Posts Tagged ‘sinus node dysfunction’

Syncope in CHB is due to unsafe escape rhythm, changing focus of VPDs,  extreme bradycardia, (<20 /minute),  pause induced VT, (Usually polymorphic and torsades is quite common .)  ultimately may end with convulsions,  ventricular fibrillation, and death.

Syncope in SND is due to extreme slowing of SA node . Sinus pauses or even arrest can happen resulting in ventricular standstill. Fortunately, a stable escape rhythm ensues more often than in CHB. (It may just be around 20 or 30/mt. still, ventricular arrhythmias are uncommon. ) This implies an important fact that stability is more important than slowness.Fatality is rare in SND.However, the mechanism of syncope in  SND is influenced by the integrity of AV conduction also. If it is severely impaired it can trigger ventricular arrhythmias as well as the escape focus becomes unstable infra hisian location.

Paradoxically, in patients with SND, an episode of palpitation due to AF  or sinus tachycardia precedes the episode of syncope. An intelligent patient may recognize this as a warning and can take lying posture after runs of palpitation.This is because of tachycardia-induced suppression of  SA node prolong the sinus node recovery time still further.

How to differentiate cardiac syncope from simple vasovagal syncope?

Cardiac syncope  is differentiated by common vaso-vagal syncope (VVS) as the latter occurs during erect posture . It may be entirely due to vascular component and hence it may simply represent hypotension without a true cardiac limb .(Vasodepressor syncope)

Hence the pulse rate and volume may take some time to recover in VVS, while Stokes  Admas of CHB  usually have a well-formed bounding pulse in the recovery phase, as the rate is low and systemic hypoxia is a consistent feature.

How is the respiration during Stokes – Adams syndrome ?

Intact. Oxygenation in the lungs goes on for time being. The pooled pulmonary blood gushes after the termination of syncope and causes  the classical flushing. Since the hypoxia causes systemic vasodilatation the flushing is more obvious.(Unlike vasovagal syncope where they are often pale)

History of stokes Adam’s syndrome Morgagni is the  one who gave credit to their  discovery

Though Morgagni first described the clinical picture of this syndrome in 1761,  It was published much later by Two Irish Physicians  Stokes, Adams. Wish this entity is referred to as Morgagni-Stokes-Adam’s syndrome


1.R. Adams. Cases of Diseases of the Heart, Accompanied with Pathological Observations. Dublin Hospital Reports, 1827, 4: 353–453.

2.W. Stokes. Observations on some cases of  permanently slow pulse. Dublin Quarterly Journal of Medical Science, 1846, 2: 73–85

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As I expected ,  my earlier algorithm “An Idiot’s approach to tachy-arrhythmias” has  elicited  mixed reactions  .Some  EPs calling it a dud while few  physicians termed it awesome . Here is  a follow up .

Heart rate of a tachycardia is the most neglected parameter by physicians .  They are often seen spending  hours together for decoding  arrhythmia , splitting the brains   for P wave  location , VA conduction, Fusion beats etc .Finally they end up  either administering  Amiodarone a broad spectrum anti arrhythmic agent or DC shock.

Here is an unusual algorithm  for arriving at a diagnosis in all tachy-arrhythmias  based only on heart rate and the width of he qrs complex.

(Click over the table for high resolution image )

approach to cardiac arrhythmias narrow qrs vs wide qrs brugada wellens criteria

General principles in diagnosis of tachycardia

Narrow  qrs tachycardias.

90 % rule : If regular It is sinus tachy if irregular it is A-FIB . Take some efforts to r/o sinus  tachycardia . (In children and young adult it can be extremely difficult at times )* Please note : Sinus tachycardia can show some irregularity due to sinus arrhythmia and  frequent  APDs and JPDS . Further at  fast rates P may fuse with T it should not be confused with  A-fib .

Wide qrs tachycardia

Common things  are common , if  you sight a large animal with a huge trunk  in a Kenyan safari ,  it is most likely to be an  elephant and not a Dinosaur !  Please diagnose VT  when you encounter wide qrs tachycardia by default especially when the BP drops  !

  Management issues

It  would be  foolish to split our heads for decoding an arrhythmia when a patient is unstable .Any hemo-dyanmic unstable tachycardia needs DC shock . (Synchronized will be better unless it is dire emergency )There are very few arrhythmia where DC shock is contraindicated   ( MAT/Dig toxicity/Underlying sinus node dysfunction )

Only if the patient is hemo-dynamically  very much stable   the  physicians  have enough time to  confuse themselves  and the real  ordeal begins .Please remember  the 5 arrhythmias  constitute 98  % of all known tachy-arrhytmia . So where ever  you practice ,  whether  in remote Nigerian village  or  sophisticated  Cleveland  university hospital , when you are  confronted with a tachycardia  the diagnosis  should be one among the  following  five  !)

  1. Sinus tachycardia .
  2. AF/A-fib
  3. Atrial tachycardia  with  or without blocks
  4. ventricular tachycardia /VF
  5. AVNR/AVRT with or without aberrancy

All  other tachy-arrhythmiaa  are  largely  academic !

Regarding  drugs

Knowing the mechanism of  arrhythmia genesis  is less important  at bed side . They are  triggered , sustained, and maintained by either functional or structural component .Ionic basis operates in every arrhythmia  , but it is the anatomical  substrate that maintains it .This happens in only diseased heart.The only point worth remembering regarding mechanism of arrhythmia  genesis  is ,  automatic and focal tachycardias  will not respond to DC shock . All other can be termed some form of re-entry . Micro reentry  for all practical purposes behave like  triggered  activity. Ischemic and electrolytic VTs are primarily ionic based and often polymorphic.Structural VT are commonly mono-morphic. Any VT just prior to degeneration to VF become polymorphic

Every patient with cardiac arrhythmia should be checked for hypoxia,acidois , electrolyte defect or exposure to any  pro arrhythmic drugs. (The commonest  cause of tachycardia in any  IMCU , is inotropic induced (dopamine /doubtamine ) tachycardia .

We  have  5  pharmacological options

  1. Blocking  adrenergic  receptors(IV Esmolol, Metoprolol)
  2. Blocking calcium channel (Dilitazem,Verapamil)
  3. Blocking potassium channel  (Amiodarone  ,Sotolol Adenosine  to a cetian extent )
  4. Blocking sodium channel . ( Procainamide , Lignocaine (Wonder drug almost forgotten now ! ) Flecanide Mexilitene etc)
  5. Digoxin ,Adenosine  magnesium are special  anti-arrhythmic  agent which  has very useful role in certain specific situations (Magnesium -Torsades/Polymorphic VT / Adenosine in LVOT/RVOT VT etc)

General principle is ventricular arrhythmias  are blocked successfully  by sodium or potassium blockade  Atrial and functional tachycardia are blocked by calcium or adrenegic blockade  .Of course,  there would be  some degree of overlap  when the arrhythmia  origin  hovers  around the junction  on either side of the AV  ring . This is basis of verapamil sensitive VT .Clusters of  calcium  channels are scattered  in the junctional  region

Refractory tachycardia

  1. Consider ablation  in AVNRT/AVRT
  2. ICD +Drugs  in VT
  3. Ablate and  Pace(Some A-fibs)
  4. Ablate and ICD (Some  incessant VTs)
  5. Surgery in minority

In AVNRT/AVRT 90 % success can be achieved  in most EP centers .VT ablation  is still a complex process  with  success rate around 60 % ICDs  are indicated in all recurrent VTs except incessant forms .(Where the battery will deplete within a month !) Surgical cure (Maze etc  ) is possible in selected few while undergoing mitral valve surgery.Contrary  to the modern scientific  mood ,  I can ay with conviction most A-fibs can be managed medically except a fraction will require pulmonary vein ablation / isolation .

Final message

Mastering the field of of  cardiac  arrhythmias ,  though  appear a daunting task ,  it does not  require   immense  sense  to understand real world problems are  only a  few and can be tackled in a simplistic manner !

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Heart rate of a tachycardia is the simplest of all  . . . but   neglected parameter by physicians.  They are often seen spending  hours together for decoding  arrhythmia , splitting their brain for locating P waves ,  VA conduction, Fusion beats etc Finally , most end up  either administering  Amiodarone a broad spectrum anti arrhythmic agent or a DC shock  without arriving at a correct diagnosis.

Here is an unusual algorithm  for arriving at a diagnosis in all tachy-arrhythmais  based only on heart rate and the width of  the qrs complex with acceptable accuracy.

(Click over the table for high resolution image )

approach to cardiac arrhythmias narrow qrs vs wide qrs brugada wellens criteria

Caution :

The above table is  an extremely simplified approach for tachy arrhythmias. Not applicable for scientifically inclined . But in my personal opinion ,  in an emergency room  pure science matters less !

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Tachycardia – Bradycardia syndrome is the hall mark of sinus node dysfunction.

  • The commonest tachycardia in sinus node dysfunction is Atrial fibrillation . Followed very closely by sinus tachycardia . In fact alteration between sinus tachycardia and sinus bradycardia without other pathological arrhythmia is rare . (Of course , we have a name for such an entity as inappropriate sinus tachycardia / bradycardia )
  • Atrial tachycardia occurs a distant 3rd
  • Ventricular tachycardia may be an exception (Please note , extreme bradycardias which lead to pause dependent VT is not directly related to sinus node disease )

The commonest bradycardia in SND is

  • Sinus bradycardia (This fact is undisputed unlike the tachycardia component of SND !)
  • Followed be sinus pause , SA blocks and sinus arrest .
  • AF with slow ventricular response ( Bradycardic AF) We are not sure about the rhythm here (Is it truly junctional /or conducted atrial ? )
  • Associated AV block can occur up to 20 % of patients .If AV block is present the true nature of SA node disease is masked and it’s function becomes almost irrelevant .

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Atrial fibrillation is one of  the common tachycardias encountered in cardiology practice.In this condition even though atria fibrillates  up to 600 times a  minute, only a fraction of that reach the ventricles. Thanks to the AV node.It acts like an electrical sink . Hence in  most  episodes of AF ,  the ventricular rate will  be   manageable and hovers   between 150-220 .We  also know ,  in the presence of  accessory AV nodal pathway there is a risk of 1:1  conduction and  result in  ventricular fibrillation and risk of sudden death. (Sudden death in WPW syndrome)

A case scenerio

The other  day  my resident called  me  to inform about a  patient with   atrial fibrillation and  hypotension    .

I told him  , to  control  the heart  rate with Amiodarone  and  I  shall come in shortly ,

He replied ,  the rhythm looked  to him  like a bradycardia  !   I  asked him to wait  , when  I went there  , it  turned out to be  an  interesting  ECG . 

This was  a  73 year old man  in our  ER with  a  syncope  .

  1. Atrial fibrillation with ventricular bardycardia

Magnified view of lead V 1 and V 2. Note the ventricular rate of 40 /mt even a the coarse f wave are recorded > 300 mt .He had a structurally normal heart .This patient has been adviced a VVI pacemaker .



While atrial  fibrillation is primarily a tachycardia , occasionally  like the  above patient  it   may present as bradycardia ! 

 How this happens ?

As mentioned before  AV node  acts like  an electrical sink .

How AV node is able to  filter out much of the  incoming impulses is not clear. This property of AV node is actually the major physiological property of AV node .This is  refered to as decremental conduction (The  faster it is bombarded with electical stmuli the longer it will take rest !)  When this filtering function  of  AV nodal tissue  is too much   we call it  pathological  AV nodal response.Some believe  ,  it is an expression of  associated   pathological  high-grade AV nodal  block .  Others belive it is simple vagotonia.

Another possibility  is  it is a sequale to  complete  AV block and what you witness is nothing but  a  junctional escape rhythm ( But here RR interval  would be fairly regular )

Excessive AV nodal blockers (Digoxin/Verapamil )  can mimic the same picture .

What is  the  relationship between sinus  node dysfunction(SND) and atrial fibrillation  ?

AF with slow ventricular response is common in elderly population with sinus node dysfunction.

AF can be associated with SND in two ways

  1. Atrial disease  and sinus node dysfunction is known  to occur  together   .  This is not surprising,  considering the close proximity they live. SA node is surrounded by  atrial tissue in its entire length and  breadth .When degenerative and infiltrative  disease of atria occur it  may trigger a simultaneous SND  ,  as well as  atrial fibrillation .
  2. While another possibility is that   AF is a default electrical response to SND . There is  some evidence  to suggest  the atria may  release a   ectopic escape rhythm  which  may  either degenerate into AF  or  mainfest a  primary  AF .

What is controlled ventricular rate and what is slow ventricular rate in AF ?

  • This aspect is not well-defined  in literature.
  • Controlled response generally  means  HR  70- 90/mt
  • Slow  ventricular response would be <60 /mt
  • Pathological bradycardia is diagnosed with  HR < 50  or at  any  symptomatic slow rhythm .
  • Holter or event monitors would help in these situations.

What is the incidence of AV nodal disease in SND ?

AV nodal disease is seen in significant population of SND.(Some series show up to 30 %) .Further ,  the incidence of  new  onset  AV block  increase   with every year of follow up ) Reversible forms are commnly due to drugs and electrolyte disorders. The AV nodal disease has another importance as they determine the selction of pacemaker  mode .SND with intact AV node function can be  managed with atrial based pacemaker ,while  ventricle must be  paced in patients with AV block or in whom the risk of AV block is high.

  Is there a clinical advantage of   having  some AV nodal disease in AF ?

It may seem so , as long as the AV nodal disease  do not lead to severe  symptomatic  CHB.A slow ventricular rate is a desirable response in patients with  angina and cardiomyopathy (especially tachycardic ). While we continue to  debate for years  about the superiority of   rhythm  control  over rate   control  ,  if the AV node  chooses to slow down by natural means  , ventricles would   welcome it with pleasure !  

Final message

Atrial fibrillation is  primarily a  tachyarrhytmia ,  occasionally it may present as  bradyarrhytmia .In this scenario one has to suspect  hidden AV nodal as well as sinus nodal dysfunction. ( This entity was also refered to as Tachy brady syndrome )   It is important to recognise this entity  because many times  dangerous bradycardias   have occurred with a single dose of  Amiodarone  bolus or  DC shock . These episodes  represent   “unmasking  effect”   of   occult AV nodal  disease.

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A man  in his 40s presented with an episode of syncope and followed by recurrent episodes of near syncope.

His ECG showed (See image)

  • ECG shows absolutely no evidence of sinus activity . That is  sinus arrest.
  • He lives by the mercy of his AV node.(“Great  escape” junctional rhythm  ! ) . Please note ,  It  fires at less than its intrinsic rate indicating AV nodal sickness as well.
  • The Heart rate is around 18/mt.

SA node is dead(Sinus arrest ) as evidenced by absent p waves. AV node is sick(Depressed) because the junctional rate is less than 20 /mt.

At what  heart rate a person  would develop syncope and near syncope ?

There is no fixed cut off rate for  syncope. It all depends upon the baseline LV function, his exercise capacity, vascular tone etc.

Most will develop some symptoms at  a heart rate less than  40/mt .

Dizziness occur and 30, syncope is sure  when hear rate  dwindles  less than 20 /mt.

A heart rate of 10-15 circulation tends to stall. But still few men are found alive at this rate.

What is the  risk of this patient dying suddenly ?

Contrary to the expectation SCD is not common in  isolated sinus node dysfunction .

It is more common with AV block. The reason being as long as the AV node is fine it will support the rhythm at least at about 30 or s0.

The cause of death in SND is extreme bradycardia induced phase dependent VT /VF.

Will you do a  EP study for him  ?

No. He  does not require it. He is symptomatic ,  and his  ECG shows  tell- tale evidence for SND with AV node depression.

So the there is not even the  necessity to assess  AV nodal status. But .one should  be aware  , there is a battery of tests for SND evaluation (SNRT, cSNRT SACT, etc*) .These are  done only when diagnosis is in doubt or for an academic purpose in teaching hospital.

What pacemaker will you use ?

  • DDDR
  • AAIR
  • VVIR

AAIR can not be used as we have evidence for AV nodal  slowing .

DDDR may be ideal.  In India we still  use VVI mode extensively . Ventricular pacing always safe when you have no EP facilities.  It makes EP study to assess AV nodal function  redundant.

* In all patients with severe bradycardia , a complete workup for systemic diseases like hypothyroidism and other chronic inflammatory pathology must be ruled out. Drug induced bradycardias can exactly mimic pathological  SND. Recognizing these entities could avoid  inappropriate pace maker implantation for  transient reversible bradycardias.

* SNRT – Sinus node recovery time. cSNRT -Corrected sinus node recovery time .SACT-Sino atrial conduction time.

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SA node is  the ultimate   power  center  of heart located in the junction of SVC and right atrium .In normal physiology  it fires  at a rate of  60 -90 /minute   that  dictates  the  ventricular rate  .

SA node is a linear  spindle shaped structure with a length of  1.5cm . The P cells with unique mitochodria  are  responsible for pace making activity  . The ion responsible for pacemaker current is mainly  calcium  with the initial 25 % push given  by  sodium current as well .  These cells are predominately under vagal control.Even though  pace making activity  is normally restricted to the SA node  , the vagal innervation is such that  the pacemaker  has a  potential to shifts it’s activity  both functionally  geographically.

In fact , there is constant flux of pacemaker activity  with  the entire length of SA node.The  cranial   aspect  SA node has more fire  power than its caudal tip . It is possible Sinus tachycardia  and sinus  bradycardia could represent  minor changes in the firing focus in its cranio-caudal axis.Further the P cells of  sinus node can spill all over the atria and even up to AV node.

What is wandering  atrial pacemaker ?

This entity is poorly defined  in literature.  With pace making cells scattered all around  there is no surprise to note dynamic pacemaker  shifts  even in healthy people. This is  especially common in young athletes.

Wandering can occur

  • Within SA node ( Shift of focus of p cell firing .No visible changes in ECG )
  • Within SA node and atria
  • Between SA node and AV node. (Sino-Junctional rhythm )

Effect on ECG

  • Baseline bradycardia.
  • Changing P wave morphology
  • Change in PR intervals
  • Intermittent absent (Rather concealed  )  P wave if  is also possible
  • RR interval can also show minor variation.

Image Modifed from http://www.eheart.org

Clinical significance of  Wandering pacemaker(WAP )

  • A Benign condition generally has no clinical significance.
  • It is often an expression of  high vagal tone.
  • Usually transient.
  • Can be unmasked by beta or calcium blockers.
  • Severe forms of wandering  pace maker can be a marker of sinus node dysfunction  and  would need  further evaluation
  • In  the coronary care units it is  associated  with infero-posterior MI when the vagal fibers are  insulted.

Differential diagnosis .

  • Some times it  need to  be differentiated form ectopic atrial rhythm /Low atrial/Coronary sinus rhythm etc .
  • Sinus  slowing  followed by a  functional escape and  reemergence of sinus beat   can be a termed as a form of wandering  pacemaker

Final message

WAP : This attractive and  descriptive ECG entity  is   largely insignificant in clinical cardiology .

It should not be confused with more dangerous cardiac arrhythmia  like sinus pauses and arrest .

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In pacemaker science ,  any pacemaker that maintains AV synchrony is often referred to as physiological pacemaker. This is  of course , a  wrong reasoning .None of the pacemakers available today can be claimed to  be completely physiological .All  pacemakers  which paces the right ventricle  induces IVS dysynchrony (Including  the modern DDD)

Single chamber physiological pacing


Paradoxically ,  the most primitive of pacemakers AAI can be the near perfect physiological  pacemaker . The simple explanation  is ,  In AAI mode , expect for the origin of pacemaker impulse the entire depolarisation and repolarisation  is through the normally existing physiological conducting system .(AV node, HIS, Purkinje etc)

(It not only has atrio ventricular synchrony but also  has ventriculo ventricular and intra ventricular synchrony )

So, technically AAIR  is most physiological pacemaker possible .But  the practical utility of such a pacemaker is limited.It can be used  only in  isolated sinus node dysfunction with intact AV conduction . (The problem is the AV nodal conduction can develop later )  To over come this DDDR pacemaker can be programmed to AAIR as a default mode.


This rate adaptive pacemaker  ,  to a  certain extent  can be termed physiological as the heart rate can improve with exercise . (Still it is unphysiological as it  paces the RV )


This is based on the concept ,  for pacing to be physiological , it  requires  atria  to be  at least sensed not necessarily paced.This mode which has a floating sensor attached to the lead as it crosses the atria.This facilitates atrial sensed ventricular pacing .But many believe  the atrial sensing is not consistent in VDD mode.Currently this mode is not popular.There is scope for improving the atrial sensor technology .

Dual chamber physiological pacing


Both  these are the prototype dual chamber physiological pacing modes.

Bi-Ventricular or triple chamber pacing  ( one atria two ventricle)   are our  elusive answers for attaining perfect physiological pacing . it need to be realized, we simply ,  can not mimic the natural cardiac  conduction system.It is  estimated to be more than 10 miles long specialized fibers .

Final message

In our quest for physiological pacemaker we often forget the fact  , AAI is the most physiological pacemaker mode  available .(It even has  VV synchrony !  )

We should use it liberally whenever possible .Of course ,we cannot use it in complete heart block .Still 50 % the  permanent pacemaker  we implant is for sinus node dysfunction. Many of them could be candidates for AAI mode .If current generation cardiac physicians feel out dated to insert a AAI pacemaker, at the least they should program the DDDR into AAI mode with a mode switching to ventricular pacing modes whenever required.

In spite of all  advantages ,  why atrial based pacemakers are not gaining popularity ?

  • Ignorance
  • Lack of expertise
  • Technical difficulty of fixing atrial  lead
  • Perceived fear of lead dis-lodgement.
  • The fact remains  the  ventricular based pacing  is always safe  in case of sudden AV block due to any reason .

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Sick sinus syndrome  or sinus node dysfunction (SSS, SND ) is one of the common cause of  symptomatic bradycardia .The other cause for  pathological bradycardia is complete heart block.Together , these two entities share 99% of indications for permanentpacemaker implantation.

The sinus node can get affected in various diseases . The commonest cause for SND is age related.This is manifested  as inappropriate bradycardia .The  other common presentation of  SND is exaggerated bradycardia to betablockers and calcium blockers.In fact , some consider drug  induced bradycardia  is  nothing but  , unmasking of underlying SND.Pathological states that result in SND include  hypothyrodism , infiltrative   and inflammatory diseases . (Surprisingly ,  ischemic  SND  is a lesser  clinical problem when considering  the  rampant CAD in our population )

What is  is a fundamental difference between SND and complete  heart block* ?

Sinus node is the proximal most pacemaker of the heart. When it fails the chances of  a  subsidiary pacemaker coming to the rescue is far greater than  a complete AV block. Further the quality and stability of the escape pacemaker is better in SND. In fact , in pure SND  ( With out AV nodal disease)  a sinus arrest is rarely fatal as escape rhythm  occur without fail.

* It should be emphasised  ,  there can be associated AV nodal disease in  significant (10%)  number of patients with SND .This may be present either at the  time of diagnosis or it can develop later in the course .This has important implication in the selection of   pacemaker .The discussion here is confined to isolated SND .

How common is ventricular escape rhythm in SND ?

It is very rare. the ventricle never gets a chance to come to the rescue as invariably junctional pacemaker takes over at times of extreme sinus pause/arrest.For the same reason , pause dependent VT (Brady dependent ) is also less common in SND .

What is  stokes Adam’s attack ? How  common it is  seen in SND  ?

It is the cardiogenic  syncope due  to extreme bradycardia. This classically occurs in complete heart block , when

the the escape rhythm becomes either very slow or temporarily goes for sleep .This results in a huge  pause (unlike sinus pause  of   , the pause  here is  ventricular pause  , this is  actually an  asystole  )  it  can  immediately trigger an VT or VF .

If  SND is not life threatening why pace maker is indicated in them ?

The pacemaker is primarily indicated for prevention of dizziness , near syncope or syncope.So primary impact is on improving quality of life  , not reduction in mortality. While in CHB  pacemakers improve  symptoms and survival.

Which form of SND can be dangerous ?

When SND is associated with rapid atrial fibrillation  some times it can trigger a VT/VT if ,  these patients also have

a fast accessory pathway with short refractory period. (<250msec)

Final message

If you have only one pacemaker at your disposal , but there are  two patients ,  one with SND and other with CHB please put the pacemaker to  the patient with CHB , even if the later has insurance coverage and the former is not .You are justified in  diverting  the pacemaker !

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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



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.


  • 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 ?


                                                              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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