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Posts Tagged ‘heart’

We  are at the mercy  of  the three major coronary arteries (LAD,LCX,RCA) that sustain our life . Their  job is clear cut  .It has to perfuse   about 300 Grams of   live bundle of energy  for  an average of 6-7 decades.

What are the hurdles it  faces ,  how it overcomes these obstacles  forms the fascinating story of   “survival  of  human heart”

When coronary blood supply is confronted with a sudden compromise  as in ACS  ,  often the heart has little  time to respond . Hence the damage  and risk of death is  more. Even here there are lots of safety mechanisms and natural lytic process that limit the loss of life to less than 30 %  of all STEMIs. This implies nature protects against the death in 70 % of individuals and help  them  to reach hospital.*

*Among those  who reach hospital , we  the cardiologists  try to reduce the  mortality to about 6-7 % (20% without treatment ) with all  those hi-tech gadgets .It is a  different story and will be addressed elsewhere .

When it comes to  chronic insults ,  the heart has a unique potential to  stage  long haul battles. It has many tricks  under its  sleeves when challenged in a slow fashion.

The main weapons are two

1. Coronary collateral circulation.

2. Ischemic preconditioning.

Here is a patient who fights his life even after all his  three coronary arteries   totally blocked and surviving with one of the branches of left main -Ramus intermedius .

If you have thought his RCA was the savior  you are  mistaken  .

To every one’s   surprise  his  RCA was awful  as well !

He had angina which was  troublesome  but manageable .Was able to live a life with acceptable standards (Indian standard )  After the angiogram he  received  CABG.  A turbulent post operative course ensued  due to various reasons . He  struggled but   fully recovered  . . .  and  ultimately  reached the  previous  standard  of life !

Final message

Modern cardiology is all about not trusting  powers of nature .

But youngsters should realise the enormous potential of those invisible powers.It may sound philosophical , but please  remember  . . .after all . . .  philosophy  is nothing but  search for truths. Atleast believe in them  once in a while !

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Humans have roughly 5 to 6 liters of blood at any given time in their  body  . Out of  this*

50% (2500ml)  is located in the systemic venous compartment.
18% is within the pulmonary circulation participating in the vital oxygenation
12% (500-600ml) is within the cardiac chambers.
8%  is in the arterial tree of  the body.
5%  is  within the  capillaries.
2%  is in the aorta.
* Source : Best & Taylor Physiological basis of  medical practice 1966, 8th edition

What is the implication of this predominantly venous distribution of blood  at rest ?

  • A competent venous tone is essential  for the human beings to maintain the erect posture.
  • Bulk of the cause of syncope in humans is due to peripheral  mechanism like loss of vascular tone and resultant venous pooling.
  • The  concept of venous reservoir is so important in emergency situations like  hypotension  as  simple elevation of legs  is equivalent to  infusing 500 -800 ml of intravenous saline .
  • Similarly during acute left ventricular failure trunk elevation and legs dangling down can reduce the pulmonary congestion very significantly and reduce pulmonary capillary wedge pressure (LVEDP)

 Autonomic dysfunction and venous insufficiency

 Autonomic dysfunction and resultant  orthostatic hypotension is directly related  to venous reservoir dysfunction.Increasing effective circulatory volume by elastic stockings or administration of mineralocorticosteroids like fludrocortisone (.5mg/day ) can be useful in this condition

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It is a well known fact squatting is a simple compensatory posture adapted by children with cyanotic heart disease during exertion to get relief from breathlessness. The children with tetrology of Fallot and related conditions have baseline hypoxia due to right to left shunting .This gets aggravated during exertion. Squatting promptly relieves this exercise-induced worsening of dyspnea. The oxygen saturation improves immediately after assumption of squatting posture. The exact mechanism by which squatting relives the dyspnea is not clear.

Apart from squat induced po2 raise there is a fall in the concentration of pco2 and raise in blood Ph that pacify the sensitive respiratory centers,thereby bringing down the tachypnea

Hemodynamics of squatting has two phases

  • Immediately ( First 15 seconds) after squatting there is a sudden drop in venous return.
  • Sustained squatting for 1-2 minutes result in steady increase in venous return, raised systemic vascular resistance.

Both these effects help the children with TOF. The initial trapping of highly desaturated blood in the lower extremity gives a quick relief as soon as the child assumes this posture. In the next 15 seconds or so the systemic vascular resistance increases and bring the aortic after load sufficiently high to divert the blood into the pulmonary artery.

The net effect of squatting is there is a transient or sustained (as long as child squats) increase in pulmonary blood flow and this is made possible by the relative reduction of right to left shunt as the aortic and systemic resistance is raised by this posture.

Other explanations

There is one more possible effect of squatting. By, compressing abdomen (Knee chest) cause a mechanical push on the splanchnic blood pool into the aorta which has high o2 saturation. This is thought to provide immediate relief to brain hypoxia and avoid the vicious respiratory/ hemodynamic cycle

What is the clinical inference from squatting in cyanotic heart disease?

Squatting implies there should be a large VSD, associated with a delicate right to left shunting very much dependent on the degree of pulmonary stenosis or ( any RVOT obstruction) and the systemic vascular resistance.

How common is squatting history in pulmonary atresia with VSD ?

It can occur with collaterals are sparse.The mechanism of relief is slightly different.

The likely mechanism of relief with squatting in Pulmonary Atresia, VSD is two fold.

1. The Initial relief is due to trapping of deoxygenated venous blood in squat posture, which is similar to TOF

2.The sustained benefit is due to raised systemic vascular resistance which favors more flow across MAPCAs from Aorta.

The second one has no authentic reference , but its a hemodynamic plausiblity as there is zero RVOT flow in PA with VSD.

What are the other cyanotic heart diseases in which squatting is reported ?

  • Tricuspid atresia
  • Double outlet right ventricle with pulmonary stenosis
  • Any combination of large VSD and RVOT obstruction
  • Rarely in Eisenmenger syndrome(10%)

Squat equivalents

Assuming a squat position has cultural issues. Grown-up children may avoid these public places. Standing with legs crosse is a common posture. In fact, the mother holding a crying baby in a chest with knees folded promptly prevents a spell . This can be called “squatting by proxy”

*Though squat equivalents do give relief from dyspnea they are given less significance in terms of diagnostic value of TOF

Reference

1.Paul R. Lurie ,Postural effects in tetralogy of Fallot The American Journal of Medicine Volume 15, Issue 3, September 1953, Pages 297-306

2. Warren G. Guntheroth. M.D.Beverly C. Mortan. m.Venous return with knee-chest position and squatting in tetralogy of Fallot American Heart Journal Volume Volume 75, Issue 3, March 1968, Pages 313-318

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                                                   Infective endocarditis is a serious clinical cardiac problem. The disease has evolved over many decades and now we are witnessing the  most virulent forms of the disease . Infection of heart , can occur in a native healthy valve, native diseased valve, or a prosthetic valve. Further, IE can occur either as  an acute (usually non diseased valve) , or sub acute form (usually in diseased valve).The changing microbial pattern has made this entity very complex. The vigorous   treatment protocols are available for IE. Still  the  prognosis and outcome with medical management is  dismal even in best centers.So the role of surgery in IE has increased over the years.We propose here,  a radically different approach to the problem.

 Traditionally there is a set of criteria for surgery in IE  :  These include

  •  Abscess formation
  •  Worsening valve lesion
  •  Refractory cardiac failure
  •  Persistent fever even after  2 weeks of  appropriate and adequate anti microbial therapy .
  •  Vegetation of more than 10mm size.
  •  Failed medical treatment

(The list is not exclusive)

In any large tertiary  hospital  series, if you  apply the above rule  more than 50 % of all patients with IE will be the candidates for  immediate surgery.

In the remaining 50% the mortality in medical management is very high. The reason being,  the  medical treatment is often prolonged over weeks. Many  of the complications occur  during the course of medical treatment.The common ones are abscess formation, embolic episodes, renal failure etc.Once a complication set in we call it as failed medical treatment and ask our surgical colleagues  to operate.By this time patient’s  general condition  deteriorates and either the surgeon refuses to take  up the case or  patient dies on the table.

So the key point  is , failure of medical treatment  is so common , it is simply not acceptable  to delay  the surgery in these patients as  majority of  them are  doomed to  fail  the trial of medical therapy.

What is the incidence of failed medical management, how to recognise it ? what is the impact of recognising it late ?

  • Failed medical therapy is around 60-70%  even in best centers.
  • Failed medical patients  constitute the greatest  surgical risk .
  • So it is proposed all IE patients should be triaged  early and the  dominant theme should be surgery (Commonly valve replacement, or valve repair)   .
  • If there is large vegetation surgery may be done for the sole purpose of physical removal of the vegetation*.

Final message

In Infective endocarditis experience has taught us, surgery  should be the default management protocol and medical therapy should be offered  to selected few who don’t require surgery.This is especially true in preexisting  rheumatic valve disease.

*The fundamental principle of management of infectious diseases, state that when there is a  resistant focus of infection .Always  remove the focus whenever possible.

 

 

 

 

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Pulse deficit is a clinical sign wherein , one is able to find a difference in count between heart beat (Apical beat or Heart sounds ) and  peripheral pulse .This occurs even as the heart is  contracting , the pulse is not reaching the periphery.This can occur in few clinical situations .

1 . Atrial fibrillation.

2. Very early diastolic  ventricular  ectopic beats

3. Some patients with Pacemaker.

The mechanism is  , the ventricular contractions are  too weak and unable to open the aortic valve  (Or opens feebly*)  , but at the same time they are good enough to close the mitral valve. To open the aortic valve it has to generate atleast 60-80 mmhg pressure , while mitral valve closes even  as LV generates  8-14mmhg  .(LV/LA pressure cross over). So intermitently the  second heart sound  is missed while S1 is retained,  producing more heart sounds and less pulse count in the periphery. The S1 is either felt or heard at the apex but the corresponding pulse is missing . Further , this intermittent absence of  S2  results in totally irregular S1 /S 2 relation.

 

 

Why some of the contractions of LV is too weak to open the aortic valve ?

Because the RR interval varies , the ventricular filling also varies , diastole duration is constantly changing some of the diastole are too short  and LV hardly gets filled , as the LV force of contraction is directly decided by the LVEDV and LV  fibre length these contractions are too weak.

Other published studies

There has been some doppler observations ,where there is a midventricular LV blood flow reversal in atrial fibrillation that could  explain the pulse deficit . Mechanism of production of pulse deficit in atrial fibrillation: assessment by blood flow dynamics

Second Department of Internal Medicine, Kagoshima University School of Medicine.

 http://www.ncbi.nlm.nih.gov/pubmed/3221309

What is the clinical significance of pulse deficit ?

Currently there is no great clinical significance of this phenomenon. But an astute clinician will pick up this sign and it may indicate underlying LV dysfunction. In patients with PPM,  pulse deficit  suggests  pacemaker malfunction .Some patients with cardiac tamponade &  pulsus paradoxus  systolic  blood pressure falls too low to make the pulse feeble or not palpable in the periphery .This situation may mimic a pulse deficit if not recognised.

Dr.S.Venkatesan ,Madras Medical College , Chennai, India

* What is the evidence for intermittent absence or feeble Aortic valve opening in Atrial fibrillation ? I could find this from the book written by Harvey Feigenbaum. whom we consider Father of Echocardiography

 

 

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Is it a crime to do a plain balloon angioplasty in 2008 ?

Plain balloon angioplasty,   the greatest  innovation in   cardiology  when it was introduced in 1977 in a Zurich cath lab , has now become an  ugly  word for most of the cardiologist !

Why this turn around ?  Has technology ,  really overtaken a great procedure and made it obsolete now ?

The answer is a definite ” No”

The restenosis which was the villian in the plain old angioplasty has never been overcome even today. Stents initally used as a bail out procedure during  abrupt closure , later it was used conditionally, followed by provisional stenting and now in 2008  we are made to believe  it is mandatory.

When we realised , bare metal stents are equally  bad (If not slightly better ) in arresting the restenosis drug eluting stents came into vogue with a big bang in 2002. It was projected as the ultimate breakthrough in interventional cardiology and  in 5 years the truth was exposed and it not only failed to prevent the restenois but also had a dreaded complication of acute stent thrombosis.

Now we know , metals  inside a coronary artery  carry  a life long  risk of sudden occulusion , and we talk about biodegradable stents (With poly lactic acid ).

 Common sense ( Unscientific truths)  would suggest

Plain balloon angioplasty still has a major role in our global  cardiovascualr population.

Since restenosis is the  only issue here, ( about 30% )  we can choose patients in whom even if restenosis is likely to happen  no major harm is done . A vast majority of chronic stable angina patients  fall in this category.

Aggressive lipid lowering with plain  balloon angioplasty has never been tested properly . In future also it is unlikely,  such trials will be done as it would be considered unethical . But that would be a premature conclusion.

The other major issue is the cost of stenting , the procedure of PCI/PTCA  has become unaffordable for most of the population in developing countries .The primary reason being the PCI without stenting is considered  ” A untouchable” . If only we remove this stigma from the cardiology community   a signiificant population will be benefited.

A patient with chronic stable angina treated with POBA ,if develop further angina after few years , he  is likely to get a recurrence of  relatively safe  stable angina.  While in a post PCI patient  any angina after the procedure becomes a unstable angina ( Braunwald classification)  and requires emergency care . Angina in a  stented patient is can not be taken lightly as  the the course of angina is unpredictable .

POBA in primary PCI ?

Many may think it is a foolish idea . It has been found many times,  when we rush the pateint to   cath lab after a STEMI  we are in for a surprise !. About 30% of times it is a very complex lesion profile  like diffuse disese,  tight bifurcation lesions , loaded with thrombus or a left main disese.

We fail to realise a basic  fact  , the  initial aim of primary PCI is to salvage the myocardium ,and the next comes the prevention of restenosis . It may even , be argued salvaging  myocardium is the only aim ! Myocardial salvage sould be done urgently . And even  removing the thrombus and opening a IRA can be suffice in a patient who is crashing on table.  Of course stenting can be done whenever possible. But for IRAs which has complex anatomy attempting a perfect stent PCI   (Some may require more than few stents)  as an emergency procedure invariably affects the outcome. One should spend  shortest possible time  inside the  illfated coronary artery. Prolonged manipulations within the coronary artery in an unstable patient  aiming at  longterm patency of an IRA  is to be avoided .The pending procedures can always planned in a next stage. 

Final message

So it is not a crime to think about plain balloon  angioplasty  in some of  our  patients  with acute or chronic coronary syndromes .  Hope Gruentzig  is listening from the heaven and hopefully agree with me !

Dr.S.Venkatesan, madras medical college, chennai, India .

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CCU’S can also save  patients with cardiogenic shock

Many of us would say ” never” or some may say “rarely” but in reality the answer is “yes it can ” slightly lower than  Primary PCI . One could save atleast  few  lives every month by  intensive medical  management alone (Inotrope, vasodilator,pacing if needed ) in any coronary care unit.

So the message here is, not offering or doing  a primary PCI in a patient with cardiogenic shock is not  synonymous with  inferior treatment or death.  After all, in the much hyped SHOCK  trial a significant no of patients survived in medical limb .

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Thousands of dissections happen in cath labs  all over the world every day  very rarely it is painful . The answer is not clear. Both have rich vasa nervorum. Aortic dissection  involves media and smooth muscle . Coronary dissection may also be a  equally painful  , probably we are not recognising it ! or we attribute   all  chest pain in ACS  to ischemia .

Deep dissections into the smooth muscle should be painful.  Type c nerve fibers carry pain signals from heart

Answers welcome.

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Heart is a muscular pump .But it contains more of  non muscular cells than contractile cells.

The average human heart which weighs 300 -400 grams . Contrary  to the popular perception heart is not purely a muscular organ. In fact myocytes constitutes only 30% of heart mass. Rest formed by

1.Fibroblasts

2.Endothelial cells

3.Purkinje cells

4.Interstitial cells

5.Collagen

6.Fibrous skeleton

7.Extracellualr matrix.

Why is this important to recognise ?

Cardiac failure is not synonymous with myocardial failure .

Many times cardiac failure is due to supporting structure failure like in connective tissue disorders.

Exceesive fibroblast proliferation and resulting in fibrosis of heart.

Cardiac interstitial failure is new emerging clincal entity.

In future individual cell based therapy will aim  at replacing specific cells that are defective or depleting.

 

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