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Archive for the ‘cardiology- coronary care’ Category

What is the Ideal time window for rescue PCI ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , on March 31, 2013| Leave a Comment »

Answer :

In cardiogenic shock it is A . In all others it is probably  C.

While D may be  considered as  an  essential target criteria  for completing the  rescue PCI

Read also

Why-we-often-follow-a-reckless-time-window-for-rescue-angioplasty ?

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I am damn sure this MCQ will trouble you !

Posted in cardiology -Therapeutics, Cardiology hypertension, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , , on March 31, 2013| Leave a Comment »

Answer

The tie is between “B” and “D ”

We know in hypertensive hearts LV primarily fails in diastole . Lungs get congested due to raised LVEDP .Here is a catch . . .  if diastole is  terribly dysfunctional  how can be systole be near  normal  ? (After all  . . . systole is not a  distant cousin of diastole !)

How is  that  high blood pressure maintained in spite of LV failure* ?

Is it due to  well-preserved  EF and cardiac Index ?  or Is it due to extreme levels of peripheral sympathetic activity mediated by catecholamine surge triggered by LVF.

We have attempted to measure  LVEF in patients with flash pulmonary edema and acute severe hypertension .It was a real messy echocardiography . We could not conclude much but one thing is  clear in acute hypertensive  LVF   the LV was vigorously contracting in , probably making the option D  more correct .

* The other way of  reasoning is    . . .  it is because  of high blood pressure the LVF  has occurred . LV contractility has no contribution in maintaining the high BP ( Not in line with  the age  old concept of LV contractility  a major determinant of systolic blood pressure !)

(Having said that  . . . we also see patients with severe LV dysfunction with  severely  stunned , ventricles in association with hypertension and LVF . In fact many of the reversible DCMs are due to sudden surge in blood pressure )

Other mechansims of LVF and lung congestion is

  • Extreme tachycardia and shortening of diastole
  • Mitral regurgitation
  • Assocaited  CAD unmasked by sudden raaise  in heart rate .

Postamble

If  this article has confused  you a little  , It has achieved  one of it’s  objective .  !  I expect more  from   young cardiology fellows to address the issue !

Reference

This NEJM article   authored by Sanjay  Gandhi  has almost answered the hemodynamics of acute LVF and HT .

mechanism of acute lvf in hypertension flash pulmonary edema lvedp in ht nejm 2005 sanjay gandhi

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Why we often follow “A reckless time window” for rescue Angioplasty ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, tagged , , , , , on March 28, 2013| Leave a Comment »

Myocardial salvage is like  coronary fire fighting.When fire is fought  very early after the accident  , benefits are accrued  more . Text book primary angioplasty is . . .  fire engine arriving at the scene when the house is on fire .

Rescue angioplasty is asking for more force ,  when the initial fire fighting  was inefficient to control the fire. So , it is obvious the rescue efforts should be fast and brisk.In fact the pace should me more than the primary (The the second engine should  reach the ground zero  faster than the first !  – Read as  door -balloon time ! )

But what happens in real world ? We would tell  time window for primary angioplasty even in sleep ! but will struggle to come   with clear cut  answer for the  same in  rescue angioplasty  even in a  fully awake state !

CaptureWiz

It is  an overwhelming fact , we have  not taken enough efforts to define strict time limit  for rescue .( Even though guidelines say it should not be beyond  24  hours , common sense will tell us rescue PCI should not go beyond 12-15 hour window ! .One more definition for rescue PCI could be within 3 hours after diagnosing failed thrombolysis. In real world  it is a race against time in a different perspective .In many centers  rescue angioplasty “enjoys time less windows “

I was funny witness in a big private  hospital  when a  colleague  of mine  has posted  a case for  “elective rescue angioplasty” and was  waiting in the side cabin  for his turn !

Coming back to the title question

Why we often follow  a reckless time window for rescue Angioplasty ?

The reason is simple

Time is not only  muscle . . . time  is  money too !

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Can we give Nitro-Glycerine in a hypotensive patient who is in acute pulmonary edema ?

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, critical care ccu, tagged , , , , , on March 25, 2013| Leave a Comment »

An elderly man  with past H/o CAD  was admitted with ischemic LVF and hypotension .Blood pressure was  90/60 mmhg  and pulse rate was 140 . Urine urine output  in the immediate past hour was 50 ml . Saturation was 95 % .He had fairly extensive  crackles in both lung fields.

A bed side echo showed  moderate LV dysfunction , with wall motion defect in LCX territory and  mild  MR .A dignosis of post  MI -ischemic LVF was made .

He  was  put on intensive anti failure protocol. I asked my  fellow to administer IV NTG  and left the ward .

On my next visit after few hours  . . . the patient was in much bad shape  , and when I enquired , I learnt  NTG was never administered . I was curious to know why the fellow  dis- obeyed my instruction .

He felt sorry  .  .  . But he earnestly told me  , he  could not comprehend the principle of administering NTG in a  patient  with shock ! . I was happy  to  note his  genuine concern  for   the patient  !  But  . . . I had to take a brief  lecture to convince the importance of NTG in some forms of shock !

What is the cause for hypotension in ischemic LVF ?

Lungs are flooded due to  very high LVEDP . Blood  not only struggles to  enter the LV  but also finds difficult to   leave the LV ,  former due to defective relaxation later due to poor pumping.

The extremely high pre-load actually stuns the left ventricle in diastole . (Primarily diastolic stunning  )  . Here is a hemodynamic paradox . Excess pre-load  occurs in  terms of pressure , but  in terms of volume there is miniscule amount  blood  that  traverses LV  .

This is pre-load mismatch  at play .Empty ventricles with high wall stress  and that is reflected in aortic afterword as well .

We have to some how reduce the  very high levels of LVEDP . IV NTG can  dramatically  reduce the pre load  ( and reduce the LVEDP .) The other major  benefit is ,  NTG   can reduce the MVO2 by improving sub endocardium coronary perfusion and de-stress the heart.

Once  LVEDP  is  lowered  , the ventricle will tend to recover and gain at least some  original elasticity ( Frank starling forces) . Of course it will be defective due to ongoing ischemia . Even slight fall of LVEDP (say from 25 to 18 mmhg  can have  significant benefits as the LV function curve labors on the steep shoulder region !) .

This is one situation where NTG can increase the blood pressure once the hemodynamics is favorably altered.

*Yes  . . . heavy doses  of  Frusemide injection can do the same job but it largely depends the kindey’s cooperation to flush out fluids  .In a shock like situation one can trust the kidney perfusion  !

Additional benefits of NTG

Mitral  regurgitation  is a serious destabilizer of LV function .NTG can reduce the regurgitant fraction in acute MR effectively .

Caution

NTG may worsen the hypotension of RV infarction . Make it very sure , you are not dealing with this unique  pre-load dependent circulation.

What happened to this patient ?

He  did show  improvement with IV NTG . Of course it was not dramatic as I have projected in this article .Still it was really helped him .He required simultaneous dobutamine infusion as well .The BP did not fall  further and lung congestion was relieved  .He went on to recover fully by 48 hours and was posted for elective cath study .

Final message

                                             We tend to  worry  more about falling blood pressure  when administering  NTG. . .It is a wonderfully effective drug especially in the setting of ischemia and cardiac failure  even if  the blood pressure is low !

Acute cardiac hemodynamics  is  complex phenomenon .No one has mastered it .Paradoxes are common . Hypotension in the back ground of  acute pulmonary edema  especially due to ischemic LVF  can be corrected by NTG . Of course physicians  need  some  courage to administer NTG in patients  with a systolic pressure of  80-90mmhg.

This should ideally be done with intra arterial line in place and a simultaneous inotropic line (Doubtamine /Nor-epinephrine ) back up in case of worsening perfusion pressure .

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A comprehensive , evidence based . . . “unethical” STEMI guidelines !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, cardiology-ethics, tagged , , , on March 24, 2013| 1 Comment »

Acute MI kills a few million people world-wide every year .It does not differentiate rich from poor. Logic would  tell us  , principles of management  should  not differentiate  the people  when  dealing with a myocardium in distress .

Unfortunately , we scientists do it with passion !

The problem is enormous  . . . the rich is suffering from too much* care and the poor is suffering from want of care !

The following flow chart  is a result of my observation from close quarters  about the management strategies in corporate as well as Govt hospitals .

The first chart exposes the problem .The second one tries  to address the issue

Please bear with me . . .  if the  stuff  sounds  too crazy !

* Too much care is also referred to as inappropriate care

Practical and ethical guidelines for stemi management corporate

And for the solution  . . . try this

Practical and ethical guidelines for stemi management

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CTO : The most important factor that determines the successful PCI ?

Posted in cardiology- coronary care, Cardiology-Coronary artery disese, cath lab tips and tricks, cto chronic total occlusion, Hardware techniques tips, tagged , , , , , , on February 27, 2013| Leave a Comment »

chronic total occlusion cto tips and tricks

Answer :

While each one of the above factor appears very much important  morphology of the lesion is the  clear winner  ( Which includes , the content of the lesion , hardness , micro channels , thickness of the proximal and distal caps, the length and   tortuosity   of the CTO     ( which is invisible ) the collateral status will ultimately determine the success)

It is becoming increasingly clear  cardiologist expertise is getting less and  less important .

Finally ,  it must  be told to our  younger generation of cardiologists , crossing a  CTO and deploying a stent  is not synonymous with success .It should result in long term sustained distal flow and make a significant impact on the patients symptoms (If at all any !) and survival.

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Can RV infarction occur with Anterior MI ?

Posted in Cardiology -unresolved questions, cardiology- coronary care, tagged , , on January 31, 2013| Leave a Comment »

Traditionally  RVMI  is  suspected   only with infero -posterio MI .

Can RVMI occur with LAD disease ?

Yes , it is reported up to 13 % of  Anterior MI (Cabin AHJ 1987)   .  Right  ventricle has an anterior wall  and blood supply to this area is from LAD .

Have a look at this ECG

isolated rvmi right ventricular infarction due lad disease st eelvation in v1 v2 v3

Reference

1Cabin HS, Clubb KS, Wackers FJ, Zaret BL. Right ventricular myocardial infarction with anterior wall left ventricular infarction: an autopsy study.  Am Heart J. 1987 Jan;113(1):16-23.

2. http://www.nejm.org/doi/full/10.1056/NEJMicm030315

RVMI famous review article in NEJM 2 1994

Final message

RVMI   is not an exclusive  complication of Infero -posterior MI.

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Stunning images of left main in routine echocardiography !

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, cardiology-Anatomy, Cardiology-Coronary artery disese, Echo library and gallery, echocardiography, great illustrations in cardiology, tagged , , , on January 23, 2013| Leave a Comment »

If only  . . . we get  an  image like this , echo can help rule out most  left main disease with conviction .

Have a close look  at it ! One can get a good image of  coronary ostia in short axis view . But , here it is well visualized  in long axis .

left main

I tried to put color flow within left  main .

left main color flow

What about pulsed  Doppler across left main ?

After all it needs 2mm sample volume and this left main was near 4.5mm . So keep trying !

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An Idiot’s approach to tachy-arrhythmias : A follow Up !

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Arrhythmias, Clinical cardiology, Uncategorized, tagged , , , , , , , , , , , , , , , , , , , , , , , , on December 30, 2012| Leave a Comment »

As I expected ,  my earlier algorithm “An Idiot’s approach to tachy-arrhythmias” has  elicited  mixed reactions  .Some  EPs calling it a dud while few  physicians termed it awesome . Here is  a follow up .

Heart rate of a tachycardia is the most neglected parameter by physicians .  They are often seen spending  hours together for decoding  arrhythmia , splitting the brains   for P wave  location , VA conduction, Fusion beats etc .Finally they end up  either administering  Amiodarone a broad spectrum anti arrhythmic agent or DC shock.

Here is an unusual algorithm  for arriving at a diagnosis in all tachy-arrhythmias  based only on heart rate and the width of he qrs complex.

(Click over the table for high resolution image )

approach to cardiac arrhythmias narrow qrs vs wide qrs brugada wellens criteria

General principles in diagnosis of tachycardia

Narrow  qrs tachycardias.

90 % rule : If regular It is sinus tachy if irregular it is A-FIB . Take some efforts to r/o sinus  tachycardia . (In children and young adult it can be extremely difficult at times )* Please note : Sinus tachycardia can show some irregularity due to sinus arrhythmia and  frequent  APDs and JPDS . Further at  fast rates P may fuse with T it should not be confused with  A-fib .

Wide qrs tachycardia

Common things  are common , if  you sight a large animal with a huge trunk  in a Kenyan safari ,  it is most likely to be an  elephant and not a Dinosaur !  Please diagnose VT  when you encounter wide qrs tachycardia by default especially when the BP drops  !

  Management issues

It  would be  foolish to split our heads for decoding an arrhythmia when a patient is unstable .Any hemo-dyanmic unstable tachycardia needs DC shock . (Synchronized will be better unless it is dire emergency )There are very few arrhythmia where DC shock is contraindicated   ( MAT/Dig toxicity/Underlying sinus node dysfunction )

Only if the patient is hemo-dynamically  very much stable   the  physicians  have enough time to  confuse themselves  and the real  ordeal begins .Please remember  the 5 arrhythmias  constitute 98  % of all known tachy-arrhytmia . So where ever  you practice ,  whether  in remote Nigerian village  or  sophisticated  Cleveland  university hospital , when you are  confronted with a tachycardia  the diagnosis  should be one among the  following  five  !)

  1. Sinus tachycardia .
  2. AF/A-fib
  3. Atrial tachycardia  with  or without blocks
  4. ventricular tachycardia /VF
  5. AVNR/AVRT with or without aberrancy

All  other tachy-arrhythmiaa  are  largely  academic !

Regarding  drugs

Knowing the mechanism of  arrhythmia genesis  is less important  at bed side . They are  triggered , sustained, and maintained by either functional or structural component .Ionic basis operates in every arrhythmia  , but it is the anatomical  substrate that maintains it .This happens in only diseased heart.The only point worth remembering regarding mechanism of arrhythmia  genesis  is ,  automatic and focal tachycardias  will not respond to DC shock . All other can be termed some form of re-entry . Micro reentry  for all practical purposes behave like  triggered  activity. Ischemic and electrolytic VTs are primarily ionic based and often polymorphic.Structural VT are commonly mono-morphic. Any VT just prior to degeneration to VF become polymorphic

Every patient with cardiac arrhythmia should be checked for hypoxia,acidois , electrolyte defect or exposure to any  pro arrhythmic drugs. (The commonest  cause of tachycardia in any  IMCU , is inotropic induced (dopamine /doubtamine ) tachycardia .

We  have  5  pharmacological options

  1. Blocking  adrenergic  receptors(IV Esmolol, Metoprolol)
  2. Blocking calcium channel (Dilitazem,Verapamil)
  3. Blocking potassium channel  (Amiodarone  ,Sotolol Adenosine  to a cetian extent )
  4. Blocking sodium channel . ( Procainamide , Lignocaine (Wonder drug almost forgotten now ! ) Flecanide Mexilitene etc)
  5. Digoxin ,Adenosine  magnesium are special  anti-arrhythmic  agent which  has very useful role in certain specific situations (Magnesium -Torsades/Polymorphic VT / Adenosine in LVOT/RVOT VT etc)

General principle is ventricular arrhythmias  are blocked successfully  by sodium or potassium blockade  Atrial and functional tachycardia are blocked by calcium or adrenegic blockade  .Of course,  there would be  some degree of overlap  when the arrhythmia  origin  hovers  around the junction  on either side of the AV  ring . This is basis of verapamil sensitive VT .Clusters of  calcium  channels are scattered  in the junctional  region

Refractory tachycardia

  1. Consider ablation  in AVNRT/AVRT
  2. ICD +Drugs  in VT
  3. Ablate and  Pace(Some A-fibs)
  4. Ablate and ICD (Some  incessant VTs)
  5. Surgery in minority

In AVNRT/AVRT 90 % success can be achieved  in most EP centers .VT ablation  is still a complex process  with  success rate around 60 % ICDs  are indicated in all recurrent VTs except incessant forms .(Where the battery will deplete within a month !) Surgical cure (Maze etc  ) is possible in selected few while undergoing mitral valve surgery.Contrary  to the modern scientific  mood ,  I can ay with conviction most A-fibs can be managed medically except a fraction will require pulmonary vein ablation / isolation .

Final message

Mastering the field of of  cardiac  arrhythmias ,  though  appear a daunting task ,  it does not  require   immense  sense  to understand real world problems are  only a  few and can be tackled in a simplistic manner !

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Does Troponin gets released in plasma during Ischemia ?(Without myocyte necrosis )

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, Cardiology -unresolved questions, cardiology- coronary care, STEMI-Primary PCI, tagged , , , , , on November 20, 2012| 1 Comment »

Does Troponin release during  Ischemia  ? (Without myocyte necrosis )

How often this happens ?   . Some believe , it is rare . Here is a possible explanation for it .I feel the mechanism is still not clear . It all depends upon the degree of ischemia.

 

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