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Posts Tagged ‘vaso vagal syncope’

A strong willed  person rarely develop syncope.  We know  weak hearted (Or is it weak brained ?)   men and women may  faint  when  the emotions swing unexpectedly  .The  commonest cause of syncope is  neuro-cardiogenic  syncope (NCS) . (Formerly  called as  vaso-vagal syncope  VVS ). Few facts need to be  emphasized  here . There are  many  critical  circuits  and components to  common syncope.

  1. Trigger
  2. Afferent
  3. Center
  4. Efferent
  5. Fall /Near fall
  6. Prompt recovery after the fall.

Trigger can be emotional or mechanical (Prolonged standing ,  dehydration , etc )  . It occurs generally  in an emotionally  charged  environment with a high  basal sympathetic tone .

Afferent for  NCS   is  mostly sympathetic but it can be  para- sympathetic also (Sensitive GI tract ,  Micturition etc )

* Many times a  trigger and afferent pathway can overlap with each other.It is still unclear what exactly constitutes the afferent , since  triggers can be either sympathetic or para- sympathetic .  ( Pain, GI stimuli, vascular puncture etc) .  Further , afferent  can be be same as the trigger and reach the brain  stem directly  or touch  the heart en route .  ( Cardiac axis  in classical NCS)

The  center is  in the medulla  . Both vagal and sympathetic centers  are involved with potential  spill over on either side.

Final efferent  pathway is the strong  vagal surge resulting in bradycardia and peripheral vasodilatation , cerebral hypo-perfusion  and the person usually falls .( Near fall or aborted NCS  is also a common theme )

                                        If stress increases the blood pressure , absence  of stress  will have to  lower the blood pressure . If anxiety cause hypertension  ,  depression is expected to   cause hypo-tension.

These  inferences  may  appear  correct by logic . As  is always in medicine ,  such   logic works only partially ! ( We are told  the  Sadhus of Himalayas rarely record  blood pressure  beyond 100mmhg systolic  !)

There are strong reasons to believe common syncope (NCS)  is primarily related to the state  of mind and  the neural regulation. Dizziness ,  giddiness  near syncope  are closely related  to  psycho-somatic disorders. Strong willed men and women rarely develop   syncope.Their vascular   tone is well in control even in critical times .This fact has been  well observed  in  the setting of   traumatic  and hemorrhagic   shock  in critical care units  ,  where  some  hold their blood pressure well  even in   adverse circumstances  and few sink without any fight .

Is psychogenic , situational , pain syncope  same as NCS ?

Technically it may not be same. But all of  them  share at least 50 % 0f the  circuits of  NCS.  .However  there is no consensus  to call  psychogenic and   pain syncope  as  types of  NCS.

One critical aspect of  the debate is ,  we do not know whether the  cardiac axis is involved in these  syncope or not. It is preferable to call these types of syncope  as neural syncope (NS)

While in the classical NCS  heart has a  central role in generating hyper active sympathetic afferent from  myocardial stretch receptors. In psychogenic and pain syncope cardiac stretch receptors  are not much stimulated instead ,  the  spillover occur  directly from sympathetic to parasympathetic  nucleus in medulla.

In pain induced syncope parasympathetic limb  gets vigorously stimulated in isolation  to cause a severe  vaso-dilatation  . But once the syncope sets in we often observe bradycardia  and cardiac  limb may get activated as well.

* Presence or absence of cardiac limb in NCS and NS is critical with reference to efficacy of  beta blockers in NCS. The current guideline of NCS  management(  ESC 2010) is strongly biased against beta blocker (Class 3 -level A)  which we feel is  incorrect . Bulk of the patients with NCS respond well to long term beta blockers  .

Please realise , beta blocker  is the only drug which  can break the  NCS  circuit at multiple levels .(Sympathetic trigger, sympathetic afferent, cardiac stretch !

So what is the message ?

It doesn’t require great brains  to realise  vascular  and neural system are  intimately linked  . We know today,  NCS  is primarily a neural phenomenon  hence the  mental status has a  dominant  control over the vascular system especially at times of stress .

The confusion between classical  NCS and psychogenic  / situational  syncope can be largely avoided  , if  only  we call these entities  as simply neurogenic / neural syncope (NS ) ( Omitting the word cardiac is helpful ,   as cardiac axis is not vital  here  ? Non existent  )

Clarity is still  elusive  in defining the  trigger  and afferent limb for the NCS  , fortunately  the final common  efferent pathway that makes the patient fall is indisputably   vagal  !   .  Medullary  vagal nucleus  though fires independently  , also gets  powerful central  parasympathetic flow  from  cortical areas  . Paradoxically ,   controlling sympathetic outflow (Anxiety ) is often an easier  way to reduce parasympathetic flow. This is referred  to as competitive , accentuated  antagonism.

One can prevent recurrent  syncope  by vigorous  mind  control at times of  extreme stress. This is  confirmed  indirectly , by the fact  reassurance is the key to successful  management  in vast majority of  patients with NCS .We learnt this  simple fact  after trying exotic methods like DDDR pacing  and so on .

Final message

Power of  the mind can never be under estimated even in cardio- vascular hemodynamics .  When  pathologically high,   it can spike the blood pressure and break  few vessels in brain , while  if it  is inappropriately  low ,  may induce a syncope or result in persistent  hypo-tension .

Let us learn to use  our  mind over  body  properly .Yogis do it style  and live for 100 years !

Reference

http://europace.oxfordjournals.org/content/12/4/567.full.pdf+html

http://europace.oxfordjournals.org/content/12/4/466.full.pdf+html

 

Iam surprised why this post has been looked so negative by the readees. Almost all  rated it  as very poor.

Iam still pondering over it. Realised to lable patients as weak minded could be one of the reasons.

I think what I wanted to convey was there is link between mind and vascular system.

Please let me what is seen as offensive, let me learn and correct in future.

 

 

 

 

 

 

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It is  a well proven concept   beta adrenergic blockers have a useful role in controlling   the  frequency, and intensity  of  vaso- vagal syncope .

One may wonder how an anti adrenergic drug help to counter hyper vagotonia syndrome !

This is because  during  vaso -vagal  syncope ,  the  inital trigger is  sympathetic . A   sudden hyper adrenergic  surge occurs   that stimulate the vagus, ( Which  overshoots the   initial  quantum of adrenergic signal)   and  cause a systemic vasodilatation ,  hypotension and bradycardia.

How does adrenergic surge stimulate the  vagus?

By two ways

  • Brain stem spill over effect in medulla (Vasomotor to tractus solitarius)
  • Cardiac  stretch caused  by hyperadrenergic activity . This stretch initiates a  vagal reflex  especially from  the base of the heart (Similar to Bazold Zarish reflex ). This  mechanism is  thought to be more important than brain stem spill over  , that’s why  it is referred to as  neuro-cardiogenic syncope .

How does beta blocker help?

  1.  It   sedates  the  adrenergic centre which  modulates the trigger  .It  also blocks the  sympathetic  afferent limb of the syncope circuit.
  2.  Anxiety  and panic reactions are close associate’s of vaso- vagal syncope. They are  not only  considered as  prodrome for syncope  but also act as  important triggers.This is effectively tackled by beta blockers .
  3. Finally , beta blockers  soothes the mycardial  stretch  receptors by reducing the  ventricular shear stress (Reduced contractility and wall stress )  hence neuro-cardiogenic  axis is  pacified.

It is important to remember beta blcokers can only  prevent/  reduce  episodes  of  vaso vagal syncope. It  may aggravate  the situation   if administered  shortly  after the event , as bradycardia and hypotension  is dominant  in the recovery phases.

*During an episode of vaso vagal syncope atropine group  of drugs is most useful .

Which beta blocker ?

Propronolol is the prototype  as it has non selectivity and good penetrance  of  blood brain  barrier ,  which is  the most appropriate site for suppressing hyper adrenergic drive.

Cardio selective beta blockers  do have a role as cardiac stretch  receptors is  one of the two target sites .

Final message

Ironically ,   in the long term management of  vaso-vagal syncope , anti adrenergic drugs  have a major role  rather than atropine like drugs .

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The commonest cause of syncope is the neuro-cardiogenic or vasovagal syncope .

The following is  the possible neural  circuit  of this syncope . In fact . it is a  “Neuro -vascular circuit”

The afferent* (Two components  are present  -Both trigger sympathetic signal )

  1. Sympathetic (Prodrome /Anxiety /fear )
  2. Cardiac mechano /stetch receptors  located mainly in LV .(Can be in Aorta/Carotid )

* In some cases sensors  and afferent can be same entities.

The centre – Medullary Nucleus ambiguous /Tractus solitarius

The efferent -Strong parasympathetic overshoot and sympathetic withdrawal

Parasympathetic excess lead to bradycardia primarily, while sympathetic  withdrawal lead to

hypotension

Syncope recovery

As patient recumbent posture ; LV gets filled and  LV mechanoreceptors are passified .

Final message

The exact pathophysiologic basis of this syncope  still  not elucidated.But one thing is clear , the syncope is due to sympatho- parasympatho signal mismatch( and sort of a rivalry reaction)  !In this neural game , heart’s behavior is all the more funny , it initiates the reflex  while  the brain stem  “Boomerangs” it back to heart and vascular system ,  with a vagal onslaught .

To call this  simply as vasovagal  is not proper , that is why neuro -cardiogenic syncope was used.

Ideal terminology  would be  to call it as  cardio -neuro -cardiac syncope   as the cardiac component form the afferent limb as well as the efferent (target organ )

Reference

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                                                             Syncope by definition is a transient loss of consciousness due to cerebral hypo perfusion and loss of muscular tone, and the patient falls but  recovers fully and gets up either assisted or spontaneous.The cardiac and vascular counter response to syncope is most often intact .This makes syncope characteristically transient . If a patient does not recover from syncope it could either be a prolonged loss of consciousness( Stroke etc)  or if he never gets up he will be called a victim of cardiac arrest or  a SCD ! (Sudden cardiac death ) . So technically by defintion ,  all  patients  will  have to  survive  the  syncopal episode.

But the following questions need to be answered   

  1. How prolonged  a syncope can be ?
  2. Can syncope lead onto  sudden cardiac death ?(SCD)  
  3. What are  life  threatening syncope and non life threatening syncope ?                           

What is the link between, syncope and SCD in patients with ventricular arrhythmia’s ?

Some case of long QT syndromes could be life threatening especially in children as they inherit sudden death. A patient with a non sustained VT  may develop syncope  if  the  VT  becomes sustained especially  if there is underlying heart disease and LV dysfunction . Among this  few , may degenerate into ventricular fibrillation and patient may die.  

How common is syncope in acute myocardial infarction ? 
 Syncope is a very  rare presentation of acute myocardial infarction. 
 
Can syncope precipitate  or precede a  cerebro vascular accident  ?   

 

Prolonged syncope , TIA,  stroke in evolution and completed stroke   can be a continuous spectrum in patients with carotid and cerebrovascular  disese . But when a syncope evolves in to a stroke the   patient is not considered to be a victim of syncope but  they enter the stroke protocol.

There is a big list for the causes of syncope

But to put it simply

A.Cardiac

  •    Purely electrical ( Arrhythmic- Brady, Tachycardia)
  •    Mechanical( Valvular obstruction, and other structural heart disease etc)

B. Non cardiac

  • Vasovagal (Commonest 90% of all syncope)

C. Metabolic*

  •  Anemia
  • Hypoglycemia
  • Hypoxia
*Metabolic causes  coupled with simple  vaso vagal(Neuro cardiogenic)  constitute the bulk of causes of syncope .Siezure disorders are very  common and a close  mimicker of syncope and need to be ruled out.

How to work up  a patient with syncope ?

                   First ,  one need to confirm  it is indeed a syncope . If the initial examination is not clearcut   one  need to  go back to the  history and ask for  circumstances under which the syncope occured  and  details of prodromal symptoms  if any . Patient’s  family members who witnessed the event can give useful information . It  is the most  cost effective ( Comes free of cost infact !)  investigative tool available .Cardiac syncopes are usually sudden, vasovagal often have environmental or emotional factor. Apart from routine investigations , ECG, Echocardiography, holter are done generally, head up tilt test, Loop, event recorders may be reuired in few.

Final message

                                          Syncope is one of the common symptoms in cardiology and  general medical practice. Many times the diagnosis is easy . Common syncope is  never fatal but , ruling out dangerous  tachy and bradyarrhythmias is a key aim.  In a significant number (20-30%) identifying the cause could be really  difficult and  may never be made in spite  of the modern diagnostic tools. These syncope of unknown origin is grouped along with the neurocardiogenic category.

The one,  positive thing about syncope is (unlike chest pain) , it is rarely fatal in it’s first episode ,  gives the physicians to  investigate and correct the underlying problem.

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