Posts Tagged ‘clinical cardiology’

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Dear friends,

It all started in 2008. This is  6th year of my attempt to share knowledge in cardiology.The followers of my blog is the only  strength that sustain my writing .

Wishing you all a Happy , wonderful  and  a prosperous , New year 2014

But . . . please be reminded we don’t require a New year to bring a bout of happiness , it is sitting right in our minds every day  !

On this day let me quote my most revered quote of Hemmingway.

Ernest hemmingway quotes

Ernest Hemmingway the Nobel laureate  who was born in USA, Lived in Paris , fought in world war 2 , lived in the deep forests of Africa with wild animals during the fag end of his life .He had a Intimate relationship with Cuba,  made a passionate appeal to end the man made disaster called wars in this planet , before his life ended in 1961.

To connect with  this noble (Nobel ) soul  reach through Wikipedia Link

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Recently , I came across a   young women  who underwent the following three tests for one episode of syncope after witnessing her pet dog bleeding with  an Injury !

  1. Carotid doppler
  2. Holter monitoring and event monitors
  3. Brain MRI /MR angiogram

This was followed up  by Head up tilt(HUT)  in a premier hospital

After 1 week of investigation ,a diagnosis of  Neurocardiogenic syncope was made and she was reassured and no drugs were prescribed.

(The collective yield of the above three investigation in fixing  a specific diagnosis is  less than 10 % of all known causes of syncope )

Syncope  approach  evaluation

To diagnose  common syncope . . . we need common sense !

Syncope is a dramatic  symptom.It is one of the commonest symptom in ER as well . Life time incidence of syncope is at least one episode in 50% all human life ! The definition  of syncope until recently , was liberal .Any transient loss of consciousness with spontaneous recovery  was termed syncope.

This includes

  1. Hypoglycemia
  2. Anemia
  3. Siezure disorders
  4. Structural  neurogenic (Including ,  brain tumors , Dural hematomas etc )
  5. Panic attacks (psychogenic)

Cardiologists wanted to fix syncope as an exclusive disorder of  circulatory insufficiency.By bringing in a modification in the definition  , ie  syncope is  now defined as a transient loss of consciousness due to   reduction in cerebral perfusion  .

This definition helped cardiologists  to exclude the above entities . Still many would include all in single basket as patient should be seen as a whole and we can’t expect them to  land according to our convenience and classification.

Here is an incomplete* list about causes of  syncope (* 99% complete ?)


  • Vaso- vagal syncope in young ( Neuro-cardiogenic , Common , Benign)
  • Autonomic dysfunction of elderly ( Including postural hypotension )


Arrhythmic ( Sinus node dysfunction /CHB/Idiopathic VT/Long QT syndromes)

Structural heart disease

  • Valvular  heart disease  (LVOT/RVOT obstructions)
  • Myocardial disease
  • Rarely ischemic heart disease


  • Severe pulmonary hypertension (Including PPH ,  pulmonary Embolism )
  • Paradoxical embolism.
  • Aortic arch disease -Takayasu related arteritis .


We have a sophisticated array  of investigation for syncope .It can be a never ending exercise , ranging from  spinal cord evoked potentials to diagnose Shy-drager syndrome ,   . . .  to implanting long-term loop recorders to decode  heart beat behavior.

However , evaluation of syncope is the ultimate wake-up call  to all current generation cardiologists  . . . Why clinical cardiology  should  never  be allowed to die (and  it  will not ! )

Common sense begins with answering  few simple questions . Is it really syncope ?

If  you ask this question three times and with  specific leads to the patient  and the witness ,  truth will come out  . 90% of times it may not be syncope at all (Near syncope, accidental  fall, dizziness ,extreme blurred vision, drowsiness  etc)

If it is syncope , Is there a non cardiac cause ?

It may related to the Hypoglycemia / Anemia /Panic attacks.Get a neurologist opinion , it would be terrible mistake if you miss a space occupying lesion  within the brain. (Missing chronic silent sub dural hematomas is  frequent   in the evaluation of syncope of elderly !)

Ruling out  cardiac syncope is relatively easy

In the remaining  patients  basic investigation like routine blood tests,ECG, ECHO   will help us  rule out most serious cardiac disorders.Similarly  bulk of the electrical cardiac syncope can be diagnosed.(Holter , carotid study in selected few )

Need for neurologist -cardiologist interaction.

Syncope due to VBI,  transient Ischemia attack , Senile vascular dementia  is a grey zone . Many have complex neuronal -vascular mechanisms . What is Consciousness ?  and  What is LOC ?  :Is it the lack of blood or severely depressed nerve signal in the reticular activating system? Lots of interaction between cardiologist and neurologist is required to clear our ignorance.(I  have one such  elderly patient who is intermittently awake ! I call this chronic syncope !)  .

Undiagnosed syncope is not  a crime

Realise the most important lesson in Medicine . If you  have ruled out all serious  causes of syncope you should have the courage to be satisfied with that !

Scientific pursuits has a limit. Searching for the mechanism of a psychogenic  fainting attacks with intra cerebral electrodes is a clear case of  physician acquiring a psychotic  behavior !

Final message

Syncope is not only a dramatic symptom for the patient , it also unfolds a drama of costly  investigations  . .  . many  with  dubious value.

Talk to the patient personally for  10 minutes in a quiet room, try to apply that elusive  clinical sense  . . .   it would rarely let you down !

After thought

What is the true clinical value of * Head up tilt Test (HUT)?

Will be posted soon

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Spinal cord is a busy  neurological  highway to brain .It  runs  24/7  non stop  with unlimited  horizontal and vertical lanes .It is such a compact  structure , it can  easily  get confounded   when multiple signals converge,  diverge, summate , deduct , reflect back,   or cancel out .
A 64 year old women came to me for  second opinion  regarding   chest pain . A  cardiologist  had  just adviced her  an  emergency   coronary  angiogram and also suggested she may require an  urgent  PCI  as well .
I listened to her history in my office  . . .  In  her own words .
Doctor , I am  getting  sudden   compressing  type of  pain which  starts in the centre of the chest and soon transmits to the left shoulder and  gradually reach the inner aspect of the hand up to the little finger . And occasionally it is very severe and some times i feel like sweating as well ! I am unable to predict when it comes doctor !
It was  so convincing  but one  feature was  not fitting In . She said , she used to walk  daily   and do all house hold work with no pain . She also  recalled about the  acid peptic disease , and neck pain periodically due to cervical spine problem.
Her resting ECG was normal .She was  afraid to do a stress test . After thinking  for a minute , I had no  other option  but  to endorse  my colleague’s view and asked her  to go for coronary angiogram .
One  thing I  suggested differently was , I told her it was not an  emergency , I also  conveyed my gut feeling  that it is unlikely to cardiac  pain . One week  later  CAG through radial route  was done . Both of  us were  happy  to find a  normal  coronary  angiogram !

Final message

Pain is a  feeling . It can be  perceived  at  multiple levels  . The site of origin , spill over on transit and at the level of brain .  A patient with multiple  potential source for pain can either summate , deduct , reflect  or cancel out .This can confuse the clinician in a dramatic fashion as it did to us ! . To complicate the matters  further , gastric pain can trigger a cervical  pain and vice versa . (Spill over effect)

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You are asked to see a patient with a pulse rate of 45 /mt .  Is it sinus bradycardia  or  complete heart block  ? 

Only one condition , . . .  you must conclude in the bed side !

  • Heart rate  may give a clue ( HR of  30-40 is common in CHB . Less common in sinus bradycardia.)
  • Pulse volume is large in both (More so in CHB )
  • JVP  shows occasional cannon waves hitting the neck  in CHB. Cannon wave can never occur in sinus rhythm
  • S 1 intensity may vary in CHB (As  Marching through  of  P waves  occur in CHB  ,  when it falls close to QRS  , it results in a  short PR interval  and a  loud S1   . Since marching through is a intermittent phenomenon S 1 intensity also varies.)
  • A short systolic murmur may be  heard intermittently due to   trivial MR/TR in CHB  ( Competitive AV valve movement )
  • A  simple bed side test  . Ask the patient  to exert for a minute -Sinus bradycardia raises  the HR with a fair regularity  to 80-90/mt  or so. CHB doesn’t  (Note :  CHB with  junctional rhythm can  sometimes increase the HR  significantly )
  • Finally response to Atropine   is prompt with sinus bradycardia.

Final message

Bed side skills in recognising cardiac arrhythmias are still relevant even in the current  era of carto and 3d electro anatomic mapping .

After all ,  the 19th century clinical wizard Wenke back recognised the second degree  AV  block at the bed side  well before  the ECG machine  was invented. He meticulously observed progressive prolongation of a-c interval and subsequent drop of c wave in the jugular  vein !

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Most important MCQ in clinical cardiology

Many cardiologists  would love to do away with detailed  clinical examination because  . . .

  1. They think it is an inferior job to do  . By skipping  it , they get a false sense of superiority.
  2. It is a time killer  and eat into precious cath-lab  time
  3. They no longer believe in  these “perceived – primitive” medical methods.
  4. Fear of colleagues making  fun of hem if they  indulge  in detailed clinical examination.( At-least in India ! )
  5. To give more job opportunities  to para medics.
  6. They are no longer confident about making a good clinical examination as they  are neither  trained  adequately nor interested in it !

Answer :  All of the above can be true .  The 6th response is  likely to be  more  correct !

While cath labs can prevent few deaths occasionally . . . it is the general wards and OPDs that add life every day

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Probably , this is  most important question  for a  modern-day cardiologist.

Q : Clinical cardiology as a speciality is  . . .

A.Hale and healthy

B.Dying slowly  and steadily

C.Terminally ill

D.Dead long ago

If your answer is A , it would be a  blatant lie ! If the answer is D , you are a pessimist .

The  real answer could be  somewhere between C and D , more towards  D “

 Why  clinical cardiology has  plunged  in  to  such a sorry state of  affairs  ?

 Why it has become an objectionable sub -speciality among current generation cardiologists ?

You blame it on anything, but the real culprits are pseudomodernity , commercial onslaught and the glamourous mindset of  many cardiologists. In every walk of life  tradition, culture and heritage of the past is preserved except in medicine .There  is rarely a backward journey in medicine  . This ,  in spite  of the fact there are lots of hidden treasures  left by our elders.

Image courtesey : Jupeter Images

Now , cardiology  as a specialty is  in a miserable  state .It has almost become synonymous with putting stents across the obstructive coronary arteries. There is a perception among  juniors (  seniors too ! )  Choosing  clinical cardiology is an inferior  pursuit of cardiology .

Many belive clinical cardiology  means ,  measuring blood pressure , looking at JVP , apical impulse, S1 S2 etc  .Clinical approach  does not end with  Inspection , palpation and auscultation of the  heart .

Then , what could be the defintion for clinical  cardiology in the current era ?

It is the process of application of our mind in toto on the patients symptom and it’s  impact on the overall health  with specific reference to cardiovascular system  .It also refers to  the thought process that will decide the optimal  managemnt strategies .( That puts the patient’s interest first )

In simple terms being clinical , is being sensible  and ethical

For example, a comfortable post MI patient with near normal LV function should be sent home for a later evaluation (If , and only if  he develops significant symptom ) This  is clinical cardiology working at it’s best .

If such a patient is sent to cath lab directly  , clinical cardiology is deemed to have doomed !

Similarly , a patient with Atrial fibrillation with the rapid ventricular rate should receive  digoxin or a beta  or calcium  blocker for rate control as a first measure . If a physician refers such a patient to an  university EP  lab ,  clinical cardiology is deemed to have doomed !

If a patient with ASD with less than 2:1 shunt is adviced device  closure clinical cardiology is considered  failed.

If a patient with renal artery stenosis is blindly stented ,  clinical cardiology is in the highway to death .

If you prescribe a latest generation sartan for your hypertensive patient instead of advising physical activity, diet and lifestyle modification , it implies  clinical cardiology is  given a death sentence and being publically hanged.

 Finally ,   it is the ultimate  mockery of clinical cardiology ,  when a physician diagnoses  cardiac failure  by pro BNP and CVP  , even as the  patient’s lungs are sounding with crackles and the neck veins are violently pounding .

Worse still ,  the same patient miay be  ruled out of cardiac failure  , if  the BNP level  is within normal levels  !

As you  come across   any of  the above situations ,  too often , one  can predict the future of clinical cardiology.

My impression is ,  the mortality  of  clinical cardiology at this point  of time  is ,  it may not survive too long and the  5 year survival  rate appear dismal. Of course ,  in many institutions    especially  the corporate ones ,   it is  already  been packed and sent to the  mortuary !

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Cannon Sound

A loud first heart sound (S 1)   which is  heard intermittently in patients with complete heart block (CHB)  is  often referred to as  cannon sound .

What is the mechanism of loud S1 in CHB ?

We know , the intensity of S 1 is  mainly determined by the  relative position of mitral leaflet (To be precise, the  anterior mitral leaflet(AML) )   at the onset of systole.  We also know the  PR interval  has an intricate relationship to  mitral leaflet  position .

The shorter it is ,  wider the leaflet separation  and a longer PR interval makes a mitral leaflet assume a almost closed position   by the time the ventricle contracts.this happens because  a long drawn PR interval fills the ventricle more completely and LVEDV  reaches the maximal levels and LV blood column lifts up the mitral leaflets , and hence the LV  contraction  which follows does not close it with a  bang. In a short PR interval the opposite happens and hence a loud S1 .

In CHB we have variety of PR intervals ranging between  very short to long   ( falling just before the qrs complex) It is not difficult to understand this , as P waves are totally dissociated with the QRS complex  in CHB.In fact p waves have a liberty to fall any where in the ECG tracing , some call this as marching through the qrs complex !.

Hence typically the S1 is variable in intensity , varying between loud to soft.  When  P wave falls just behind a QRS complex , it generates a very  loud S 1  that is called cannon sound .This happens intermittently.

Cannon wave

This is entirely different phenomenon except that it shares the word cannon . Cannon a wave is  a visual finding on the jugular venous pulse.(JVP) .It is a systolic event . It is also seen in CHB as like a cannon sound

This is a giant a wave  in  JVP  when the right atrium contracts against a closed tricuspid valve. In physiological situations atrium contracts with an open AV valves , so that ventricle gets  filled . So atrial contraction  does not does not cause any reflux of blood back into vena cava.

But, when the atrium  contracts and  finds , the AV valve closed  there is no other option   for the incoming blood  to reflux  back into  the neck veins. This is seen as giant a waves called as cannon ” a “waves

With reference to ECG  location ,  this cannon”  a” wave occurs   whenever p wave falls within the ventricular systole ie  the QT interval .The cannon waves also occur intermittently like the  cannon sounds.

What is the  peculiar relationship between cannon a wave and   sound ?

In fact , it is  a non- relationship.  Though  , both the sound and wave   can occur in a given  patient with CHB ,   they can not occur simultaneously .This is because ,  for cannon sounds   to occur  the  P  wave has to fall before  QRS  and for cannon waves to occur the  p   waves must fall after QRS  ie with QT interval .

Clinical significance  of  cannon wave

Complete heart block is the most common situation for cannon waves to occur.

Ironically ,the VVI pacemaker which is used  to treat CHB does not prevent the cannon waves , and atrial contractions continue to occur at random , causing various degrees of intermittent venous reflux into the veins .This may produce, worrisome venous palpitation in some (Usually settles down after few weeks !)

Some attribute , the so called pacemaker syndrome ie giddiness, dizziness to this abnormal venous waves triggering the carotid baroreceptors (Venous -artery spillover )

Will DDD pacemakers  eliminate venous cannon waves ?

We hoped so , it does in fact . But,  it really happens only if the A sense V pace mode . A pace V pace mode with programmed PR interval is not a realiable way to produce AV synchrony. It is  common ,  many of the DDD pacemakers fall back to VVI mode either intentionally or by mode switching  for various reasons.


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Heart is externally covered by two layers of pericardium .  Pericardial space is formed between parietal and visceral layers of pericardium . It is a narrow space which is normally lubricated with pericardial fluid up to 25ml. When these two tissue surfaces  come into contact ,  pathological  rub takes place.It is heard  whenever the pericardium is inflammed . Pericardial rub is a distinctive but uncommon  clinical sign .

Common clinical conditions

  • Acute pericarditis
  • Uremic pericarditis.
  • Rheumatic pericarditis
  • Post myocardial infarction

Pericardium has two layers .

There are four  possibilities for pericardial rub to take place.

The rub can occur

1.Between the two layers of pericardium

2.Between the visceral pericardium and the epicardial layer of  heart*.

3.Between parietal pericardium and the  chest wall

4.Pericardium can rub with the adjacent pleura( Pleuro pericardial rub )

The second and third mechanisms are very rare.

An update

We have realized one more possibility . Diaphragm forms the floor of the heart on which the hanging heart  rests . Rubbing of pericardium over diaphragmatic surface is a beat to beat affair that lasts the entire life !. In inflammatory states of  diaphragm especially  the contagious  ones from abdomen  , can result in pericardio- diaphragmatic rubs .These rubs are almost impossible to hear clinically.

pericardial effusion rub plural pleuro pericadial

*The anatomic mystery : Is epicardium same as visceral layer of pericardium ?

Some anatomist feel that both are same entities. If that is the case myocardium can never split its relationship with visceral pericardium.But it is also a anatomical fact visceral pericardium engulfs the coronary artery and  are located sub epicardially.

How many components of pericardial rub are clincally heard ?

Pericardial rub  classically has three components. Systolic, mid diastolic, and pressytolic atrial components. Pericardial rubs are typically described as to and fro rub. Systolic component is most consistent. In atrial fibrillation mono component pericardial rub is heard.


Superficial , scratchy, high pitched ( Can also be low pitched)


Left sternal border , left 2nd or 3rd space  .Best heard in  sitting , leaning forward in inspiration. Many times the rubs are transient and evanescent . Since it has multiple components it may be mistaken for added heart sound like S 3 or S 4.

What is the mechanism of pericardial rub in the immediate post MI phase ?

Presence of pericardial rub post MI indicate a transmural involvement or atleast significant epicardial involvement . Recognition of this is important as presence of pericardial rub increases the risk of rupture  and hemorrhagic effusion if anticoagulants are used.

What is the  relationship between  pericardial effusion and  pericardial rub ?

Generally it is said with the onset of effusion pericardial rub disappear.But this is not necessarily true.

Rubs after contusion chest and fracture ribs can be with the chest wall and may have  no relationship with effusion.

Is pericardial rub a painful condition ?

Pericardial  rub associated with acute inflammatory pathology is severely painful (like a pleuritis).But pericarditis associated with chronic inflammatory conditions are less often generate pain.The exact reason is not known.

What is pleuro pericardial rub ?

This  clinical entity is poorly defined , often taught by veteran professors  in clinical auscultation classes.It can be heard in the mid segment  or diaphragmatic pleuritis with or without pericardial effusion in patients with  atypical pneumonias.

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