Archive for July, 2012

Caution: This is a fairly lengthy article . Optimal Reading time  15  minutes

Cardiac failure is a progressive systemic disease  ,  even though the primary problem originates in the heart .Most of the symptoms and clinical features are related to Neuro-Endocrine activation instigated by poor pumping function.When the diminishing cardiac function exceeds the compensatory mechanisms , full blown cardiac failure sets in and get into a vicious downward spiral unless  intervened.

The conventional treatment model involves  on three targets.

  • Reduction in pre -load(Diuretics)
  • Improving  contractility (Inotropics)
  • Reduction in afterload  (Vaso- dilators)

Though the concept looked attractive  there are many missing links . Medical treatment   lags far  behind  the desired goals. Still , it  can stabilize most of the patients with cardiac failure till they reach very late stages.


Inadequately  treated  CHF is not  synonymous  with refractory failure  . But  ,  practically it is the commonest cause for refractionaries . Hence  , every patient must be scrutinised meticulously for adequacy of treatment.

Primary mitral  , aortic valve  lesions causing cardiac failure need  not be considered as refractory  cardiac failure . In the strict sense myocardial disease /damage  either  idiopathic or secondary to CAD  would form  bulk of refractory failure .

(For example a patient with critical aortic stenosis with severe LV dysfunction is   technically  refractory cardiac failure but functionally it could be a  simple  expression of  after load mis- match )

COPD -Cor pulmonale /Primary pulmonary  hypertension  / End  stage congenital  heart disease  and   Eisenmenger syndromes   form separate  group of  CHF and would not be discussed  here.

The valves , the fibrous skeleton, the  pericardium are integral parts  of the heart . Individual disease process can affect these compartments in a differential pattern .

When we  refer to  refractory heart failure   it amounts only two  large disease groups.Ischemic and idiopathic  cardiomyopathy.The whole myocardium is a single unit. If it is destined to fail  it will fail in toto.  There can be reversible factors that can be addressed.

The coronary artery   though not a part of heart has a major say in the outcome of cardiac failure as they determine the cardiac muscle  integrity.In every patient with refractory cardiac  failure , an attempt must be made to rule out  any  re-vascularisible  lesions.

The primary difference between ischemic and Idiopathic DCM   is ,  in ischemic DCM left ventricular  segments  are predominantly involved . RV function  is relatively   preserved until very late stages.

Patient factors

Age , gender, body weight , systemic illness that increase metabolic demands have an adverse impact . Diabetic patients fare poorly .

Fluid management  and  diuretics

In refractory cardiac failure the renal blood flow is reduced .Diuretics usage will further worsen this if ECF is depleted .

So it is obvious we have to use it very judiciously .

Why only  certain patients with cardiac  failure   develop significant edema while others do not ?

This lies in the response of neuro -humoral  activation of secondary RASS system.

Both inadequate  and excess diuretic can perpetuate the  status.

Intra vascular hypovolemia and effective renal blood flow reduced

Diuretic strategies

  • Increasing the dose
  • Adding another ( Switching over to another loop diuretic like Bumetanide, or Toresemide  can be tried )
  • Sequential nephron blockade ( Add  metalazone a powerful thiazide acting in proximal tubule  to be used with caution risk of hypokalemia)
  • Continuous IV infusion  is an option

Ultra filtration  can be  used  in severely volume over loaded  patients.

Refractory diastolic failure .  How common is that ?

The incidence of significant LV filling defect are more commonly observed.There is no specific  drugs  available to tackle this .It may be argued digoxin and other positive inotropes worsen diastolic dysfunction.This  may not be true in the bed side.Unless severe  LV restriction feature are present  digoxin can be continued.

The simple and effective way to improve LV filling in the presence of diastolic filling defect ,  is to slow down the heart rate. At low heart rates  diastolic filling period prolongs and dysfunction tend to vanish.Beta blockers usefulness  in   DCMs  is attributed to this phenomenon

Specific  therapeutic targets

RV dysfunction

RV dysfunction is responsible for systemic congestion .RV function improvement alone can improve the functional class in  many .Controlling and targeting pulmonary hypertension is beneficial . There can be a role for off  label use for chronic pulmonary hypertension associated with DCM.

Importance of  weight reduction :

We can comprehend  complex equations  in  cardiac failure  , still we often  forget a simple logic  . Body wieght is an  indirect but powerful determinant of aortic after load.  A 80kg body needs more heart power than a  body with a 40 kg  mass. If a  patient with EF of  25 %  loses 50 % of his body mass,   his heart can serve  his body  for   100 % longer duration.   (Of course ,  this happens  in certain patients  by a mechanism  called  cardiac  cachexia !  shall we call  it as  natural adaptation ?  )

 Inflammation   control

Tumor necrosis factors and Interleukins are responsible for systemic reaction . These levels are high in CHF. Anti -Inflammatory drugs and diet would help. Statin usage is shown to be beneficial.

Metabolic modulation

ATPs ,fatty acid are fuels for the  heart .Ailing hearts  require  it in plenty. Certain drugs like Trimetazidine, L carnitine has been shown to be useful .

Cardio-Renal syndrome

This is nothing but raising renal parameters  as heart failure worsen .This  essentially  involves fluid and electrolyte management.

Natural course of refractory cardiac failure

It is sort of a  delayed near death sentence . 5 year survival is comparable to many cancer inflicted patients.Basic medical care  remain the corner stone. CRT /ICD*  , LV  assist devices are slightly more effective with substantial  risks and cost involved. Indicated only for  rich  and  insurance infested  population who can tolerate both scientific and  financial excesses.

ICDs* do prevent sudden electrical deaths.

 There is a  fundamental flaw  of  electrical and mechanical device concepts  in refractory heart failure .It  forgets  ,  CHF is a  systemic disease .A  cardio centric approach rarely works to perfection .

Cardiac transplantation  is the ultimate . It works well beyond any doubt. In best centers  like  Stanford 85 %   for 5 year survival is expected. Heart transplantation is limited by donor  availability and  surgical infra structure.Total artificial heart is a distant dream , but will be definitely accomplished

Role of surgery

CABG ( Strictly Indicated only in absolutely deserving .The habit of  revascularising scarred, akinetic DCMs to be abandoned )

Ventricular reduction( Batisda -seems to work only in Brazil!)

Mitral valve  interventions

Some  exotic interventions in cardiac failure

Mitral splinting to  reduce secondary mitral regurgitation in DCM


Newer drugs  and experimental drugs

Nesiritide, (Synthetic Brain naturetic peptide )  Tolvapton ( Vasopressin antagonist) are used with varying  success .

20  point bed side prescription tips  for refractory failure.

  1. Correct the  underlying causes  and triggers.Try to correct any  critical coronary lesion if any by PCI /CABG ( Not a major game changer ! )
  2. Restrict activities (Better to remain in class 3)
  3. Admit  only if  persistent  class 4 .(Intermittent class 4 does not require admission )
  4. Do not try vigorously to move up to class 2  with inotropes  you may  end up in class 4 !
  5. Advice mild passive and active movements. (6 minutes walk > 300 -400meters)
  6. Educate the entire  family / Ask them to shun Internet  (Internet acquired half baked medical knowledge is more injurious to health )
  7. Restrict salt intake
  8. Continue  Digoxin till toxicity develop  or maximum  dose  is reached  (Milrinone /Amrinone make  no major difference )
  9. Optimse diuretics.  Add Metalazone to Frusemide.
  10. Maintain good hemoglobin level (Erythropoitin does not work !)
  11. Add beta blockers  in every one including many of the  class 4 (Not necessarily Carvidilol)
  12. ACEI remain a key drug . Titrate to maximum tolerated dose. (Additional ARBs not much useful)
  13. Aldosterone antagonist has  unique role (Anti-fibrotic ? )  Caution required in diabetic patients  in monitoring renal function .
  14. At-least One metabolic modulator like  Trimetazide  could be tried (ATP utilisation amplified)
  15. Fatty acid metabolism enhancer  L carnitine  may be useful (Recall 1st year medical school basics  . . . Heart thrives on fat energy more  !)
  16. Nephrologist consult  is recommended if electrolyte / ECF status fluctuations are more.
  17. Avoid dobutamine infusions unless patient  insist.
  18. Narcotics like morphine can be used liberally in terminal heart failure  (Both for hemo-dynamic  and  neural benefits )
  19. As far as possible do not send these  patients  to big tertiary hospital unless heart transplantation is planned.
  20. Don’t  be a party  in  exhausting the  personal finance resources of the patient by ordering exotic investigations . Let him not suffer from additional worry ! (By the way . . .  having a hefty health insurance limit  is not an excuse  . Depleting  it  for futile purposes   would make the national economy weaker ! )

Final message

 Three  principles of  management in  refractory  cardiac failure  

  1.   Systemic approach  is the key .
  2.   De-mystifying   cardio centric  interventions  is essential.
  3.   Psychological support is vital .

Functional capacity   has a  poor correlation with LV contractile function . The skeletal  muscle  integrity , blood flow , and its  metabolism has critical say in this. Optimal medications  , properly regulated  locomotion  , weight reduction   can have a major impact.

The secrets of living a good quality of life    in  cardiac failure   ,  lies  not in modern technology  but in the  rare commodities  called  common sense and compassion.

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Angina is the classical clinical counterpart   of  myocardial Ischemia.

True  Ischemia , by electro- physiological rules  must elicit some sort of  ST segment shift .(Usually  ST depression rarely Elevation  )

But  . . .  we know Ischemia and ST depression do not always go together !  Dissociation can occur in both ways.

ST depression without angina is more prevalent  (often referred to as silent ischemia)  , while angina without ST depression is  less common but by no means rare .

We observe both these  phenomenon  during EST.  The  critical issue  here is ,  any pain without ST depression during a EST , the physician is likely to reject it as  non cardiac.

How wise  it is ,  to ignore such chest pain  ?

If a patient  complaints  true  compressive , squeezing  pain  it should be taken as angina  and EST should be  stopped and labelled as positive   even without  ECG changes .

According to the much   famed (De ) theory on ischemic cascade chest pain is supposed to come last. Time and again the rule of ischemic cascade  goes awry in the bed side. Clandestine angina without any ECG evidence be more important clinical entity than we realize.

                                      The argument against this ,  “If you start believing  patient’s  word  more than  ST depression  then the very purpose of EST documentation is lost  !

According to the now  de-famed theory on ischemic cascade ,  chest pain is supposed to come last. Time and again the rule of ischemic cascade  is found to go awry in the bed side .Clandestine angina without any ECG evidence be more important clinical entity than we realize.

Another clinical situation where we  encounter  ST segment  : Angina dissociation is ,  during balloon inflation of PTCA.

Two  explanations can be offered  for Angina in the absence of ECG changes .

1 .Cancellation of ST vectors  due to ischemia of two diagonally opposite areas of ischemia.

2. Electrical  blind spots  in 12 lead ECG. This  is especially common with LCX ischemia  where most of the electrical events are directed to back of the chest.Conventional leads can easily miss .

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LAD is  graded into three types according to

Type 1  :  Falls short  of Apex

Type 2 :   Reach up to the LV apex

Type 3 : Wraps around LV apex and travels some distance in the posterior Inter-ventricular groove.

Clinical  Importance of Wrap around LAD

As the name implies , LAD   should descend only in anterior aspect  in about 15 %  population it can take a posterior descending course as well .

When LAD  wants to conquer more areas of heart is it a clinical advantage  ?

When LAD wraps around the LV apex,  anterior MI due to LAD occlusions can show changes in inferior leads. (Antero Inferior MI )

In ideal anatomic /Physiologic conditions  LAD  should nearly  meet the  PDA   to prevent any water shed  area.

There is usually a trade off between the  terminal LAD and  length of PDA ( whether it arises from LCX or RCA.)

There is some evidence to  suggest the site of ventricular rupture in anterior MI is related to the gap  in the LAD/PDA drainage zones.

Patients with Type  1 LAD  are at risk of   LV apical  ischemia if the  dominant LCX /RCA is  not supportive .

Final message

A long LAD is definitely a  hemo-dynamic  advantage   in physiology ,   Of course  it goes  without saying    . . .   when  it’s   likely  to get  obstructed it is always better to have a Type 1 !

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The other day a patient developed acute left main occlusion within 20 minutes of a  what looked like a successful PCI. When the angiogram was analysed  there was a distinct possibility of left main dissection.

The common causes  for left main injury during PCI include

  1. The guide catheter can it self  injure the tender left main ostium  by  size mis-match
  2. The frequent adjustment of  guiding catheter to get a co -axial alignment caries a definite risk
  3. The guide catheter slipping and subsequent repositioning  with the guide wire precariously snaring the left main ostia is the single important cause for left main injury.

How to prevent left main injury ?

  • Optimal guide catheter size and shape is vital.
  • Smaller the size it is better .(6 F is ideal for most )
  • As for as possible minimal handling of guide catheter is adviced . (Hands always  on guiding catheter  approach  is to be discouraged )
  • Deeper  engagement of guide catheter  as far as  possible  without hemo-dynamic compromise.This will ensure  not only better support for guide wire and balloon ,  low chances for guide wire to injure the left main ostia
  • Tapering guiding catheters with  soft ends are ideal. ( Which are available I think !)
  • Finally  and most importantly keep  the PCI procedure as short as possible ,  come out quickly  . After all ,  we  play  the   dangerous    coronary  game  right  in the mouth of the mysterious   coronary  cave  ( of Alibaba ! ) called Left main !

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Identifying the P wave is the key to decode  any  narrow QRS  tachycardia . Though the  the relationship to  p and  qrs is vita ,  many times it is  not  easy to  relate them.More easily one  may  get  a  clue to the mechanism by analysing   P wave timing .This is the basis of calling narrow qrs tachycardia as short RP and long RP.

Wonder   . . .  why  the  relation “P to R” became  “R to P” here !

Since  in the   common narrow qrs tachycardias  AVNRT/AVRT  ,  atria  activates  the atria  in a  retrograde manner , we look  for the relationship of qrs complex on subsequent P wave . Hence the interval between R to P become the focus.

In other words RP interval indicates retrograde  conduction property of AV tissue .

If it is slow the P wave will be well separated from QRS .

If it is fast it will be close to QRS complex .

If it is ultra fast as in some AVNRT ,it can fall within the qrs complex and completely invisible .

(The so called  r’ prime in classical AVNRT is nothing but a distorted p wave on the terminal qrs complex.)

Based on  RP interval  the following classification is used (List is incomplete)

Short RP Tachycardia

  • AVNRT (Slow-Fast )
  • AVRT

Long  RP tachycardia

  • Atypical AVNRT(Fast -slow)
  • Atrial tachycardia*
  • Sinus tachycardia*
  • SA nodal re-entry*
  • Some forms of AVRT

* Please note ,  here the P wave is not determined by the preceding qrs unlike other tachycardia in the list.

What is the  cut off point to call it is Short RP /Long RP ?

It is arbitrary . Following may help

If RP interval > PR interval it is long RP.

If the absolute RP interval is >  100  ms  with the heart rate of > 160 it would  generally  Indicate a long RP tachycardia .

The timing  of  retrograde P can be very complex than we believe  as the following factors heavily influence it.

  • The autonomic tone
  • Site of retrograde atrial  breakthrough point .
  • Atrial size ,
  • Atrial  refractionaries
  • Effect of drugs
  • Intact-ness of inter atrial conduction
  • Chances of the retrograde atrial activation capturing Internodal pathway

Final message

The P wave location in narrow qrs tachycardia is primarily determined by the retrograde VA  conduction and less  on the antegrade AV conduction  . Looking at the interval between R and P is a  quick way of getting the VA conduction in the bed side.

Once we get an  idea how the VA  circuit  conducts , we can narrow down the possibilities  in  Narrow qrs tachycardias !

Comming  soon

What determines the morphology of retrograde P waves in AVNRT/AVRT ?

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Rheumatic valvulits , Valvular inflammation and edema  is the traditional answer .A detailed Echocardiographic study from All India Institute of medical sciences New Delhi  ,India  which was published in circulation 1996 answers this question most authentically .

From a meticulous  Echocardiographic  study of about 70 patients  (with both first and recurrent episodes of carditis ) the following findings were observed.

After reading this article one should be able to answer variety of  questions in RHD  such as

  • How common is MVPS in RHD ?
  • How often MR dissapear with Aspirin etc ?
  • Echocardiographic correlates  for care -coombs murmur ?



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