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Posts Tagged ‘VPD’

Sinus node is the electrical high command of our heart .When it gets injured  seriously (or shot down   as in sinus arrest ) there is utter chaos in the lower ranks !

This is what happened  in this patient .

trigeminy group beating vpds sinus node dysfunction escape capture

The lower pacemkers can either passively release  themselves as escape rhythm or actively fire with a  ectopic focus  . Any combination of escape / ectopic  beats can  occur .If occasional sinus beats capture the ventricles things  can become further complicated .

It is obvious , this  random intra-cardiac  shooting  makes the life of the  myocardium miserable . It is a perfect setting for syncope, tachcyardic cardio myopathy , extreme brady induced VT , VF  even SCD.

*Meanwhile , It is  heartening to note  SND   rarely lead to  sudden death in spite of all the chaos .However  extreme  bradycardias  that occur in  complete heart block  does  not enjoy this immunity as fatal complications are common if not intervened .

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What will be the pulse rate in a patient who has ventricular bigeminy in ECG with a heart rate of 90 ( 45 sinus beats 45 VPDS/minute ) ?

A.Exactly Same as HR , ie 90/mt

 B.Exactly half of HR , ie  45/mt

C.Can be anything between 45 to 90/mt

D.Any of the above can be true

 The  answer is D . 

I have  noted  ,this simple question in cardiology resident examinations cause great anxiety among students .

Why is it difficult to arrive at an easy answer to this question ?

Traditionally , ventricular ectopic beat were also called extrasystole , implying every ectopic beat shall produce a peripheral pulse .Since ,  we learnt this is not true , we started refering them as VPDs.(Simple ventricular depolarisation which may or may not have a mechanical activity ) So , in a patient whose alternate beat is a VPD  , things become little complicated.

What determines a VPD to acquire  mechanical  energy  or simply  remain as an  electrical event ?

  •  Timing of the VPD* .
  • LV residual volume(LVEDV ) at the onset of  VPD
  • Force of contractility of LV( Of course ,  it is directly related to LVEDV)
  • Temporal relation to  aortic valve opening**

If  the VPD is too early or too late it can not have a mechanical activity . It should be optimally timed midway between two sinus beat to have a good mechnically active VPD. Some refer this as an interpolated VPD .Here, the VPD  becomes a  true extra systole for that individual. So , in patient with ventricualr bigeminy in ECG the pulse rate is usually half , can be same as HR when the coupling interval is optimal or it can be totally irregular as someof the  VPDS gain a mechanical activity and some do not (as often occurs multifocal VPDs. )

* Among the above  four factors timing of the VPDS is the most crucial as it can influence all the other three factors.

** Whatever be the timing or force of contraction aortic valve should be opened to generate a pulse wave. If for some reason this does not happen  there can be intermittent mechanial activity what  we refer to as pulse deficit .

Read a related phenomenon:  Ventricular  paired pacing

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Ventricular ectopic beats are the most common cardiac electrical abnormality for which cardiologist’s consultation is sought.VPDs are one of most benign observations in ECG and  and almost every  heart experiences it. In 24 hour holter recordings it was reported up to 25% of healthy  individuals .

In spite of this ,  the fear of  noting a VPD in a given tracing of ECG is genuine both for the patient and his physician.This is because  VPDs  can be  a forerunner of dangerous ventricular arrhythmias.

  • VPDs are often graded according to the count and morphology and frequency.(Lown’s ,Bigger’s grading)
  • VPDs that occur in single are less fearsome.( It may not be so . . .)
  • VPDs in couplets and  triplets raise considerable anxiety.( Again it need not be . . .)
  • A series of VPD lasting for 30 seconds is called non sustained ventricular tachycardia(NSVT)
  • If it exceeds 30second it called sustained VT.
  • VT may remain as VT in many.
  • VT may degenerate into VF  ventricular fibrillation in minority( ie cardiac arrest)

The importance of VPDs do not lie  in the number ,  morphology or frequency  but most importantly  in  the underlying etiology. If it occurs in a structurally normal heart it is largely benign.

New onset VPDs should be investigated thoroughly. The commonest symptom is palpitation.

vpd ectopic

Friendly VPDs : Some of  situations where VPDs are  commonly observed and has little significance are.

  • Exercise induced VPDs
  • Pregnancy induced VPDs  (PIH /Peripartum DCM are  rare possibilities)
  • Thyroid associated VPDs
  • Alcohol /Smoke related

What are the VPDs that could be clinically  important ?

VPDs with chest pain(Ischemic etiology )

VPDs in patients with dyspnea.(CHF , COPD)

Drug induced VPDs(Digoxin etc)

Renal failure associated VPDs

VPDs due to hypoxia/Hypokalemia

In patients with pre existing heart disease.(Congenital, valvular, myocardial disease)

What prevents a non sustained VT from becoming sustained ?

No one really knows the answer.Most of the NSVT self terminates.A healthy heart some how gets the capacity to self terminate the arrhythmia.The normal  LV  fails to sustain the abnormal electrical circuit . A diseased heart may not be able to do so . Further if there is electrolyte abnormality (low potassium), or lack of oxygen it may maintain a VT.

What are the most dangerous forms of VPDs ?

  • VPDs that occur during  acute coronary syndrome.
  • VPDs associated with cardiomyopathy( Ischemic , nonischmic,)
  • Some forms of primary electrical disorders of heart( Brugada syndrome, ARVD , CMVT etc)

How do you investigate patients with VPDs?

General medical work up in all.

Echocardiogram is usually necessary in most.

Holter monitoring in occasionally.

Coroanry angiogram rarely

Electrophysiological study in high risk category

How do you manage  patients with VPDs?

  1. Generally do not require any specific drugs in vast majority of individuals .
  2. Reassurance is the key
  3. Ask them to avoid potential triggers like smoke, alcohol, coffee, tea and related bevarages.
  4. If palpitation is troublesome beta blockers( Propronolol, Atenolol, metoprolol can be used.)
  5. Anxiolytic may also be given.

*If the patient has  systemic disorder like hyperthyroidsm , anemia  or underlying heart disease he has to get the specific treatment.

Caution:It has become fashionable for the physicians  to use powerful antiarrhythmic drugs like amiodarone (Cordarone) liberally in patients with asymptomatic VPDs with structurally normal hearts.this practice must be absolutely avoided as amiodarone is one of most toxic  cardiac drugs known  with great pro arrhythmic activity.

When to refer a patient with VPD to a electrophysiologist ?

Physicians   can  treat   most of these patients. But the following will require EP consultations

  • Patients with syncope
  • Patient who have LV dysfunction(Low ejection fraction EF%)
  • Has had an episode of ventricular tachycardia
  • Cardiac arrest

What will the Electrophysiologist  do ?

These patients will be evaluated for inducibility of VT/VF and if the LV function is poor (EF<30%  MADIT 2 criteria ) many would receive implantable cardivertor defibrillator(ICD) or life long anti arrhythmic  drugs.

Some times radiofrequency (RF ablation)  waves are used to ablate the focus of VT.This is possible only if it occurs close to endocardium as  intracardiac catheters do not have access to epicardial  focus. Among  ICD and RF ablation later could be preferred whenever feasible as it eliminates the arrhythmia , while  the former only tackles it only after it occurs .( Hence ICDs  , even though a technological marvel can not be labelled as curative ! )

Final message

VPDs are the   most common cardiac arrhythmia .Most of them are benign. Few of them require extensive investigation.

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Ectopic beats or premature depolarisations are the commonest  cardiac arrhythmia encountered . Human heart , is a  non stop  electro mechanical organ ,  and it is not surprising   ectopic beats are so common  and can literally originate  from every cell of heart. But , generally it   emanates  primarily from  the special conducting cells . At times  ,  even  other cells (Myocytes, interstitial cells )  can generate abnormal electrical potential.These ectopic electrical potentials  can be compared  to  electrical load shedding when there is excess electrical strain .

Vast  majority of ectopic are benign  in human population. When this occurs ,  in the milieu of underlying heart disease or during ischemic  episodes they become clinically important and initiate a sustained arrhythmia.

Classically and traditionally ectopic beats are described in the

A.Ventricle :      Ventricular premature beats, (VPD)

B.Atrium:             Atrial premature beats(APD)

C.AV junction : Junctional premature beats.(JPD)

If you note , one important structure is missing from the list.

Yes , it is  SA node.  Can it result in premature depolarisation ?

When do you suspect a SPD(Sinus premature depolarisation)

  • It manifests a  an sudden unexpected , sinus beat exactly as the previous sinus beat. Followed by a pause.
  • The P wave morphology exactly is similar to prior p wave.
  • Many times we miss this entity as we tend to over  diagnose APD than SPD.
  • SPDs tend to occur in bigeminy rhythm.

Differential diagnosis

  • Sinus arrhythmia and pause
  • APD
  • SA node echo beats (Part of SA node reentry)
  • SA blocks

How do differentiate  a sinus arrhythmia from sinus premature depolarisation (SPD ) ?

Sinus arrhythmia occurs in a baseline bradycardia environment.

It does not not come as   “on -off ” pattern . It has a gradual onset offset dynamics.

Clinical significance

This is a clinically unimportant arrhythmia* .This  is probably the reason , it is not a popular concept .

*But it can confound in the diagnosis of  , other important rhythm  disorders.it could be a expression of  sinus node dysfunction and a precursor of  inappropriate  sinus tachycardia The significance could be substantial in atrial triggered  based  pace maker rhythm

Final message

When you confront an unexpected , early , sinus beat not accountable to sinus  arrhythmia  or APD

suspect SPD.It is  not rare , it is a  grossly under diagnosed entity.

Reference

Sinus premature systole  http://www.chestjournal.org/content/64/1/111.full.pdf?ck=nck

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Pulse deficit is a clinical sign wherein , one is able to find a difference in count between heart beat (Apical beat or Heart sounds ) and  peripheral pulse .This occurs even as the heart is  contracting , the pulse is not reaching the periphery.This can occur in few clinical situations .

1 . Atrial fibrillation.

2. Very early diastolic  ventricular  ectopic beats

3. Some patients with Pacemaker.

The mechanism is  , the ventricular contractions are  too weak and unable to open the aortic valve  , but at the same time they are good enough to close the mitral valve. To open the aortic valve it has to generate atleast 60-80 mmhg pressure , while mitral valve closes even  as LV generates  8-14mmhg  .(LV/LA pressure cross over). So intermitently the  second heart sound  is missed while S1 is retained,  producing more heart sounds and less pulse count in the periphery. The S1 is either felt or heard at the apex but the corresponding pulse is missing . Further , this intermittent absence of  S2  results in totally irregular S1 /S 2 relation.

Why some of the contractions of LV is too weak to open the aortic valve ?

Because the RR interval varies , the ventricular filling also varies , diastole duration is constantly changing some of the diastole are too short  and LV hardly gets filled , as the LV force of contraction is directly decided by the LVEDV and LV  fibre length these contractions are too weak. 

Other published studies

There has been some doppler observations ,where there is a midventricular LV blood flow reversal in atrial fibrillation that could  explain the pulse deficit . Mechanism of production of pulse deficit in atrial fibrillation: assessment by blood flow dynamics

Second Department of Internal Medicine, Kagoshima University School of Medicine.

 http://www.ncbi.nlm.nih.gov/pubmed/3221309

What is the clinical significance of pulse deficit ?

                                  Currently there is no great clinical significance of this phenomenon. But an astute clinician will pick up this sign and it may indicate underlying LV dysfunction. In patients with PPM,  pulse deficit  suggests  pacemaker malfunction .Some patients with cardiac tamponade &  pulsus paradoxus  systolic  blood pressure falls too low to make the pulse feeble or not palpable in the periphery .This situation may mimic a pulse deficit if not recognised.

 Dr.S.Venkatesan ,Madras Medical College , Chennai, India

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