://circ.ahajournals.org/cgi/reprint/48/5/1028

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    Management issues in acute pulmonary embolism : Should heparin be started only after thrombolysis ?

    Posted in Uncategorized, tagged , , , , , on October 8, 2010| Leave a Comment »

    Acute pulmonary embolism is a vascular  emergency.Massive pulmonary embolism needs immediate thrombolysis or embolectomy. Success rate  of  thrombolysis  appears good . But , the symptom improvement  is slower .

    Sterptokinase is the commonly used drug to dissolve the pulmonary thrombus  . (Except in USA , where they  prefer the much costlier TPA )

    The sterptokinase  adminstered with the following protocol

    • 2.5 lakh Unit bolus over 30 minutes
    • Follow with 1lakh unit /per hour for the next 48 hours (Up to 72 h)

    When to start Heparin infusion ?

    For TPA ,  there is no confusion .Heparin must be started immediately after the completion of TPA infusion (100mg in 2 hours)

    Cardiology community is divided for heparin protocol with  streptokinase. Because , streptokinase is administered over 48hours it is thought heparin is not required during  this period.But in reality , it  implies , we  deny a role for this  powerful anti thrombin  in the critical hours of ongoing  intra vascular clotting . Hence  logic demands  to start heparin  along with  streptokinase.

    There is further concern that,  the dissolved thrombus generate pro coagulant  debri , that will negate the benefits of thrombolysis. Oral anticoagulants  are supposed to be started  as soon as the diagnosis  of pulmonary embolism is made. In that case , heparin will be required  much earlier as  warfarin has to be overlapped with heparin.

    We would  argue for  , a careful simultaneous infusion of heparin (May be 500units/hour ) .Strict monitoring of APTT is warranted.

    What does the clinical  trials say ?

    There are few studies address this specific issue .I am still searching the data base. Once i get it i will post it. The readers  may also try to find an answer .

    http://ats.ctsnetjournals.org/cgi/content/abstract/62/3/880?ijkey=cdcd223289bd75ffb49a8d1cd1c73d35fe76e08d&keytype2=tf_ipsecsha

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    When does planimetery errs in estimating mitral valve orifice ?

    Posted in echocardiography, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , , , , on October 6, 2010| Leave a Comment »

    Planimetery is the age old method to measure the mitral valve  area( MVA) by echocardiography.

    Advantage

    • Simple modality
    • 2D echo  is enough
    • Doppler errors avoided
    • In the presence of MR, planimetery orifice has an edge over other methods

    Disadvantage

    • Optimal gain setting becomes  important .There is  significant inter and intra observer variability.
    • Shape of the orifice is not constant  ( MVO is funnel like) . Narrowest diameter is usually measured.
    • Planimetery is  a purely an anatomical orifice,while blood flows through both primary and secondary mitral orifices .Sub valvular fusion makes secondary MVO the  narrowest point  . Measuring it becomes difficult as it has no defintion of border.
    • Gross errors possible in calcified valve.
    • In post commissurtomy  the  lateral extent of split is often  not tractable

    How to improve the accuracy of planimetery ?

    Color Doppler aided  2D  planimetery . This can improve some of the limitations , as  it provides a hemodynamic MVO(Some what physiological ) Of course  , pressure halftime derived MVO is purely a physiological orifice .

    Other options to measure MVO

    1. Pressure half time
    2. Continuity equation
    3. PISA method

    Advantages and disadvantages  of Pressure half time derived MVO will be posted soon.

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