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Archive for the ‘Cardiology – Clinical’ Category

Anticoagulation protocol in pregnancy with prosthetic valve

Posted in cardiac drugs, Cardiology - Clinical, Uncategorized, tagged , , , on November 16, 2010| Leave a Comment »

A simplified animation strictly  meant  for understanding the concept

Link to the review article on the topic

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The most important article on hypertension ever to be published :Loose cuff hypertension !

Posted in Cardiology - Clinical, Cardiology hypertension, Uncategorized, tagged , , , , , , , , , on November 13, 2010| Leave a Comment »

Blood pressure  measurement ,   probably  is the commonest investigation done  in our patients  in  the entire field of medicine . It is such a common thing ,  both physicians  and patients  fail to perceive  it as  an investigation . (It indeed is !)

Even though BP is  considered as a  clinical sign , measuring it requires a device called sphygmomanometer  . The BP apparatus has to be properly calibrated  with the mercury  , the tubing, the bladder  , inflation balloon  etc   need to be perfect.

The following fallacies are noted in the measurement of  blood pressure . Some of them are rampant* !

Patient

  • Posture of recording
  • Anxiety -White coat /Gender

Device

  • Cuff width/Length
  • Arm circumference

Ocular errors

It is surprising , such an important tool has a scale of 2mm markings which is prone for parallax errors of light with  mercury column undulating .

Physician factors*

  • Hasty cuff syndrome , Rapid deflation .
  • Absent minded recording – Failure to note phase 4 to phase 5  due to inattention
  • Failure to hear phase 4 muffling  (Aging  medico  -Auditory insufficiency !)

It is  not at all  surprising  to note,   two BP readings rarely match ,  even if it is recorded by the same person with  same machine at the same time !

There are many  articles that describe in detail  ,  how to record blood pressure properly. But this article from  a relatively unknown  journal   from Purdue university  ,  tells  us  most   scientifically  , what  has been taken for granted  by the medical  community for so long  .

Loose cuff  hypertension (Link to the journal of  Cardiovascular engineering )

How much  stiffness  is to be applied in  the arm for optimal pressure recording ?

What is the incidence of hypertension due to  loose cuff  ?

Final message

The BP apparatus ,  though appears  as  an   innocuous   machine ,   the readings  that emerge  from it  determines ,  how millions of our fellow human beings are going to be labeled  ! ( High pressured  humans ,  slaves to  anti hypertensive  drug marketeers    for  rest of their  life ) .

So , realise  how important  it is , to measure  the blood pressure properly    !  Never be casual . . . with  this  machine .

Experience has taught us ,  while  it is very easy to name an  individual  wrongly as hypertensive  , it  often needs  Herculean  efforts  to remove this medical tag from their neck . The reasonings  are  many .( Academic , non academic and patient factors included )

Finally , in this funny planet  it is  a personal observation ( Or is it  an imagination ?)    some  men and women   tend to  enjoy  ,   being  referred to  as  high pressured !   Loose cuff  or tight cuff   ,  it simply do not bother them  !

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Clinical implications of Inter atrial septal aneurysm

Posted in Cardiology - Clinical, cardiology congenital heart disese, tagged , , , , on October 25, 2010| 1 Comment »

This is a relatively common abnormality of IAS. It is  often observed  as  IAS bulging  into left  or right atrium  in routine echocardiogram.If this happens without  atrial hypertension it is termed as IAS aneurysm .

This is due to valve of foramen ovale bending into the RA/LA*  cavity for various distance. By definition , the radius of curvature of  the bulge should be more than 10 mm to label it as IAS aneurysm.

*Bulging into RA more common

Click on the Image to see the animation

General features

  • Mostly a benign entity.
  • More often observed  in  association with PFOs or ostium secundum ASD.
  • When occurs in isolation does not result in any shunting across it
  • The septal bulge can be static or  dynamic . It could swing  into LA, RA, and back to LA or vice versa.
  • Anatomically 5 types are proposed.
  • Multiple fenestration in the aneurysms have been noted.
  • Aneurysm  formation may aid in spontaneous closure of ASD.

Clinical  implications

  • IAS aneurysm tend to aggravate  stasis of LA  blood flow and predispose to minute LA clots and systemic thrombo embolism .
  • IAS aneurysm can act as an arrhythmic focus , generating focal atrial tachycardias.
  • A non ejection click  may be occasionally heard as  the IAS aneurysm  bulges and tenses within LA/RA cavity .

Reference


1 . Olivares -Reyes A, et al. Atrial Septal Aneurysm: A new classification in 205 adults. J Am Soc Echocardiogr
1997;10:644-56.

2. Longhini C, et al. Atrial septal aneurysm: echocardiographic study. Am J Cardiol 1985;56:653-67.

3. Gondi B, Nanda NC. Two-dimensional echocardiographic features of atrial septal aneurysm. Circulation 1981;63:452-57

4. http://www.fac.org.ar/revista/00v29n4/congreso/premio3.PDF

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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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    How will you manage failed pulmonary thrombolysis in acute pulmonary embolism ?

    Posted in Cardiology - Clinical, cardiology -Therapeutics, tagged , , , , , , on October 10, 2010| Leave a Comment »

    Acute massive  pulmonary embolism is a dreaded medical  emergency  . In the past,  surgical embolectomy was the main option . Now , we have thrombolysis as a viable option.But , it does not work in all cases.* (90% success ?). It is critical to evaluate the success of thrombolyis , before embarking upon rescue embolectomy.

    As it is often in critical care  medicine , this decision making is not easy .

    The key question is how long , we shall wait before labeling  thrombolysis a failure !

    In-fact , premature  assessment is the commonest cause for failed thrombolysis. True failure is different from deemed to be a  failure . This  is often related  to  , lack of patience  among  the   members of  treating team . Unlike acute MI ,there is not a  strict time window to  follow .The issue hear is ,  not lung salvage but  restoring VP/VQ and  dead space ventilation . The assessment is made , by clinical ,   MDCT ,Echo  parameters.

    When there is difficulty in judging success , clinical parameters will prevail over medical images !

     

    Key clinical parameters for monitoring

    • Heart rate
    • Saturation
    • Blood pressure

    There are  four  options  available to manage in  failed pulmonary thrombolysis.

    1.Emergency embolectomy in an unstable patient *

    2.Elective , planned embolectomy  in a sable patient **

    3.Repeat thrombolysis ***

    4.Continue Intensive heparin regimen  for up to a minimum of   72hours  and up to a week .

    *  Dismal outcome .

    ** Best option (Ironically,  these are the  patients , who improve  with medical  management , as well !)

    ***This is especially useful  when  partial success  is noted in a stable patient . ( For rescue thrombolysis it is  logical tom use TPA if SK was used initially and vice versa.) The logic here is the initial dose was  either insufficient or ineffective  to lyse the thrombus completely. If TPA is not available /or not affordable,  repeat SK can still be considered .It can be  safely administered within the 5 days of initial dose.

    **** Least popular and considered inferior but has worked wonders in many .

    How to manage a relatively  stable patient with a large thrombus load  in his pulmonary artery ?

    Option number 3 could be tried. Prolonged  monitored heparin

    What  are the surgeons concern about  management in failed pulmonary thromolysis ?

    Every  surgeon( Especially  the  cardiac  surgeons)  loves  to operate in a stable patient . If you hand over  a case  for pulmonary  embolectomy  ,  with  sinking  O2 saturation  and  falling  blood pressure  ,the outcome can be  easily predicted !

    Further, RV dysfunction  is notoriously known    for pump dependency  .  CT surgeons are vastly experienced   in  the intra operative tips and tricks of  managing  LV dysfunction (They may not be  in  so  in RV dysfunction !)

    Bleeding risk  is also high especially  in the milieu of   intensive anticoagualtion and thrombolysis .

    The mortality could be as high  as 30 % in many centers.

     

    Final message

    • The incidence  of failed pulmonary thrombolysis  is  often subjected to the whims and fancies of treating physician  and the imaging modalities used.
    • Timing of assessment is critical .One need to give a long rope for medical management  , in spite of the urge , to do something more. .
    • Clinical improvement should be the main guiding force.
    • Normalisation of tachycardia   ,  improving  trend  of  o2 saturation(  >90-95%)  , regressing  RV size are useful parameters.
    • Thrombus load  detected by a repeat  CT scan  ,  need not be  the   sole guiding parameter.In -fact , mobilising these patients for CT scan by itself is fraught with a risk of  worsening the hypoxia.
    • The issue of  tackling the source of thrombus should  be addressed separately .Luckily, the same anticoagulant protocol takes care of this issue also. It is rarely a emergent issue.
    • Deploying an  IVC filter as an emergency procedure is a bigger controversy .At best , it is useful in few high risk individuals with high risk mobile ileo-femoral clots .
    • Finally, not every one can handle this  situation .Ideally such  patients  should be  to be  shifted to a well established cardiac surgical  set up .

    From Chest journal

    http://chestjournal.chestpubs.org/content/129/4/1043.full.pdf+html

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    Laughter and enothelial function

    Posted in Cardiology - Clinical, tagged , , , , , on September 24, 2010| 1 Comment »

    • Endothelium is the largest vascular organ in the body .
    • It is constantly being serviced by both the circulating blood  from the luminal side as well as from the abluminal plane.

    • The discovery of nitric oxide and endothelin  was a breakthrough .
    • They are under neural, mechanical and endocrine control .
    • Negative emotions like anger and depression has a high correlation with hypertension and cardiac event
    • Positive emotions like laughter and happiness is expected to have good vascular tone

    This fascinating  study from Japan and USA (Texas)  published  in American journal of cardiology , discusses how a comedy movie possibly releases nitric oxide profusely from our endothelium

    Link placed with the courtesy of AJC

    http://www.ajconline.org/article/S0002-9149(10)01050-7/abstract

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    50th anniversary of cardiac resucitation had just gone by . . . silently !

    Posted in Cardiology - Clinical, Cardiology-Land mark studies, tagged , , on September 23, 2010| Leave a Comment »

    In 1960 , exactly 50 years ago , a group of doctors from Jhon Hopkins published their observation in 20 cases. It went on to become , one of the most remarkable discovery  in the history of cardiology .

    They taught us how to use  a pair of hand  ,  as an  artificial  heart and save lives

    They are . . .

    1. Dr Kouwenhoven*
    2. Dr  James R. Jude, and
    3. Dr G. Guy Knickerbocker .

    * He was not a medical doctor but an electrical engineer at Hopkins but he worked in the medical school as well .

    They meticulously documented , each patient’s case history ,  whom they were able to successfully revive , (It was in the same  period , the  AC/DC shock was also invented  in the  Hopkins ) .One of  the  highlights of their paper was ,  with each chest compression  they were  able to elevate the carotid pressure  up to 90mmhg and was recorded in a pressure tracing .

    We have to thank the  JAMA (Journal  of American medial   association )  for  making this  original  article   available  free in their website .

    Must read for every cardiologist

    http://jama.ama-assn.org/cgi/reprint/173/10/1064?ijkey=33bb40fe3062331bae50e10c8a04263f3e26b317

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    How to manage complete heart block during pregnancy ?

    Posted in Cardiology - Clinical, cardiology -Therapeutics, Uncategorized, tagged , , , , , , on September 19, 2010| 1 Comment »

    For the lay public   the term complete heart block (CHB) often convey a sinister message . When  encountered in   pregnancy,  it is   frightening    for the  physicians as well .  One need not  say  . . .the anxiety to the Obstetrician !

    Congenital complete heart block is the usual etiology. Though there are other important causes of CHB in general population , it is very rare to  get an  ischemic or  degenerative heart  blocks  in the reproductive age group.

    There are  many  ways it can present .

    How does it present ?

    • Symptomatic CHB detected  first time during ante natal screening
    • Asymptomatic CHB detected incidentally during ante natal screen
    • CHB first time recognised during active  labor. Either symptomatic /Asymptomatic
    • A more familiar  situation  is  CHB  diagnosed in child hood . Women in question can undergo an  elective marriage and a managed  pregnancy.

    * The success of modern medicine  lies in the  mantra  of  “early  diagnosis ” .Ironically , early detection  of CHB in  pregnancy adds  considerable anxiety  to mother , family  and the treating physician  . So ignorance  can be a  bliss here ,  as 99/100 with CHB  would not require any intervention during pregnancy  .But , in this hyped up scientific world  one  needs  lot  of courage to  simply watch a pregnant mother with a heart rate of 45  !   .You are tempted to do something . We have seen CHB presenting  in labor room as emergency and delivering successfully  by vaginalis .

    Where is the pathology in congenital complete heart block ?

    It is  usually due to anatomical discontinuity between AV node and the bundle of his. The most fortunate thing  here is ,  these patients  develop a junctional escape rhythm at around 40-45/mt .This is enough for most basal activities. Further this junctional rhythm can increase   up to 100 in many, or  even up to 120 at times of stress.(Accelerated junctional  rhythm )* .An ECG which shows a narrow qrs  complex is nearly  100 %  specific  for a stable junctional escape rhythm.

    What is the hemodynamic stress of pregnancy ? Will a heart rate of 50 /mt enough , to support the labor or cesarean section ?

    Nature  is a wonderful equalizer. What the pregnant mother requires is a good cardiac output to nourish the baby as well as herself. A heart rate of 50 is often able to sustain and support the entire pregnancy with ease.

    How it is done  ?  . . . is  it not simply  amazing ?

    In pregnancy there is less of  systemic vascular resistance due to various reasons (Low impedance  placental circulation, reduced sensitivity to Angiotensin 2  ) . The heart can always increase it’s out put by increasing  the heart rate or stroke volume.  In  patients with CHB , as the  rate can not be increased much , the heart  accepts  the  alternate option quite easily without  any protest  . The low SVR also facilitates  increase in stroke volume. This  is the reason pregnancy  is  often well tolerted  even with the heart rate < 50 /mt.

    But , at the time of delivery increase in heart rate may be important in some.We do not know , who will require this HR support .This makes it mandatory to have a  temporary pacer standby.

    What are the ominous signs and symptoms of CHB in pregnancy ?

    Having discussed a lot about the benign nature of congenital CHB ,  one need to realise it is also a potentially dangerous heart rhythm . Syncope, symptomatic hypotension  (BP<90) and some times  signs of PIH ,  all possibly indicate a pacemaker support .

    Can we do an exercise test  to  assess  the chronotropic competence in pregnancy ?

    Tread mill test is generally not done  in pregnancy. It is a good option ,  to test the adequacy of heart rate increase during activity . If the heart rate increases up to 100 -120 it is a good response .

    What about holter ?

    A less predictive , but more acceptable investigation is the 24 hour holter monitoring  that gives a rough idea about lowest and highest heart rate. If there is a  long pause > 5 sec ,  she will be a technical candidate for permanent pacing !  once you have documented this ,  we will be sued if not paced however asymptomatic the patient is ! So beware of this investigation !

    Atropine stress test ?

    This again is a simple test , that will measure the chronotropic reserve. A concern for fetal tachycardia is genuine !

    Pre-conceptional  counseling

    A patient with congenital complete heart block should never be adviced against pregnancy.

    “Pace and become pregnant ” strategy is also not warranted.This is based more on the perceived  scientific approach the and  litigation  fear  than reality !

    Only issue is we have to make sure ,  the women in question has  adequate hemodynamic reserve. This  can be easily accomplished  by asking some basic questions about exercise capacity .Or , she can be put on a  tread mill (or atropine stress test). If the heart rate increases up to 100/mt  there is absolutely , no need to put  permanent pacemaker.

    Peculiar  issues in   pregnant  women with permanent pacemaker

    The paradox of modern medicine  felt at it’s  best here !

    We think ,  we are  implanting   a  pacemaker in CHB of  to provide good hemodynamic support  during the stress of labor. But a  fixed rate VVI pacemaker will not do this job . The real reason  to put a pacemaker is to avoid a dangerous bradycardia during the labor .

    Hence ,   patients  with CHB carry equal  concern (if not more !)   during labor as the pacemaker fires at a  fixed  rate of 70/mt and  the native rhythm is often suppressed due to long-term pacing . Hence their heart rate often fail to increase   beyond the pacemaker rate of  70  . Paradoxically , patients with untreated  CHB (with their native rate ) , can increase their  heart  rate often up to 100-120  at times  of stress .This is possible because  their AV node is still under the control of autonomic system , while artificial  pacemakers* are not !

    *Some of the current pacemakers have overcome this problem with rate adaptive pacing .

    Mode of delivery ?

    • Natural , expected
    • Induction  of labor
    • Elective cesarean
    • Emergency Cesarean

    Can complete heart block per se , become an  indication for cesarean section ?

    No. It is always an obstetrical indication .It  is better to avoid GA / Regional anesthesia  in cardiac disease. The stress of  second stage of labor is always less than   that of   surgery provided it is not unduly prolonged .

    Assisted /accelerated vaginal delivery is the  best option .However , one should be ready for any intervention. Some obstetricians  feel  that, elective cesarean section  could  be less stressful than  labor( which could be prolonged for some unpredictable reasons  ) while a ,  Cesarean section  can not  be a  prolonged one  !

    Cardiologist’s role in the labor room

    The role of cardiologist is to provide support to the obstetrical and anesthetic team   prevent   extreme bradycardia. Inserting a temporary pacemaker with back up pacing of 50/mt is preferred.Trans-jugular approach is ideal .In difficult cases fluroscopy guided temporary pacing in cath lab is advised.

    Role of temporary trans cutaneous pacing  as stand by ?

    This method of pacing with two sticky electrodes in the chest wall  with external pacing .It is proven , efficient useful modality of pacing in coronary care units  .However this can be a substitute for  only few hours of support . May have patient discomfort .In places from expertise for temporary  pacing is not immediately available  this can be used .However presence of such a machine increase the comfort level of physicians.

    Is there a rate adaptive temporary pacing available ?

    Currently available temporary pacemakers  are not rate adaptive , and hence we have to pace  roughly at  about 90 or 100 give  allowance  for labor related demand  (We would not know, how much  the mother is compensating with increasing with  stroke volume ) in this case pacing rapidly may  reduce the net cardiac output as the mother’s heart is  used to operate  at different  point in the  frank staling curve right  through the 10 months

     

    Anesthetic issues in complete heart block  during cesarean section

    Anesthetists have a concern here.(Genuine one of course)  A cardiologist  with a standby temporary pacemaker is  to be arranged. Cardiologist  will decide whether to have sheath or sheath plus lead  in standby mode .

    Many anesthetic drugs have an adverse effect on heart rate. Drugs to be avoided are  Fentanyl ,suxamethonium, neostigmine  Induction with propofol has risk of worsening bradycardia . Controlled epidural anesthesia is preferred .This ensures slow onset anesthesia and limits hemodynamic instability.Bupivacaine is known to cause depression of heart rate .(Even with epidural route )

    Miscellaneous questions

    A often debated  query among obstetricians : Should I refer a CHB patient  to a cardiologist or electro-physiologist ?

    There  is no  academic answer  to this question.Logic demands conservative (without compromising patient/baby  safety ) management .Electrophysiologists are rarely conservative

    Radiologically how safe it  is ( for the fetus ) to undergo permanent  pacemaker implantation ?

    For implanting a permanent pacemaker, about   15 minutes of  fluro time is required which could be significant .So it should be used in  exceptional situations only.

    What is the effect of maternal  complete heart block on the fetal hemodynamics?

    Nil or almost nil (Surprise ! surprise)

     

     

    Issues during  weaning of pacing  in postpartum

    Post partum period can be troublesome in few as fresh  blood volume  injected from contracting uterus.If temporary pacing has been done , it is usually possible to wean by 48 hours. Permanent pacing  is rarely required

     


    Final message

    1. Congenital complete heart block* during pregnancy is  a well tolerated rhythm.
    2. The panic  this   entity creates is  largely unwarranted. This conclusion is derived from decades of observation by eminent clinical cardiologists.
    3. The heart  rate reserve can be estimated by a  minimal exercise test .(Atropine test with caution )
    4. Insertion of either permanent  pacemaker is not necessary* in most .
    5. If there is symptomatic hypotension /syncope during any time during pregnancy  pacemaker becomes mandatory .
    6. During labor /or cesarean section  insertion of temporary pacemaker  “may be” needed. Hence a cardiologist stand by with a temporary pacemaker  is advised to tackle any  emergency(Which is anyway  highly unlikely  !)

    .

    * This rule is applicable only in  isolated congenital CHB.  Ischemic CHB  or CHB  with associated LTGV,AV canal defects etc  need special attention.

    References

    Books

    Elkayam

    Journal articles

    The famous paper which first described safe outcome four patients with CHB in preganancy without pacemaker

    http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2003;volume=49;issue=1;spage=98;epage=98;aulast=Mehta#ref3

    http://medind.nic.in/iad/t06/i1/iadt06i1p43.pdf

    http://www.joacp.org/index.php?option=com_journal&task=check_subscription&id=1077

    anesthetic issues in pregnancy and CHB

    http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_12_number_2_1/article/labour_analgesia_in_a_patient_with_complete_heart_block.html


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    A new coronary risk factor : Community smoking

    Posted in Cardiology - Clinical, Cardiology -unresolved questions, tagged , , , , on September 10, 2010| 1 Comment »

    Coronary artery disease  can be termed  as   “New age plague” afflicting the mankind  !  It  probably has killed ( or Killing ) as  many lives  as   most other diseases  put together.  Why  only a section of  our  population is vulnerable is  not fully  understood .

    We are familiar with coronary risk factors for too long  . . . still  . . .

    We do not understand why 50% CAD occur in people who have no known coronary risk factor !

    There has been propositions and dispositions  of various risk factors .  The latest one is  the  Air pollution. This is quiet interesting,  as air is the staple food of human survival . We  eat , drink ,  (Rather inhale )  about 500 ml /of  air every   3  to 4 seconds  for 24 hours a day for 365 days  , for our life time !

    Does the air we breath reach the  largest cardiovascular  organ namely the vascular endothelium ?

    Yes definitely  ,  not only it  reaches   the endothelium but also injures it  (When it contains gases other than oxygen  )  .While tobacco  is a well established  endothelium  destroyer , it is no surprise   community smoking ( Air pollution !)  will do the same job  with perfection .

    What are the proposed toxins in the air pollution that harm the endothelium ?

    It is a mixed  masala gas out there  over  our   polluted cities ! .(Atmosphere,  Industrial, Automative ,Domestic, Human , and other invisible  sources ) We need to analyse further to answer this question authentically .

    Though , common sense  is  enough   to establish the  link between air pollution and CAD. We have  lots of evidence coming up  . . .

    Reference

    http://ajrccm.atsjournals.org/cgi/reprint/173/4/432?maxtoshow=&hits=10&RESULTFORMAT=&titleabstract=coronary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

    Further research

    We will be shortly reporting our experience with endothelial  function assessment  in traffic police population of our city Chennai  ,India .

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    The “must read” books on Intra-operative transesophageal echo and mitral valve repair !

    Posted in cardiac surgery, Cardiology - Clinical, echocardiography, tagged , , , , , on September 7, 2010| Leave a Comment »

    Mitral valve can be termed as  the most important valve of heart . The reason  for this  : It is the only valve that is dependent on the  Left ventricular function (The  parameter  which   determines the  ultimate outcome in any form CAD ! )

    So , indirectly mitral valve function will invariably be affected by some degree  at least in  most  patients with LV dysfunction. (After all LV free wall , is a component of mitral valve apparatus.)

    While , we have numerous modalities to assess mitral valve function  ,  the one that has fascinated the surgeons during  mitral  valve surgery is the intra operative TEE.

    Many believe TEE provides live  images  of mitral valve   which are not possible  even under  direct vision ! The eye of the  TEE sees the mitral valve  from a  posterior location , (of -course It can see at any angle !)   while surgeon can see in one angle . The  types of repair , the adequacy  of repair, the annulus status,  even a trial mitral run ,  can be done with the help of TEE.

    The TEE probe silently does  this job sitting inside the esophagus   , without  obstructing the surgeon’s operative field .

    The success of TEE as an investigative tool did not come easy.Decades of  observation , innovation and learning( Especially from  department of cardiac science  Mayo clinic USA , where they standardized the views. )  are involved .

    Now we have omni plane, real time 3D TEE probes .

    The books  which are  considered the best for  TEE aspects of mitral valve  and it’s  repair are

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