SVT

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SVT

• PREARED BY DR. AKRAM SAADEH
• Discussed BY DR ALI AL HALABI

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SVT

• Divided into 3 categories
• 1.re-entrant tachy. Using an accessory pathway.
• 2.re-entrant tachy. Without an accessory pathway.
• 3.ectopic or automatic tachy.
• 1. Is the most common mechanism of SVT in
  infants ,with an increasing incidence of AV nodal
  re-entery noted in child.

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• Tachy. Is initiated by a premature atrial beat
  that is most often conducted to the ventricle
  through the normal AV NODAL Ppathway (orthodromic
  conduction).
• Atrial and junctional ectopic tachycardias are
  more commonly associated with abnormal hearts
  (e.g cardiomyopathy ) or with postoperative
  congenital heart disease.

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Clinical Manifestations

• Re-entrant SVT is characterized by an abrupt
  onset and cessation , it may be precipitated by
  an acute infection and usually occurs when the
  patient is at rest .
• Attacks may last only a few seconds or may
  persist for hours .

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Clinical Manifestations

• The only complaint may be awareness of the rapid
  heart rate .
• Many children tolerate these episodes extremely
  well and it is unlikely that short paroxysms are
  a danger to life .
• Precordial discomfort and heart failure may
  supervene.

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Clinical Manifestations

• In young infants ,the diagnosis may be more
  obscure because of the inability to communicate
  their symptoms.
• Infants with SVT are often initially seen in
  heart failure because the tachycardia goes
  unrecognized for a long time .
• The heart rate during paroxysms is frequently in
  the range of 200-300 beats/min .

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Clinical Manifestations

• If the attack lasts 6-24 hr or more with an
  extremely fast heart rate , the infant may become
  acutely ill, have an ashen color , and be
  restless and irritable.
• Tachypnea and hepatomegaly .
• Fever and leukocytosis.
• Tachycardia occurs in the fetus.

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Clinical Manifestations

• In neonates, SVT is usually manifested as narrow
  QRS complex (lt0.08 sec). The P wave is visible on
  a standard electocardiogram in only 50-60 of
  neonates with SVT .
• If the rate is greater than 230 beats/min with an
  abnormal P-wave axis (a normal P wave is positive
  in leads I and aVF) , SVT is more likely .
• The heart rate in SVT also tends to be unvarying.

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Clinical Manifestations

• Differentiation from ventricular tachycardia is
  critical .
• The absence of ventricular to- atrial conduction
  (and thus only intermittent p waves), the
  presence of fusion beats , and wide QRS complexes
  that are dissimilar to the QRS complex during
  sinus rhythm are diagnostic of ventricular
  tachycardia .

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Clinical Manifestations

• AV re-entrant tachycardia uses a bypass tract
  that may either be able to conduct antegrade
  (Wolff- Parkinson-White WPW syndrome) or remain
  concealed .
• Patients with WPW syndrome have a small, but real
  risk of sudden death .
• The patient is at risk for atrial fibrillation
  begetting ventricular fibrillation .

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Clinical Manifestations

• Concurrently , any patient with syncope and WPW
  syndrome should have an electrophysiology study
  performed .
• These features include a short P-R interval and
  slow upstroke of the QRS (delta wave).
• When rapid anterograde conduction occurs through
  the pre existation pathway during tachycardia
  and the retrograde re-entry pathway to the atrium
  is via the AV node , the tachycardia complexes
  are wide and the potential for more serious
  arrhythmias is greater especially if atrial
  fibrillation occurs.

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Clinical Manifestations

• AV nodal re-entrant tachycardia involves the use
  of two pathways within the AV node .
• This arrhythmias is more commonly seen in
  adolescence .
• It is one of the few SVTs that is frequently
  associated with syncope .
• This arrhythmia is usually amenable to
  antiarrhythmic therapy such as digoxin or
  propranolol or to radiofrequency ablation
  therapy.

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Treatment

• Vagal stimulation-
• Vagotonic maneuvers such as the Valsalva
  maneuver , straining, breath holding, drinking
  ice water, or adopting a particular posture .
• Pharmacologic alternative -
• -Adenosine .
• -Phynylephrine or edrophonium .
• -Quinidine, procainamide, and propranolol.
• -Verapamile.
• Synchronized DC cardioversion.

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Treatment

• Maintenance therapy In patients without an
  antegrade accessory pathway, digoxin or
  propranolol is the mainstay of therapy .
• In patients with resistant tachycardias,
  procainamide, quinidine, flecainide, propafenone,
  sotalol, and amiodarone have all been used .
• If cardiac failure occurs because of prolonged
  tachycardia , cardiac function usually returns to
  normal after sinus rhythm is re-instituted .
• 
  
  
  
  

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Treatment

• Twenty-four hour electrocardiographic (Holter)
  recordings are useful in monitoring the course of
  therapy and in detecting brief runs of
  asymptomatic tachycardia .
• More detailed electrophysiologic studies
  performed in the cardiac catheterization
  laboratory are often indicated in patients with
  refractory SVTs.

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Treatment

• The tachyarrythmia can be induced by pacing and
  different pharmacologic agents can be tested for
  their ability to inhibit the arrythmia.
• These studies are necessary prerequisites to
  radiofrequency ablation .

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Treatment

• Radiofrequency ablation In patients with
  reentrant rhythms , it is often used electively
  in older children and teenagers, as well as for
  patients in whom multiple agents are required or
  drug side effects are intolerable or when
  arrhythmia control is poor .
• The overall initial success rate ranges from
  approximately 80 to 95 depending on the
  location of the bypass tract or tracts .
• Surgical ablation of bypass tracts can also be
  successful in selected patients.

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Atrial ectopic tachy.

• Uncommon.
• Variable P wave .seldom more than 200
• Identifiable P waves with an abnormal axis
• Chronicity(sustained or intermittent)
• Single automatic focus
• Identification of this mechanism by ECG while
  initiating vagal stimulation or therapy.

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Atrial ectopic tachy

• Re-entry tachy. Break suddenly
• Automatic tachy. Slow down then speed up again.
• Rx difficult to control.
• cath. ablation

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Choatic or multifocal atrial tachy

• 3 or more ectopic P with with different ectopic
  P-P cycles,freq. Blocked P and varying P-R
  intervals.
• Often in infants.
• Association with myocarditis.
• Rx uneffective.
• Terminates by 3 yr.

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JET(Acc. Junc. ectopic Tachy.)

• Non-re-entry arr. In which the junc. Rate exceeds
  the sinus node and AV dissociation results.
• Early postop.,or digitalis toxicity.
• Extremely difficult to control.
• Often disappear spontinuously.
• In the absence of surgery carries amore gaurded
  prognosis.

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JET(Acc. Junc. ectopic Tachy.)

• Rx reduce catecholamine infusion
• D/C digoxin
• IV amiodarone
• Chronic Rx amiodarone,or sotalol

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Atrial flutter

• Intra-atrial re-entrant tachy.
• Regular or irregularly irregular
  tachy.characterized by atrial activity at arate
  of 250-400.
• Due to re-entrant or circus rhythm originating in
  the atria and involving a micro-re-entrant loop
  within the atrial tissue and some form of
  anatomic obstacle that crea

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Atrial flutter

• Because the AV node cannot transmit such rapid
  impulses,some degree of AV blockis always
  present,and the ventricles respond to every 2-4
  atrial beats.
• Occasionally the response is variable and the
  rhythm appers regular.
• Older childrenCHD
• Neonatesnormal hearts
• May occur in inf. Illness,large stretched atria ,
  Ebstein anomaly, rheumatic mitral stenosis,or
  after atrial surgery.

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Atrial flutter

• Vagal stimulation or adenosine produce temporary
  slowing.
• Dx rapid regular atrial saw- toothed flutter
• Rx DC shock
• anticoagulation
• digitalis then quinidine or procaineamide
  added
• amiodarone and sotalol

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Atrial flutter

• Vagal stimulation or adenosine produce temporary
  slowing.
• Dx rapid regular atrial saw- toothed flutter
• Rx DC shock
• anticoagulation
• digitalis then quinidine or procaineamide
  added
• amiodarone and sotalol

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Atrial flutter

• Rx radiofreq. And ablation.
• Neonates who respond to digoxin may be Rx byfor
  6-12 mo.

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Atrial fibrillation

• Atrial excitation is choatic and more rapid
  300-700 and produces an irregulary irregular
  ventricular response and pulse

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Atrial fibrillation

• Most often the result of achronically stretched
  atrial myocardium.
• Most frequently in older children with rheumatic
  mitral valve dis.
• As a complication of intra-atrial surgery
• ,left atrial enlargmentdue to left AV valve
  insufficiency,
• WPW,
• thyrotoxicosis
• pul. Emboli,
• and pericarditis.or famililal

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Atrial fibrillation

• Rxdigitalis.(not in WPW).
• Quinidine ,procainamide or DC shock.
• Anticoagulaton.