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Posts Tagged ‘neuro cardiogenic syncope’

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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Vasovagal syncope is the commonest cause for syncope in our population.It is also referred to as simple syncope .The mechanism is thought to be  an abnormal overshoot  response  by the vagus  in response to a  sudden surge of  adrenegic activity  usually occurring  in erect posture following   , often an emotional or physically stress full situation .The  receptors for  this  reflex pathway is thought to be located  left ventricular myocardium .

There are  two components  for  the VV syncope

  • Cardio inhibitory
  • Vaso depressive.

The quantum of contribution  by each component in a given episode of syncope varies. Pure vasodepressive or cardioinhibitory forms can occur .

Diagnostic issue

Before labeling  a patient as simple vasovagal syncope all potentially serious , cardiac causes must be ruled out. this may require a fairly extensive investigation in some

Read the related blog  : Why syncope is rarely  fatal ?

https://drsvenkatesan.wordpress.com/2008/09/30/why-syncope-is-rarely-fatal/

Management of vasovagal syncope.

  • Reassurance is the mainstay . By this we mean , V V syncope may never kill . . .
  • Prevention  – Involves  identifying syncope prone situations  & taking precaution
  • Emotional support
  • Pharmacological approach

Some will benefit from beta blockers, fludro cortisone(Increase the intra and extra cellular  fluid space )

Since  these are   simple ,   cheap  treatments ,  we worked over time to innovate  &   find some interventional solutions for this life threatening condition !!!.  Thus ,  the indication for cardiac pacing for vasovagal syncope came into vogue .

DDDR pacemaker was implanted worldwide for thousands of patients with vasovagal syncope .

It took  many years  for our  intellectual brains  to realise ,  there are  two limbs to vasovagal syncope Pacemakers ,  at  no stretch of imagination  is expected to counter vasodepresssive component of the syncope.

And then this article came !

http://circ.ahajournals.org/cgi/content/full/108/21/2660?ijkey=ba86da897c167581c498c81743c32afe14fc9393

Water ,  (Simple  H2O ! ) administered at right time in right quantity can prevent most  episodes of vaso vagal syncope . When a tumbler of water can be substituted for a  10000 $ misadventure  (DDD pacing)  , and  further  we have  hundreds  of similar examples in modern  day health care  ,   no surprise  why our health care system is  sinking  along  with our economy !

Epilogue :

In this  21st century   medical “AVATAR ”  , we need to realise   in a strong manner,   low cost  medicines  often   provide   high  quality  cure  ” while ,”   many of the  high cost  therapies  may  end up in  low quality  treatment !

It took 50 years of intense research of  medical comunity to realise ,  a good diet , physical activity and quitting smoking has the greatest way to control  and reverse  the cardiovascular epidemic . Please , note all of them come at free of cost .

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sinus-node

 

Sinus node  as the pacemaker , orchestrates the rhythm of life . It has  to fire for the entire life time of  a person.It  can not afford to take any rest ! But it can pause a little bit , of course that pause  could  be less  than 15% of it’s basic sinus length. This variation of sinus  cycle length is called sinus arrhythmia.This is physiological. When it exceeds 15 % of the previous sinus cycle it is referred to as sinus pause.

 Have a look at this ECG

sinus-pause-2

 

What follows a long pause ?

By strict terms  of definition a sinus   pause should be followed by  a delayed , next sinus  beat only. A  sinus pause  , many times  is followed  by   JPD – Junctional escape beat.This situation should be ideally  referred to sinus arrest as the sinus node is taking too much of rest and it is not able to wake up from the slumber and it needs assistance form the junctional pace maker.

So even though sinus pause and sinus arrest is used many times interchangeably, it should be avoided. 

What are the electrophysiological mechanisms of sinus pause ?

  • Simple sinus bradycardia . The commonest  mechanism is  the  increased vagal tone. This occurs more often in young athletes. Eventhough increased vagal tone  conveys   a innocuous meaning , at times  this can also be symptomatic  and require intervention.
  • Sinus node exit block.
  • First degree, second degree, complete SA block can occur as in AV node.

First degree SA block can not be diagnosed by surface ECG. Third degree SA block is same as sinus arrest and subsidiary pacemaker will function in these patients.  Second degree SA block is usually diagnosed when the sinus pause is in the multiples of resting sinus cycles. If the pauses are not in exact multiples  sinus arrest is diagnosed. All these arrhythmia’s are collectively called sinus node dysfunction(SND)

How do you manage these patients?

Sinus node disorders can occur in number of systemic diseases*. It  needs to be  ruled out.

  • Infiltrating diseases like amyloidosis, hypothyroid states can result in SND.
  • Drug induced SND like beta blocker and calcium blockers are fairly common and should be excluded
  • Some congenital heart disease (SVC ASD) can involve sinus node.
  • Ischemic SA node disease is rare but can occur  following  infero posterior  myocardial infarction
  • Sinus node disorders are  very often related to degenerative atrial diseases associated with HT, cardiomyopathy etc

*The list is not exhaustive

A very important association is noted  with atrial fibrillation as  a part of tachy brady syndrome .The link between SND and AF  is obvious as   atrial pathology is the common denominator in both ! This will be discussed later.

When is a  pause  significant ?

Any pause that is producing significant symptoms is significant.This depends upon the overall  hemodynamic compensation of the patient.Young, and fit can even tolerate three second pause without symptoms.Underlying heart disease makes even a smaller pause symptomatic.But generally a 3  second or more  pause is almost always pathological .Pauses can be up to  5  seconds (  a 5 second pause actually means a  heart rate of 12/mt , obviously it can not go on for a minute, a patient will develop a syncope). A 3 second pause  corresponds to 20/minute.

How will you evaluate a patient with sinus pause ?

There are sophisticated electrophysiological studies (EP) available like sinus node ECG ,sinus node function studies like sinus node recovery time, activation time etc. But these are generally of  academic interest.

If a patient is symptomatic  (syncope) because of bradycardia  he requires a pacemaker and  EP study is redundant . Similarly , if  he is totally asymptomatic in spite of pauses , again  EP study is  not  indicated.

Only for patients  in the  grey zone,   further studies are indicated .This would include a extended holter, loop recorders, event monitors etc.

Another important issue to consider  is , before putting a pacemaker   patient”s   symptom  must be correlated  with their arrhythmia.

What is  the overlap  between sinus node dysfunction and neuro cardiogenic syncope ?

SND  can occur as an overlapping syndrome with neurocardiogenic syncope.(NCS ).NCS is also a very common cause of syncope .In NCS  there are two limbs .Cardio inhibitory and vasodepressive. The cardio inhibitory form can exactly mimic an SND. In a given patient  it is very difficult to pinpoint which of this limb is dominant.Head up tilt test(HUT)  might help in few.  If a patent’s symptoms are due to inappropriate vasodilatation pace maker may not reduce the symptom of dizziness or syncope.

Management

  • There is no ideal  medical therapy* available as on date
  • Withholding all drugs which might aggravate bradycardia is of paramount importance.
  • Pace maker is the specific treatment in all symptomatic patients.

*Aminophyline tablet may be useful in some patients .It acts by antagonising adnosine receptors in SA node.Other drugs which can incrase the heart rate in the short term include  Orcipranaline(Beta 2 stimulant /Alupent ) Probantheline(M 1 blocker)

The key issue is to avoid unnecessary pacemaker implants in patients who have insignificant pause.

 Which pacemaker is ideal in SND ?

pacemaker

                                                              The need for dual or single chamber pacemker will be taken by the electrophysiologist .Atrial based pacemaker (AAI)  is preferred as it gives physiological pacing .But a simple ventricle based VVI pace maker is good enough in vast majority of patients. This takes care of   future risk of AV block also. DDD pace maker is the most physiological pacemaker and it is supposed to provide better quality of life. But it has an issue of insertion and  maintenance of  two leads, multi parameters to be programmed.It should switch to appropriate modes  at different times.(Like VVI mode during atrial fibrillation etc).Trouble shooting needs expertise , while  VVI is simple,  safe , and just effective as well .(In this turbulent world, quality of life is a  too trivial an issue  to be determined by a DDD  maker)

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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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