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Cardiology quotes : Human Atherosclerosis

Posted in Uncategorized, tagged , , , , on April 3, 2012| Leave a Comment »

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We ignored NEJM for many years . . . now let us learn cardiology from Forbes for a change !

Posted in Uncategorized, tagged , , , on March 31, 2012| 1 Comment »

COURAGE , BARI 2D , JASP

What is common in all ?

These are the studies which nailed the routine PCI in chronic  stable angina . Please note these articles came in prestigious  journals more than 5 years ago.

Nobody* seemed  to listen or learn  . Now the  Archives of Internal Medicine has  come out with another punch to PCI  .

Hope we refuse to learn again   . . .  and keep the interventionist spirit high !

And for a change  read this landmark paper from Forbes

http://www.forbes.com/sites/larryhusten/2012/02/27/meta-analysis-finds-no-advantages-for-pci-over-medical-therapy-in-stable-patients/

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Beta-Blockers in Acute STEMI : COMMIT clears the Confusion !

Posted in Uncategorized, tagged , , , , , , , , , on March 31, 2012| 1 Comment »

Beta blockers are vital drugs  to limit infarct size and  facilitate myocardial salvage. Myocyte death is  prevented by reducing MVO2.These concepts originated in early 1980s when thrombolysis was not in vogue .Studies like MIAMI  and BHAT were considered landmarks.

Later on ,  when IV thrombolysis came in a big way the importance of beta blockade in STEMI  suffered a little ,  still it  held on to their  benefits.

The real problem arose when few enthusiastic cardiologists introduced early multiple blouses of IV beta blockade in the setting of Acute STEMI without realising the potential danger. (In all probability man kind must have lost many thousands  of lives with this aggressive beta blocking protocol world over for nearly a  decade !)

Fortunately  we woke up and in early 2000  , a massive study called COMMIT was  initiated  to answer convincingly the utility value of  routine early IV bet blockade. Rest is history . It clearly showed us the what we were fearing was indeed true. An unacceptably excess cardiogenic shocks were reported in the early IV beta blocker arm .In the same period of time the concept of  primary PCI  exploded and the  BBs were pushed to sidelines

It is a different story  altogether   . . .

While  the funny world of cardiology showed the door for routine early  beta blockers  in STEMI ,  it  made a stunning  U turn   in the management of CHF  , after being dumped as an  absolute contraindication  for so many years !

Still COMMIT  fails to   answer many queries

  • Beta blockers in LBBB /RBBB –     Probably need to be avoided.
  • Beta blockers in bifasicular  block –   Should  be an  absolute contradiction

How do you know  tachycardia  in STEMI is due to high sympathetic activity or cardiac reserve ?

Young men with persistent tachycardia  will do well with beta blocker started within 24  hours .

Unless there is s3 or basal rales all tachycardia are to be considered as purely inappropriate  and  adrenergic

Tachycardia in elderly, women, and diabetic especially the blood pressure hover around 100mmhg is   more often a compensatory  phenomenon.Meddling  the heart rate with BB is vested with a risk.

Finally , if you have a doubt do a rapid echo ,  if the EF is > 45% one can safely administer BBs

Should we discontinue BBs  in those who are already taking it ?

Continuing the beta blocker is  thorough the STEMI phase is adviced .(Unless specific contraindication  exists  )

Beta blocker following primary PCI

The beneficial effect of early Beta blocker even in post thrombolytic era is blunted, it goes without saying primary PCI almost nullifies these effects.

still , beta blockers is to be introduced after a successful primary PCI in all patent for long-term protection.

Final message

Do not rush into start  beta blocker  routinely following STEMI .  The  risk is not worth taking  !

Reference

COMMIT  study from Lancet 2005

ACC/AHA guidelines on Betablocker and STEMI

The following is taken from the above  guidelines   When not to administer IV beta blocker  seems  to be more relevant !

Class 3 recommendation  for  Beta blocker in STEMI (Evidence A)

1. IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 seconds, second- or third-degree heart block, active asthma, or reactive airway disease). (Level of Evidence: A)

*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock) are age greater than 70 years, systolic blood pressure less than 120 mm Hg, sinus tachycardia greater than 110 bpm or heart rate less than 60 bpm, and increased time since onset of symptoms of STEMI.

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A funny Arrhythmia called Acclerated Idioventricular rhythm

Posted in cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Arrhythmias, Uncategorized, tagged , , , on March 31, 2012| 1 Comment »

Cardiac arrhythmias by nature connote a serious implication ,especially  so  with ventricular ones. Here is an  arrhythmia which arise from the ventricle by excessive automaticity  ,   fires independently  ,   still  very   benign compared  to others ventricular arrhythmias.

Why AIVR is a stable arrhytmia ?

Primarily due to its low rate.

Since  it is a  reperfusion arrhythmia the outcome is good.

Mechanism

It is not due to reentry , it is thought to be due to enhanced  automaticity  without pathological  intra-myocytic  calcium spikes  (Like true VT )

Absence in surface  ECG does not mean it is not existent.  In-fact there  is some  evidence to call this arrhythmia as a form of ventricular parasystole.

Focus of arrhythmia

Since it is a reperfusion arrhythmia it has to arise somewhere from  re-perfused myocardium.

The fact that  it  can occur in both RCA and LCA reperfusion  indicate the focus can be  in any of the ventricle .

Usually it follows the reciprocal rule of bundle branch block  pattern  (RBBB in LV focus LBBB in RV focus.)

Septal AIVR  can have either RBBB or LBB morphology.   Usually  left axis is noted .

How to differentiate it from  non sustained VT ?

  • Ventricular rate in AIVR should be between 60 -110 .(Note -The inherent ventricular rate is 35/mt .There is three fold acceleration )
  • Basic idoventricular rhythm is about 35.  Three times accelerated
  • Characteristically   AIVR  starts with an escape beat rather than an  ectopic beat .

AIVR  is common  in  RCA or   LCA reperfusion ?

It is supposed to be more common in infero-posterior MI  as sinus slowing is an important predisposing factor  for releasing   the idio ventricular rhythm.

AIVR after primary PCI

Is not reported much as  current interventional  cardiologists  do not bother much to watch about this arrhytmias

Other causes for AIVR

  • Myocarditis.
  • Digoxin toxicity

Management

(The commonest issue with AIVR  could be    . . . Nurses  /Fresh interns may mistake it as VT and  pressing the false alarm ! )

  • Rarely  requires treatment .
  • Atropine ,Isoprenaline to increase sinus rate.

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What will be the PCWP in grade 1 LV diastolic dysfunction ?

Posted in cardiac physiology, Cardiology - Clinical, Cardiology -unresolved questions, echocardiography, Uncategorized, tagged , on March 30, 2012| Leave a Comment »

What will be the  pulmonary capillary wedge pressure ( PCWP ) in grade 1 LV diastolic dysfunction ?

  1. Significantly elevated
  2. Marginally elevated
  3. Usually Normal
  4. It depends upon  age, LA size and LV  function.

Answer is 3 . (Of course  it depends on  4 )  Normal PCWP  is  4-12mmhg

Are these patients with grade  1 LV diastolic dysfunction  are at  risk for  acute pulmonary congestion at times of stress ?

Probably not ( in  most )*

                                             The grade 1  LV diastolic dysfunction or defect is the most used (abused ! )  echo terminology .The diagnostic simplicity of this condition namely  a simple documentation of “a”velocity more than “e” , has made it  as an epidemic in echo labs  world wide. After all  , it reflects a simple  fact that  left ventricle  has  summoned   the atria  for assistance   (Which is  all the more  physiological   at times  of stress   !)

When does this physiology becomes pathology ?

As long as  the atria is  doing its job of assisting the LV without any fuss  ,  the mean pressure of LA(PCWP) is maintained  within  normal level . Only if the atrial function is stretched  beyond the limits ,  PCWP begins to raise.  It can happen  in a variety of  ways . Most commonly it happens   elderly hypertensive /Diabetics  especially with LVH .

It can also occur in healthy individuals when they become physically deconditioned. (Left ventricle   goes  for  disuse and find it difficult to relax)

Final  message

Isolated  grade 1 LV diastolic dysfunction in people  > 40 years   generally do  not indicate a serious  abnormality.

Only if they have DM/HT and myocardial  disease they need to be evaluated further.

One practical clue is ,  if LA size is normal one can rule out  significant  diastolic dysfunction.

Caution

* In elderly population ,   when they undergo any major  surgery ,  presence of even grade 1 LV diastolic dysfunction can be a marker for peri -operative LVF and  lung congestion .

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Cardiology quotes: Single vs Dual chamber pacing

Posted in Cardiology - Electrophysiology -Pacemaker, Cardiology quotes, medical quotes, Quotes, tagged , , , , on March 29, 2012| Leave a Comment »

Choosing a pacemaker  is not a child’s play . It is a  complex game played by cardiologists , electro-physiologists and their  ill-informed

patients. The  superiority of dual chamber pacing over single chamber pacing  was never convincingly proven.

Still . . . usage of  dual chamber pacing is steadily increasing over the years  for various reasons.

“Every thing hangs around a key word called quality of life . DDD pacemaker is supposed to enrich life due to their AV synchrony “

World  health organization  says  quality of life  of homo-sapiens are  determined by at least few dozen factors .They are  mostly non medical.

How an extra lead at a cost of  2000 dollars more , is  going to  provide that  elusive “quality of life”  to all those poor patients with bradycardia  in  this world  ,   which     . . . they  any-way lacked even  in their best of times  !

Scientifically also there is  a major  flaw in calling DDDR as physiological pacemaker

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Jugular venous pulse in congenital heart disease

Posted in cardiology congenital heart disese, Clinical cardiology, dr s venkatesan -Personal, My presentations, Uncategorized, tagged , , , , , , , , on March 11, 2012| 1 Comment »

Click  to down  load a PDF  version

This was presented in the cardiology fellow training course in Chennai – March 2012

(Acknowledgement : Paul wood collection , J.K Perloff , Credit to Images from open source )

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The gimmickery called routine echocardiography in pre-operative cardiac risk assesment !

Posted in Uncategorized, tagged , on February 29, 2012| 3 Comments »

Can you  safely rule out  heart disease before  non cardiac surgery without echocardiography  ?

Yes  ,  in most situations  .  Experience suggest  If the clinical examination is normal  ,  ECG and  X ray  do not show any abnormality  , significant heart disease is ruled out 95/ 100 times.

  Please note  : ECG and X-ray can not  R/O  Coronary  artery disease by  any  degree of   specificity  .Echo cardiogram  also  miserably fails to predict future CAD. But  EST / TMT does this very efficiently!

So where does the  echo comes in the   routine  protocol  in the screening of  heart disease*  ?

“No where” to be precise.  It is only a gimmick . But  many   physicians  and anesthetists are obsessed  with  echo estimated LV EF %  They     invariably   ask for pre  operative echo  for   cardiac risk  stratification.

* On the other hand EST has a strong case for inclusion as a routine screening test before surgery.

What about diastolic dysfunction  ?

ECG and X ray will not miss  a manifest myocardial disease  . However concealed diastolic  dysfunction can not be detected  without echo. It is very common to detect early forms of diastolic relaxation abnormalities in echo . Significance of this is not clear especially  if it is grade 1 . In this situation patient’s  functional capacity comes to our rescue.  In a non functional patient any degree of diastolic dysfunction may increase  the   pulmonary capillary  wedge pressure. These patients must be  monitored and fluid administration should be  be judiciously used.

Final  message

Echocardiography   rarely  comes*  in the  routine  scheme of things in the pre -operative   cardiac risk assessment.

Summary

First question to ask   before non cardiac surgery is  about the  symptoms and functional capacity . ( Do you climb 3 floors  ? Walk 6 km /hr . lift 20kg over a flight of stairs , objectively walk 9 mts on treadmill with std Bruce)  If  he is asymptomatic and his functional capacity is good , for all practical purposes he will be fit for  surgery in cardiac point of view .

Next  , we need to look  the ECG and X ray chest . If one of them shows  some evidence for chamber enlargement / q waves etc ,an echocardiography is ordered .

If  you  really suspect CAD  one should  go for EST or doubtamine stress ECHO.

* Cardiologist lack professional freedom in new age medicine  :

In this funny medical world , a cardiologist can not do what he wants to do . I have encountered surgeons and anesthetics refusing to take a patient for surgery without knowing the  ejection fraction ! Once when  I gave a  surgical fitness without taking an echo there was a furore  from the corporate  desk  of  a  big hospital . How can you  make decision without these modern gadgets they seemed  to  ask  !  Future looks lovely for cardiology !

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Importance of recognising type C RVH in clinical cardiology !

Posted in Uncategorized, tagged , , , , on February 5, 2012| 3 Comments »

RVH is  traditionally  categorized into three types . With  the  advent of echocardiography  diagnosing  RVH by ECG would  appear  redundant. Still , it gives vital information about the electro-physiologcal basis  of RVH. Knowing different mechanisms of RVH helps us decode  regional variations in RVH.

Type A , Type B  are easy to diagnose as they fulfill the conventional criteria of tall R in lead V1

Type A  RVH occur in severe  pulmonary hypertension and critical valvular pulmonary stenosis.

Type B  RVH occur in  volume overload states like ASD and moderate  forms of mitral stenosis.

( Severe  MS may cause Type A pattern  if RV pressure exceed systemic pressure)

Type C  RVH    has  no classical signs of RVH. Here  RVH  is diagnosed by proxy . Look for RAE  and a  vertical QRS axis . ( For all practical purposes RAE will indicate  RVH  except in isolated tricuspid stenosis.

Type C RVH occurs classically in COPD and in some cases  of acute pulmonary embolism .In other- words type C  RVH  reflects  predominantly  RV dilatation rather than  hypertrophy.

Why Type C  RVH is important ?

It is important  for two  reasons

  • It  is  basically a  masked   RVH .
  • It mimics Anterior MI

Missing the first  one and erring  in  later  both  can have major  implications  in clinical cardiology  especially during emergencies.

What is  the mechanism of poor  R wave in precardial leads in  Type C RVH of COPD ?

The fact that  poor  R wave  in precardial  leads occur in  most  cases of  COPD  (whether or not RVH is present or not)   convey an important message.

The  lack of  R wave  progression   is probably  less to  do  with   rotation of  RV  than  the insulation effect  lung  . Further, the  elongated lungs   drags   the heart down , and  make it more vertical and in spite of RVH tall  R  is not picked up by v1 v2 .

Unlike primary PAH and critical MS where the RVH  can dominate the LV  ,  the  quantum of  RVH is never huge in pure COPD . However , presence of RBBB  could  alter  the R wave amplitude .

ECG in acute pulmonary embolism

This resembles the type  C  RVH . The  R  waves in V 1  and  V 2 can not gain the voltage acutely.

The S 1 . Q 3 , T 3  pattern if present indicate the  acute RV strain and  the resultant  RV wall motion defect.

.

Clinical scenario : Practical utility of  decoding    RVH   by ECG ?

A  middle aged female came  to our CCU  with acute  dyspnea with tachycardia .

Echo revealed a dilated  RA and RV . She had  mild TR and moderate to severe PAH (The TR jet measured 3.8m/sec)

The MPA showed a hazy shadow suspicious of thrombus . The patient  had no evidence for DVT .

The fellows  arrived at  a conclusion about a  severe  PAH  but , the etiology was debated.

One is chronic thrombo-embolic PAH . Other groups argued for acute massive pulmonary embolism and resultant PAH.

This raised an  important    therapeutic   issue  as one of them wanted to lyse the thrombus  ,  the  other argued for simple heparin .The  argument continued as the first fellow reminded ,  presence of RA, RV dilatation is a sign of acute RV strain  . The other countered the  same  as  it could be  a  chronic response  to pre existing PAH.

How do you know  in an emergency ,  whether the RA, RV dilatation is new onset  or a chronic one ?

In spite of  good   echocardiogram  we were confused .  Then it struck  to us ,  ECG would solve our problem . It indeed helped us. She had a tall  monophasic  R  in  V1  indicating   Type A RVH , which suggested chronic PAH   and  the thrombus in MPA  in all likely hood  was a sequel  to PAH  and  not vice versa . A type C RVH  would have voted  in favor of  acute pulmonary embolism.

Meanwhile a  CT pulmonary angiogram  report was available   . It showed a small  thrombus in MPA and LPA with no clearcut perfusion defects ruling out acute pulmoanry embolism . The thrombus was probably  de-nova in- situ thrombus due to PAH.

 

 

Final message

It may  appear  funny for the  present day cardiologists to waste so much time  to analyze  the  RVH  by surface ECG . But please remember ECG remain the only simple and cheap  investigation that transmit live data from the heart instantly  .Most importantly unlike other imaging  modalities  ECG data do not vary with person who records it !

Reference

A very good referen from   Basic and Bedside Electrocardiography   By Romulo F. Baltazar

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Why AV dissociation does not occur in all patients with ventricular tachycardia ?

Posted in Uncategorized, tagged , , on January 31, 2012| 1 Comment »

AV dissociation is  the most specific diagnostic clue in VT.But this is not a constant finding. In fact one  would be  lucky to spot a fusion beat  which denotes AV dissociation . It occurs in less than 30% of patients with VT .

Technically ,  for AV dissociation to occur atria and ventricle should  not be related in either direction .

If there is  a retrograde VA association ante grade AV conduction   is not possible  and hence one can not get a  fusion beat or so.

What happens to p waves during VT ? How does atria depolarise during VT ?

Atrial chambers can not sit idle during  VT .It has to somehow get depolarized  and contract   but  the  timing    may not be appropriate .

P waves  during VT can either be antegrade or retrograde .

Theoretically both can be present   but most times  it is   the  retrograde  p waves we see.

The occurrence and timing of p waves  is related  to the VA conduction .

If there is  1 :1  VA conduction during VT there can not be AV dissociation  for the simple reason  we have VA association.In fact there is constant vigil to depolarise the ventricle  through the normal AV node and his purkinje  in spite of the VT .SA  node is aware of this fact ,  how difficult it is going to be  confront the upcoming  rapid ventricular impulse . Usually the ventricular impulse   prevails  over the atrial impulse and much part atria is controlled by the VT . In fact  the VT reaches  all the way to SA node and simply  overdrive it . At these fast heart rates  retrograde p waves are not visible. ( But surprisingly one may see a regular  cannon wave in the neck with 1: 1   VA conduction.

Mean while ,  the SA  is always under look out for a opportunity to sneak into the ventricles thorough AV node. This happens  when the VT focus slightly slows down or shifts to a new site . this sis the time  we are able to  witness the AV dissociation . When the atrial impulse capture fully or partially the ventricle fusion beats occur confirming  AV dissociation .

Final message

AV dissociation is present in  less than 30% of VT because in  70%  there is a VA  association.(Retrograde  VA conduction ) . When V is associated with A there can not be AV dissociation.

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