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Archive for the ‘Tutorial in clinical cardiology’ Category

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 ?)

Vascular

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

Cardiac

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

Miscellaneous

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

Investigation

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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Pacemaker current is   strangely  referred  by physiologists  as  funny current (I f ) . I am yet to find the exact reason .  This is the current  that  sustain  our life right from the day 22  of  embryonic life when the  cardiac jelly beats for the first time.   SA node  solemnly  follow our  entire life  before  making  a  bid-adieu !

pacemaker  potential sa node 5

 

pacemaker current if funny current poential 002

pacemaker current if funny current poential 003

What is contribution of  If  current in the overall Pace-making  activity ?
This  has not been quantified . The fact that ,  Ivabradine induced  If  current  blockade does not result in serious bradycardia indicate  , SA node has alternate reserve currents as well . ( SA node  is a such a mystery  structure , it would never be a  surprise , if we  find many more  “not so funny”  currents !)

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Guidelines are meant for simplifying  cardiologist’s life  as well as  ameliorating   patient suffering  . It should also  ensure  improving overall  outcome   with  efficient  use of human resources and  economy .

acc aha guidlines stemi 2013

These guidelines  are written from sophisticated centers  mainly for consumption  in developed countries .Though core  concepts will be same , many recommendations are neither possible nor desirable  at the exact point of delivery  in  less developed countries . Please remember these guidelines are not binding on you .Physician discretion is the ultimate principle in medicine.

So ,  let us read these guidelines apply our mind and try to  indigenise . Get maximum out of it  for the respective population .

Some  of the highlights in this 2013  guidelines
1. Therapeutic hypothermia should be started as soon as possible in comatose patients with STEMI and out-of-hospital cardiac arrest caused by ventricular fibrillation or pulseless ventricular tachycardia, including patients who undergo primary PCI.31–33
(Level of Evidence: B)

2 . Presumed or New onset  LBBB is no longer a Indication for emergency reperfusion

3 . Indication of Primary PCI has the following modification

Primary  pci Guideline in  2013 aha guidelines

Reference

http://circ.ahajournals.org/content/early/2012/12/17/CIR.0b013e3182742cf6.full.pdf+html

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Doppler Mitral Inflow velocity profile   is the key to  assess LV diastolic function . The ratio between  E and A has become most popular parameter .

In the absence of atrial contraction what shall we do ?

The answer is simple .  We have 2 D parameters of LV diastolic function.

LA dimension ( > 30 % basal dimension which is  usually >  4 cm  ) is a most specific marker of diastolic dysfunction in the absence of   mitral regurgitation or stenosis.

The only available  velocity E wave profile  can help .A short  E deceleration time in a short cycle  would suggest  significant diastolic dysfunction.High amplitude   E  wave  > 2  M/sec in the absence of MR  will suggest diastolic dysfunction .

Curiously  ,   it can be  assumed    an episode of   lone AF  per-se   ,  be an indicator of diastolic stress for the left atrium .

After all ,  why should a person all of a sudden develop an episode of AF .(Hypoxia, Ischemia ,  excluded )

Other parameters.

Mitral annular velocities / E propagation velocity   / E/E’  are other tissue Doppler parameters  can be used.

Pulmonary venous flow velocity is  largely not useful  (Since A reversal does not occur )

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There are many  organic causes of mitral regurgitation. ( Ischemic , degenerative , valvular , cardiomyopathy etc.) It is not  rare for  pure  electrical events to result in valvular regurgitation.   A 70year old  man  with SHT   presented  with palpitation  and exertional dyspnea  .He was  later referred  for  Echocardiography.  Echo revealed LVH with intermittent MR and moderate LV dysfunction.

His ECG looked like

Ventricular ectopic recorded in bi-geminal rhythm

His  echocardiogram showed

 

His echo showed randomly timed mitral regurgitation was detected .See the Doppler MR jets below.

We know ventricles are integral  part of mitral valve apparatus  .Hence  it  wouldn’t  be a surprise to note  abnormally timed ventricular contraction  can  have a major impact  on mitral valve function.

When ventricles  prematurely begin  to contract  ( As  during  VPDs) it  interferes with  opening of mitral valve. In other words every VPD  technically imparts a  sort of  diastolic dysfunction !

VPDs occur in which part of cardiac cycle ?

VPDs  occur  either in early   or mid  diastole . Thank fully VPDs can not occur in systole . (Refractory period )

What would be the status of mitral valve at times of  VPDs?

Though it depends upon the timing of VPD ,  generally it interrupts the rapid inflow period of diastole .

In fact ,  it converts the cardiac  cycle from diastole to a partial systole or  a combination( fusion ) of diastole   and systole ! *

More MR jets are visualised than LV filling waves . Note the some of the E waves are sandwiched between two MR jets. ECG gating should have made this image more interesting .Any way , we have good MR jets to time systole nicely

* Is that a funny  imagination  ?

During   diastole ,  if  LV suddenly  begins  to contract   instead of  receiving the blood  ,  what will happen ?

VPDs are such a common arrhythmia , we  rarely  wondered  ,  it can have a dramatic  consequence  in a any  given cardiac cycle .While   the cardiologists think too  technically  their  patients observe with  shrewd  sense and tell us clearly  what  they feel  is  actually a   missed beat !

(Yeh  . . .  how simple  they describe the complex  hemo-dynamics  of  missing  diastole !)  .They also tell  us ,  next systole is felt as big thump as palpitation . (Post VPD potentiation )

Just imagine ,  if a patient  has  multiple VPDs  with  different  coupling intervals   that fall in different location of diastole  also  interspersed with sinus beats ,   how chaotic  would be the  the  mitral   filling .

This is what  is recorded in the above patient with multiple random MR jets .

Why all VPDs do  not cause MR ?

The timing is critical .We know all VPDs do  not generate a powerful contraction to cause MR. Atrial fibrillation, Prolonged PR intervals , heart blocks , critically raised LVEDP all can influence the trans mitral gradient . In fact these situation can result in  an  entity called diastolic MR that would be discussed later.

Can  VPD induced MR be  referred to  as diastolic MR ?

When VPDs  occur  in  diastole  , it  interrupts the diastole  and a new systole begins. In any  particular point of time there will be  leak into the LA  if the mitral valve is open .This is technically a new systole but in true sense it is the diastole of  the  previous beat . I wonder , whether   VPD induced MR  may be referred  to as one  form of  diastolic MR.  Of course ,  this MR can spill over to true  systole as well .

This also  makes  sense (Non !) as many of the VPDs do not open the  aortic valve ,   hence technically we can’t call the phase reset  by  all  VPDS   as a true systole !

What is the effect of VPDs  on pulmonary venous flow ?

Left atrial  cannon waves can occur that can elevate PCWP .This is the prime reason for resting or  exertional  dyspnea in these patients. Some may get a paradoxical relief  during exertion   as  exercise  suppress VPDs which are frequent at rest.

If VPDs can seriously interfere with mitral valve function , why  they are  often  considered benign  ?

VPDs are well tolerated* as long as  the  LV function is intact.  If VPDs are associated with  LV dysfunction  it  can initiate a vicious cycle of   hemodynamic deterioration .  Multiple VPDs  if left untreated can lead to progressive LV dilatation  in a  significant population .  Hence patients with  recurrent VPDS need some sort of  follow up. It  makes good medical sense to suppress VPDs in the long run. (Of course the  available anti VPD  drugs  are not very safe  !  The search for non toxic ,  ideal drug should go on !)

*”Well tolerated VPDs”   in no way  means  normal physiology.  Read a related article in my site.  “3 minutes crash course on VPDs”

Final message

VPDs  though considered  largely benign , can lead to dramatic  alterations in the  functions  of mitral valve , especially in diseased hearts.

We  must  realise  when ventricular  ectopic beats occur frequently  , it  interfere with the  both opening and closing of mitral valve.

It is really surprising  ,  the literature is  devoid of  major studies  about the  impact of  VPDs on  mitral valve  physiology . . . rather pathology !

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It is tempting to fix the  “Force of cardiac  contractility” ,  to be the  prime determinant  of  systolic  blood pressure* .  Rather ,  it is  influenzed heavily  by   multitude of anatomical  and  physiological factors.

                                        ”  In most  life instances  the primary determinant  blood pressure  is not the state of cardiac contractility  “

                 For many ,  this  would  appear as  shocker of  a statement !

Fellows  should not be  confused with above inference  . What it means is ,  the  heart initiates  the blood pressure by a brief  period of  systole .The pulse wave attains a peak during ejection phase  . This is the peak systolic blood pressure  . There is nothing called  sustained  systolic  blood pressure .  The quantum and  duration of peak systolic pressure  contributed by the LV contraction  is  far less than we imagine .

If blood pressure is to be controlled   primarily  by  cardiac contractility , how is that ,  a  blood  pressure of   about 80mmhg is maintained throughout diastole when the heart is taking rest and the  aortic  valves  are closed  ?

The  major elastic blood vessels  aorta and the major branches use the potential  energy gained during systole  (Like a rubber band )  into   kinetic energy as vessels recoil during diastole . This recoil  imparts an   important component  to the  diastolic blood pressure  augmentation  and maintenance.

It is  prudent to note  since  diastole is  much  longer than systole  , integrity of the vascular tree  become  much more important  to maintain the blood  pressure  till the next systole arrives.

Note

*The cardiac contractility  , might  still be  important  in determining systolic BP  in  patients  with  severely compromised  LV function** For example ,  in  dilated cardiomyopathy  with  LV failure ,  systolic blood pressure will  be directly related to LV  function.  When LV function is critically  low , the elastic  blood vessels  fail  to  amplify the blood pressure  beyond  a limit.

**Still it is not  uncommon to find high systolic blood pressure  recorded in the back ground of with severe LV dysfunction especially hypertensive individuals.

What happens during aging ?

The  aorta and it’s major branches  gets thickened , the  vascular collagen  goes  cracking  with wear and tear of  life.  In effect , these vessels become less compliant . So , when blood is rapidly ejected  from the  left ventricle  into aorta  and their branches  it’s  distensibility   is  reduced  .This  fails to dampen the  pressure  wave  and  hence systolic  pressure spiking occurs. This we refer to systolic hypertension of elderly.

It is  important to  emphasise   major elastic arteries  has a big  say in fixing the systolic pressure. For the same cardiac output systolic pressure can surge in elderly this  is why we have kept the normal  in adults as 16o mmhg.

Another key point to be understood  is  ,  Aortic compliance  has an impact on diastole blood  pressure too ! . The  stiff vessels during diastole bring  less diastolic recoil. Diastolic recoil of large elastic arteries  determines the diastolic pressure . Hence there  could be  a mild fall in diastolic pressure with physiological aging when recoil is attenuated .  Since the  reduced diastolic  recoil ensures diastolic pressure from being elevated  the entity is aptly named as isolated systolic hypertension.(ISH)

Image courtesey :Norman M Kaplan, Lionel H Opie Lancet 2006; 367: 168–76

Final message

While the traditional  teaching  ramains  as  systolic blood  pressure  would be determined by cardiac contractility  / cardiac out put , while the   diastolic pressure is determined by peripheral  vascular  resistance .This is not an absolute reality ,  rather it is  too simplistic way of teaching circulatory physiology !

The  peak systolic blood  pressure is more often determined by the integrity of  Aortic  and major arteries   rather than cardiac contractility  and stroke volume. Similarly , aortic properties do have a  say in the diastolic pressure as well !

Further reading and debate

 The net effect of aging  on blood pressure :  Is it  physiological or pathological  ?

  Should we  treat  this  raised  pressure due to aging  related systolic hypertension  ?

There is a huge controversy going around ,  regarding the need  of  treating this mild elevation of systolic  blood pressure due to arterial stiffening .This will be addressed separately in this forum .

Reference

http://www.mayoclinicproceedings.com/content/85/5/460.full.pdf+html

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VPDs are the most common arrhythmia  that  confront  us  in  cardiology clinics .While  it can be a totally  benign   manifestation in some  ,  it may signify a sinister condition in others. ECG  is the easiest  and surest way to identify VPD.However  a shrewd echocardiographer can detect the VPDs while imaging the heart.It is often missed if one do not concentrate on the mitral valve motion.

Note :The VPD convert the typical M pattern into a inverted U pattern in mitral valve.

One of the important hemodynamic side-effect of VPD is intermittent mitral regurgitation.

Effect of VPD on mitral valve opening .

By  conventional thinking   VPDs  are expected   to impact  more on the  mitral  valve closure than it’s  opening .In reality it has indirect influence on mitral valve  opening as well. The retrograde  conduction(VA conduction) of the VPD determine the timing of atrial contraction and hence the   mitral valve opening. If the VPD gets blocked retrogradely  within AV node , the normal sinus impulse will activate the atria in an antegrade fashion .Note ,  he atrial activity  occur randomly when multiple VPDs occur.This makes the cardiac cycle too complex to assess especially the diastole. (In fact true  physiological diastole  may  not occur here !)

If  the mitral valve opening  is interfered by a   VPD  (Early diastole is  the  favorite time  for VPDs to  appear  !  )   .When it occurs the AML is    suddenly pushed  upon superiorly  by the premature ventricular activity and hence resets the  mechanical diastole. Please note electrical resetting of atrium is different from mechanical resetting.

It is also possible atria and ventricle contract simultaneously .This is the time , a cannon wave  may occur inside LA .VPDs can result in pulmonary venous canons and may even elevate pulmonary venous pressure   if  this  occurs repetitively .

Another possibility  is ,  VPDs  may not initiate a ventricular  contraction at all .It may be  simply  be an electrical event. That’s why  we changed the name of extra systole  and premature contraction into just   premature depolarisations.

Why is it important to know about M Mode motion of VPDs

Cardiologists  continue to  engage wide qrs  tachycardias   in the  wrong side  of their   brain for many  decades .The ECG debate about wide qrs tachycardia  is expected to  continue  for generations . !  Few smart cardiologists would  rapidly put  the echo probe  over the mitral valve and able to  differentiate  instantly a VT form SVT   with fair  degree of accuracy.

Detection  of regular M shaped mitral AML  will exclude a VT with a high degree of precision .(AV dissociation by echo )*

Even  presence of trivial  MR*  (More often diastolic )   which occur  irregularly  will  definitely indicate it is VT . SVT  hemodynamically   can not result in this  MR is gives us evidence for AV dissociation

* No reference for these observed indices in our lab. (Class 1 Level C expert opinion(  No one calls me as expert though ! )

What is the mechanism  of VPD induced  mitral regurgitation ?

It is well-known VPDs can cause   mitral regurgitation .Not every VPD cause MR.

  • The timing is important .
  • It can be  either systolic or diastolic MR .
  • If VPD occur in early diastole (After the T wave , the MR jet  will collide with  diastolic mitral flow. )
  • Paradoxical septal motion induced by VPDs can alter the pap muscle alignment transiently and result in MR
  • We dot not know how a LV apical VPD  differ from RVOT  VPD in the genesis of MR.
  • Logic would suggest RVOT  VPDs are unlikely to result in MR as there is  a time lag for the impulse to reach the LV base

What is  the effect of  VPD and Aortic valve opening ?

While  every VPD promptly  hits the mitral valve ,  aortic valve may or may not open with VPDs .Again timing and focus of VPD could be  important.This is the reason during  multiple  VPDs  only few open the aortic valve , that  explains  pulse deficit. (The so called missed beat )

Final message

Anterior mitral leaflet (AML) is the most mobile structure  of  the heart . Hence ,  it is not surprising to note  sudden unexpected ventricular contraction will  have maximum impact on this valve .

When VPDs occur in clusters or at random it has a complex effect on the mitral valve motion. This is responsible for  palpitation , minimal mitral regurgitation and rarely trouble some pulmonary venous cannons and raise in pulmonary venous pressure .

Careful analysis of  AML motion can give us useful clues to differentiate VT from SVT during wide  qrs tachycardia

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