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Archive for September, 2008

                              Cardioversion with DC shock  offers immediate cure in many of the dangerous ventricular and atrial tachycardias.  It is often  taught ,  any hemodynamically unstable tachycardia  refractory to  medical therapy respond to electrical cardioversion.  One should also  remember electricity is in fact be called  as a drug !  and it should be delivered in proper form and dose. Here it is the paddle size, paddle position and the axis of current flow all are important. Now we have bi phasic currents for better efficacy.

                             While it is true, most of cardiac arrhythmias respond to shock,  there are few which do not respond or respond very transiently.There are few arrhythmias  in which ,DC shock is not only ineffective but may precipitate a ventricular  fibrillation.

                            Generally arrhythmias of reentrant etiology respond well to DC shock were interuption of  electrical circuit by external current is easily possible. In arrhythmia’s of enhanced automaticity ,  and ectopic tachycardia  it is difficult  to extinguish  the tachycardia focus with DC shock .

Arrhythmias where DC shock is not going to work are

A. Mutifocal atrial tachycardia(MAT)

B. Digoxin induced arrhythmias.Patients who are on digoxin,  has  enhanced ventricular  automaticity.These patients if they  get a DC shock will unmask the  ectopic foci.

C. In elderly with atrial fibrillation and sinus node dysfunction it may be dangerous to shock them with out temporary pacing support as sinus node goes for prolonged sleep mode.

D.In electrical storm with VT ,  if more than three shocks are required within a minute,  the VT will most often going to be permanent and the  electrical therapy can be termed as a failure. These patients will require intensive pharmacological management( Including magnesium, bretyllium etc)

E. And finally , sinus tachycardia (whatever the rate)  is an absolute contraindication for DC shock.

 Verapmil is often effective in MAT  but correction of hypoxia and acidosis may be critical.For digoxin induced arrhythmias phenytoin may be tried.

What to do when the DC shock fails?

  • It will be a  tricky situation and one wonder what to do next when the so called  universal antidote for cardiac arrhythmia fails !
  • Cellular internal millieu  is altered  by hypoxia and acidosis .It may prevent the  effectiveness of cardioversion.So try to correct them .
  • Over dirve atrial  pacing  is one option for automatic tachycardia.
  • And now ablation of arrhythmic focus is possible with radio frequency waves  in some of these patients.( Diffiuclt as an emergency procedure)

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                                  Indication for thrombolysis in ST elevation MI  is mainly determined by clinical and ECG features. ST elevation of more than 1mm in two consecutive leads with a clinical suspicion of acute coronary event demands immediate thrombolysis.

                                 Early repolarisation syndrome(ERS) is a  is typical mimicker of STEMI . In ERS , ST segment elevation occurs in many leads especially precardial .This entity is estimated to occur in nearly 3-5% of population where a genetic variation in the potassium channel activation is reported.

                              If they  land in ER with some sort of chest pain , chances are high for labelling  them as ACS . It is not uncommon for  CCU physicians  to  witness  an  ERS being lysed . Even in many of the land mark trials (ISIS ) there has been many inappropriate thrombolysis , recognised later on.

What can really happen if you thromolyse them inadvertently ?

Generally nothing happens . But they are exposed to the risk of thromolysis. The ECG changes persist. And troponin will be negative and  echocardiogram will not reveal any wall motion defect.

Are we legally liable if a patient  with ERS was thrombolysed and he ends up with a bleeding complication like stroke ?

                        While the physician may feel guilty , there is no reasons for him to feel so.The guidelines are kept little lineant  for  the indication for thromolysis. When we are promoting  a strategy of early  thrombolyis  on a population based approach  in STEMI ,  there is bound to have a overlap with normality .The benefits out of early thrombolysis for eligible  patients for outweigh the few inappropriate thromolysis.

When you want to catch  a   real criminal  it is unavoidable,  one gets hold of all suspected criminals before letting them free . Unfortunately  in this exercise , some of the innocent  might experience   intimidation or even a injury  at the hands of law enforcers.

                               Similarly if a patient with ERS develop a severe esophageal spasm and typical  angina like chest pain he is absolutely certain to receive thrombolysis. (Troponin, CPK come later , and the results never veto the clinical and ECG criteria ,except probably in LBBB) .Many times critical  time dependent decisions are prone for errors in CCU.   So it may be  unscientific to ask why an ERS was  thrombolysed !

 How can one prevent inadvertent thrombolysis in ERS ?

                            Always ask for the previously recorded ECGs .If it is available and  look exactly similar to the current ECG  chances are unlikely  for ACS. In ERS ST segment is generally concavity upwards . ACC/AHA  guideline for STEMI  ,is  aware of this fact , but still  advices thrombolysis for all ST elevation irrespective of the morphology of ST segment elevation. This is propably intentional,   not  to incorporate morphology cirteria of ST elevation  for thromolysis .It would potentially  make many true STEMIs  diagnosed falsely  as ERS and deny thrombolysis.

 

What is the latest news about ERS ?

                       Now data are coming up, ERS is not entirely benign condition.Some of them ( Even a fraction of ERS population could be a significant number) can have a overlap between Brugada syndrome and they  could be prone for dangerous ventricular arrhythmia when challanged with ischemic or other stress.

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The pressure tracing between two chambers of the heart are distinctly different .

 Apart from the magnitude of the  pressure ,(LV at systemic pressure ) The morphology also changes.

  •  RV pressure curve is triangular in shape,
  •  Upstroke is not rapid , (Low dp/dt)
  •  There is no sustained peak ,
  •  There is an early fall and
  •  The pressure falls to zero which  never happens in LV.

Contary to this LV pressure curve is bullet shaped,  with a rapid upstroke, sustained peak, fall later, and does not touch zero.

RV/LV pressure curves in normal persons .Adapted from , Curtiss 1975 Circulation

Note : The shapes of RV curve will change in pathological states.Example in TOF, large VSD there will be left ventricularisation of RV pressure wave forms. Also  in pulmonary hypertension RV pressure may mimic a LV curve.

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                                       Left atrium is the posterior most chamber of the heart.  It is almost a mid line structure.  The normal size of left atrium is about 4 / 4 cm. Normal left atrial volume is 46ml in men and 38 ml in women .(Atrial volume in a normal adult population by two-dimensional echocardiography Y Wang, Chest, Vol 86, 595-601.)  Left atrium  is not an easy chamber to identify in the  X ray chest as it does not form  the cardiac border.( Except a small circumference of left atrial appendage.(LAA)

Left atrium can enlarge in multiple directions.Generally it dilates in the path of least resistance.

 

  • It is believed left atrial appendage  enlargement occur early .  LAA enlargemnet seen as a fullness beneath the pulmonary artery shadow. It may be the earliest finding of LAE in X ray. ( This may appear as straight left heart border , as in classical  mitral stenosis where MPA is also enlarged). The LAA enlargement is not necessarily in  in proportion  with LAE.
  • LA could  also enlarge posteriorly by pushing the esophagus towards the spine.This is visible only in barium swallow.
  • Then LA can enlarge either to left or right ( Usually towards right) and  reach the right heart border or over shoot it and form the right heart border by itself.This occurs very late in the course.
  • The other direction  LA goes on to enlarge is superiorly. When LA enlarges superiorly it hits on the left main  bronchus and lifts it.This is measured by the widened subcarinal angle which is normally less than 75 degrees.
  • LA can enlarge anteriorly  sometimes , but it is resisted by right ventricle but rarely right ventricle yields to the LA push and produce a left parasternal lift which could be mistaken  for RV enlargement.
  • Inferior enlargement can not happen in a significant way as it is limited by the AV groove and strong fibrous skeleton. 

With the advent of echocardiography X ray assessment of LA is redundant .(Academic value and in fellows training programs).The upper limit of normal LA size is around 4.5cm.

LA enlargement is commonly seen in

  • Rheumatic mitral stenosis, regurgitation. Gross enlargement up to 10 cms are common.
  • Hypertensive heart disese.
  • Cardiomyopathy, especially restrictive where both atria enlarge.

In all these conditions if  atrial fibrillation occurs  LA size increases further.

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Chest pain is one  of the commonest presenting symptom  in any  hospital both as  an emergency  or non emergency. Reaching an accurate diagnosis is very important. The main  purpose of evaluation of chest pain is to recognise it as cardiac or non cardiac origin . Cardiac chest pain almost always means ischemic chest pain . That is called angina. (Of course there are few important causes for non ischemic cardiac chest pain which Will be discussed later).

Standard features of typical angina.

Chest pain which falls short of typical features are called atypical chest pain . Some recommend at least three typical features to label it as angina.
After the clinical examination patients  should be categorised in one of the following .

  • Typical angina
  • Atypical chest pain
  • Non cardiac chest pain** Non cardiac chest pain is not a diagnosis. Any physician (or a specialist)  should take some effort to localise it. (Muscle, nerve , pleura , anxiety  etc) . But  generally once these patients are ruled out of cardiac pain  they become less special and are simply referred back to their  family physician, only to return back  with  another cardiac  pseudo-emergency  in a different hospital .

    Why we are diagnosing atypical chest pain liberally ?

    Currently   more number of  patients as well as  the physicians  are   aware of the looming epidemic of CAD. The other major reason is the  lack of application of mind during  foirst clinical appraisal  and examination. Many of the patients with non cardiac chest pain  (Muscle, nerve , pleura )  are termed as atypical chest pain. Though some of the popular texts use atypical  chest pain  and non cardiac chest pain interchangeably , it is not  correct to do so. For example don’t ever label a  patient with chest pain with chest wall tenderness as atypical chest pain and order a cardiac work up .It  is a poor model to  emulate , that consumes time and resources!.Instead they should be diagnosed a confident non cardiac chest pain and dealt properly.

Once a patient is diagnosed  atypical chest pain what’s next ?

They should get a  complete physical examination,ECG, and  undergo exercise stress test.   In the  screening of CAD , angina can be termed a hard sign,  atypical chest pain is a soft sign,  resting ECG is surprisingly  a soft sign again (unless you record it during chest pain). Exercise stress testing is  the ideal  investigation in evaluation of  chestpain.( 70-80% accuracy). This can be improved upon by Thallium, SPECT, stress echo etc. As of now coronary angiogram is considered the ultimate gold standard (Not pure gold !) to rule out  CAD.

It is also worthwhile to remember non anginal  chest pain can also be an emergency and life threatening

  • Pulmonary embolism
  • Pneumothorax
  • Thoracic tumors
  • Aortic aneurysm (Dissection and non dissection)  The list is not  exclusive

Final message

What do we really mean by  atypical chest pain ?

In reality we don’t mean any thing !

When a  cardiac  physician is confused or rather , unable to  rule out angina , at the same time he is not confident of calling it as non cardiac chest pain,  he has the luxury of using this terminology . It is obvious  this terminology  should  minimally  be used.  Once diagnosed  these patients  can’t carry on with this tag  for long. They should be reinvestigated , (Right from history  and clinical ex) .They should either enter the cardiac work up  protocol  or  a non cardiac source for pain should be fixed  immediately.

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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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Left ventricular hypertrophy is one of the most common clinical cardiac entity.It is recognised either by ECG or echocardiography.LVH has a unique place in cardiology as it can imply a  grossly pathological state  or  a marker of healthy heart as in physiological hypertrophy in athletes.

Logic would suggest , in this era of  stem cells and  nano medicine ,  every muscle fibre in ventricle is worth in gold !. So when the nature provides an  extra reserve of myocardium in the form of LVH one should welcome it , if otherwise not harmful.

Is LVH due to systemic hypertension benign ?

Not really, LVH has been shown to be an independent cardiac risk factor. (The famous Framingham study)Further LVH can result in diastolic dysfunction and the risk of cardiac failure increases.

But in spite of these observations, an  astute clinician with considerable experience will appreciate , patients with LVH fare better during an acute coronary syndrome !

This has been a consistent clinical observation . (Shall we call it as class C . ACC /AHA evidence ? )

Is LVH  an asset during ACS ?

  • A hypertrophied heart takes ischemic injury very easy , it doesn’t really hurt much . Another possibility is that in  LVH myocytes are relatively resistant to hypoxia .
  • Patients with LVH rarely show  significant wall motion defect following an STEMI.This is probably because the full thickness transmural necrosis is almost never possible even if extensive MI occurs.
  • This is also reflected in ECG  as these patients   rarely develop q waves in  following STEMI .
  • Persistent ST elevation and failed thrombolysis is very uncommon in pateints with LVH.
  • LVH provides  a relative immunity against development of cardiogenic shock . It requires 40% of LV mass destruction to produce cardiogenic shock.This can rarely happen in LVH. In a  long term analysis we have found none of the patient with LVH developed cardiogenic shock following STEMI.
  • LVH patients  are also protected against development of free wall rupture.

 Concluding message

“Lack of evidence  does not make a fact , a myth”

LVH , either pathological or physiological , has a hither to unreported beneficial effect .It acts as a myocardial  reserve and help limit the impact of STEMI .

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