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A. Definition and Characteristics navigator

  1. SVT refers to paroxysmal tachyarrhythmias which require atrial or atrioventricular (AV) nodal (AVN) tissue
  2. Origin of tachycardia in or above Atrium, or in the upper AV junction (AV node or AVN)
  3. Involvement of AVN or Sinoatrial (SA) node determines classification
    1. AV nodal reentrant tachycardias (AVNRT) - most common type of reentrant SVT
    2. AV bypass tracts (missing the AVN) are also very common in SVT's
  4. Characteristics
    1. Rate > 100 bpm (usually >140 bpm) with:
    2. Narrow QRS complex in most cases
    3. May be difficult to distinguish from ventricular tachycardia with wide QRS
    4. In patients with pre-existing (or rate dependent) bundle branch block, QRS may be wide
  5. Presentation
    1. Palpitations are universal
    2. Dyspnea, light-headedness, diaphoresis, chest pain, and anxiety
    3. Symptoms may be misdiagnosed as "anxiety" disorder or panic attack [2]
    4. Evaluation of such symptoms should include and ECG and an event recorder

B. Classification
[Figure] "AV Node Conduction Pathways" navigator

  1. Usually classified by regular or irregular rhythms 2, Better classified by length of RP and PR intervals [3]
    1. Short RP (RP<PR): AVNRT, AVRT (bypass node), Junctional Tachycardias
    2. Long RP (RP>PR): Sinus Tachycardia, Sinus NRT, Ectopic Atrial Tachycardia (EAT), Junctional Tachycardias, Unusual AVNRT (antergrade fast fibers)
    3. Other: Atrial Fibrillation / Flutter, Multifocal Atrial Tachycardia, WPW
  2. Regular Rhythms
    1. Premature Atrial Contractions (PAC) - normal QRS
    2. Sinus Tachycardia: A=V rate <200 bpm
    3. Atrial Flutter - sawtooth flutter (F) wave, 300+/-30 bpm, usually includes 2:1 A-V block
    4. Wandering atrial pacemaker
  3. Normal QRS Regular SVT
    1. AVNRT
    2. AV reentry tachycardia (AVRT) - accessory concealed (anterograde) bypass tract
    3. Ectopic atrial focus (unifocal atrial tachycardia, EAT) - 5-10% of symptomatic SVT
    4. SA nodal reentry - ECG appear as sinus tachycardia; abrupt initiation and termination
  4. Accessory Pathways
    1. Usually called bypass tracts because they bypass the AV node
    2. Accessory tracts are abnormal bands of conducting tissue between atrium and ventricle
    3. ~25% of bypass tracts are capable only of retrograde conduction
    4. These retrograde tracts conduct from ventricle to atrium
  5. Ectopic Atrial Tachycardia (EAT)
    1. Single (or double) ectopic pacemakers, rate >100
    2. Multifocal: at least 3 atrial pacemakers (distinct p waves, frequent in patients with COPD)
  6. Wolff-Parkinson-White (WPW) Syndrome (see below)
  7. Irregular Tachycardias
    1. Atrial Fibrillation
    2. Atrial Flutter with variable block - irregular ventricular response rate
    3. Multifocal Atrial Tachycardia (MAT) - varying P waves and PR interval
  8. Atrial Fibrillation and Flutter
    1. These are usually considered separately from SVT's
    2. Atrial fibrillation has >450 foci/min
    3. Atrial flutter - atrial firing rate ~300/min
      [Figure] "Atrial Flutter"
    4. Ventricular responses in atrial flutter are usually regular (100, 150 or 300 bpm)

C. Sinus Tachycardia
[Figure] "Sinus Tachycardia" navigator

  1. Definition: Rate >100; Less than 150-170 beats per minute
  2. Common Causes
    1. Hypovolemia
    2. Sepsis
    3. Shortness of Breath (anxiety, hypoxia)
  3. Treatment
    1. Direct therapy at underlying cause
    2. Drug therapies are usually avoided
    3. Anti-ischemic agents may be helpful in some settings

D. Atrial Reentrant Tachycardias
[Figure] "AV Node Conduction Pathways" navigator

  1. Introduction
    1. QRS narrow in ~90% and rhythm is regular
    2. Must have two conduction pathways with differing refractory periods
    3. This allows the establishment of a circuit from the atrium back up to it
    4. In the heart, the AV node is considered to have fast and slow pathways
    5. These pathways probably involve longitudinal (fast) and transverse (slow) conduction through the same muscle fibers in the AV node
    6. Thus, the anatomic location may be the same
  2. Types
    1. AVNRT - AV nodal reentrant tachycardias (more common)
    2. AVRT - AV reentrant (retrograde or concealed bypass tract) tachycardia
    3. Note that ~5% of patients with SVT (non-AF) have ectopic atrial tachycardia
    4. Ectopic tachycardia is more common in elderly persons (P waves normal or inverted)
    5. SA nodal re-entrant tachycardias may also occur (upright P waves)
  3. AVNRT
    1. ~60% of SVT
    2. Usually initiated by a premature atrial contraction (PAC)
    3. This PAC is conducted down slow pathway (short refractory period)
    4. Fast pathway is still refractory when PAC occurs
    5. Retrograde conduction then occurs up through fast pathway causing reentry
    6. Most AVNRT's involve slow pathway conduction with retrograde fast pathway
    7. Inverted p waves are seen shortly after QRS
    8. About 1/5 of AVNRT's have opposite pathways, with delayed retrograde P' waves
  4. AVRT
    1. ~35% of SVT
    2. Majority conduct down AV Node then retrograde through bypass tract ("concealed")
    3. A bypass (or accessory) tract is an anomalous band of conducting tissue
    4. Bypass tract conduction is rapid; P waves are usually inverted, occur shortly after QRS
    5. A few involve prograde or orthrodromic bypass conduction, WPW syndrome (~2% SVT)
    6. The WPW syndrome has a very short PR interval at rest due to "pre-excitation"
  5. Treatment (see below) [1]

E. Junctional Arrhythmiasnavigator

  1. Depolarization initiates (usually high) in the AV junction.
  2. Narrow QRS with retrograde p wave buried in qrs
    1. May be found just after qrs
    2. Examination of morphology of qrs
  3. Result is 30-60 bpm rhythm (junctional node firing)
  4. Retrograde P waves may then conduct, leading to a "capture" beat
  5. For automatic junctional arrhthmias, RF ablation is preferred treatment [5]

G. Wolff-Parkinson-White Syndrome (WPW)navigator

  1. Divergent sinus node impulse travels partially down two paths
    1. AV junction and parallel rapdily conducting bypass accessory pathway
    2. Impulses travel down AV junction and up bypass tract in 90% of WPW tachycardias
    3. In 10% of the tachycardias, there is a wide complex with exaggerated delta wave
    4. This is due to impulse travelling down rapidly conducting bypass tract
    5. The impulses meet again and fuse in ventricles leading to retrograde P waves after QRS
  2. Causes
    1. Most cases are idiopathic
    2. Familial cases identified - caused by mutation in PRKAG2 gene [6]
    3. PRKAG2 codes for the gamma2 regulatory subunit of AMP-activated protein kinase (AAPK)
    4. AAPK involved in sensing AMP to ATP levels in cells
    5. Downstream targets of AAPK phosphorylation are not currently known
  3. Atrial and ventricular rates are equal
  4. Characteristic delta waves on upstroke of QRS complex
    1. This is due to premature excitation
    2. Short PR interval (<120 ms) should be present also
  5. AV nodal blocking agents should be avoided in pre-excitation syndromes
    1. These block AV node sending impluse down rapidly conducting bypass tract
    2. This leads to poor synchrony of atria and ventricles
  6. Presentation
    1. Palpitations due to SVT
    2. Shortness of breath, dyspnea on exertion
    3. Tachycardia induced dilated cardiomyopathy
    4. Cardiac dilation is often reversible if bypass tract is ablated or tachycardia terminated
    5. Relatively low frequency of ventricular fibrillation (1.85%)
    6. Spontaneous arrhythmias occur in 17%, often atrial fibrillation (AFib)
    7. Sudden cardiac death is relatively uncommon (increased in high risk patients)
  7. High Risk Patients
    1. Electrophysiologic study (EPS) to induce arrhythmias is recommended
    2. EPS induction of AV reciprocating tachycardia indicates high risk
    3. High risk patients have high rates of spontaneous ventricular tachycardia and fibrillation
    4. Children with >1 accessory pathway are at high risk
  8. Pharmacologic Therapy
    1. Type 1A or 1C agents can be used (without nodal blockade) to control rate in some patients
    2. Type 1A or 1C agents should not be used in presence of structural heart disease
    3. Magnesium IV may reverse digoxin mediated tachycardia
  9. RF-catheter ablation [4,5,8]
    1. Is the preferred modality for definitive treatment
    2. Reduces risk of arrhythmia by 92% in high risk patients (defined in EPS) >13 years old
    3. Children (5-12 years) with high risk WPW should be treated with RF-cather ablation [7]

H. Multifocal Atrial Tachycardia (MAT)navigator

  1. Often in patients with severe lung disease (60% of cases), particularly COPD flare
  2. Definition
    1. More than 3 atrial pacemakers firing AND/OR
    2. More than 3 P wave morphologies must be present
  3. Ventricular response rate usually 120-180bpm
  4. Verapamil is most effective agent but arrhythmia is difficult to control
  5. Treatment and recovery from underlying cause is best therapy
  6. RF directed partial AV nodal ablation may be used for resistant cases [5]

I. Treatment of SVT [9] navigator

  1. Overview [1]
    1. AV blockers should not be given to patients with WPW or other pre-excitation syndromes
    2. Some experts recommend initial vagal maneuver such as carotid sinus massage
    3. 90% of AVNRT and AVRT are terminated by adenosine
    4. Initial dose is 6mg adenosine IV bolus; may repeat in 5 minutes, to maximum 18mg
    5. Diltiazem, verapamil, or ß-blockers may be used intravenously
    6. In recurrent SVT, calcium or ß-blockers are first line, then class IC or III antiarrhythmics
    7. Patients with intermittent SVT can be considered for "pill in pocket" - taking diltiazem or verapamil, ß-blockers, or flecainide or propafenone at symptom onset
    8. Catheter directed radiofrequency (RF) ablation is preferred treatment in recurrent SVT, particularly in young, active persons [4,5]
  2. Adenosine (Adenocard®)
    1. Rapid action on AV node to block conduction
    2. Drug of choice for diagnosis and treatment of some SVT's
    3. Dose is 6mg-12mg iv push
    4. Aminophylline (250mg iv bolus) is given as an antidote if complete heart block occurs
    5. Contraindicated in heart transplant; use with caution in patients with bronchospasm
  3. Diltiazem (Cardizem®, others)
    1. Excellent SA / AV nodal blockade with effective rate slowing within minutes
    2. Less negatively inotropic than verapamil and ß-blockers
    3. Dose is 15-25mg iv depending on weight, slow iv push; may repeat
    4. Hypotension can occur; calcium gluconate iv can reduce hypotension somewhat
  4. ß-Blocking Agents (see above)
    1. Esmolol iv (short half life), large fluid bolus
    2. Metoprolol 2.5-5mg iv may also be used acutely
    3. Chronic therapy with metoprolol or atenolol often effective
  5. Verapamil (Calan®; Isoptin SR®)
    1. Potent slowing of SA/AV conduction
    2. Strongly anti-inotropic with most patients developing significant hypotension
    3. Calcium gluconate iv can reduce hypotension
  6. Electrical Cardioversion - mainly for emergent cases (hemodynamic instability)
  7. Digoxin (Lanoxin®, others)
    1. Positive inotropic activity (see above)
    2. Mild to moderate rate reducing activity due to cholinergic (vagotonic) activity
    3. Intravenous loading (0.25-0.5mg iv) initially for rate control
    4. Requires 1-6 hours for activity
  8. Class IC or III Agents
    1. Class IC agents flecainide or propafenone in patients without coronary disease
    2. Flecainide dose is 100-300mg daily; negative inotropic effects
    3. Propafenone dose is 450-900mg daily
    4. Class III agents amiodarone or sotalol are alternatives if Class IC not tolerated
    5. Amiodarone dose is 200mg daily
    6. Sotalol dose is 160-320mg daily
  9. Radiofrequency Ablation
    1. Localization of slow pathway of AV node or to bypass tract (or ectopic focus)
    2. RF ablation near coronary sinus ostium (slow pathway) preferred over fast pathway
    3. RF ablation preferred for junctional tachycardias and for inappropriate tachycardias
    4. Transvenous electrode catheter delivers radiofrequency to specific area
    5. Although this is an expensive proceedure, it is cost effective [10]
    6. Partial or total AV nodal ablation for rate control in resistant cases [5]
    7. AVN ablation requires pacemaker implantation
    8. Appears that RF ablation improves quality of life better than anti-arrhythmic therapy

References navigator

  1. Delacretaz E. 2006. NEJM. 354(10):1039 abstract
  2. Lessmeier TJ, Gamperling D, Johnson-Liddon V, et al. 1997. Arch Intern Med. 157(5):537 abstract
  3. Pieper SJ and Stanton MS. 1995. Mayo Clin Proc. 70:371 abstract
  4. Kay GN and Plumb VJ. 1996. Am J Med. 100(3):344 abstract
  5. Morady F. 1999. NEJM. 340(7):534 abstract
  6. Gollob MH, Green MS, Tang ASL, et al. 2001. NEJM. 344(24):1823 abstract
  7. Pappone C, Manguso F, Santinelli R, et al. 2004. NEJM. 351(12):1197 abstract
  8. Pappone C, Santinelli V, Manguso F, et al. 2003. NEJM. 349(19):1803 abstract
  9. Agents To Slow the Heart Rate. 1996. Med Let. 38(982):75
  10. Cheg CHF, Sanders GD, Hlatky MA, et al. 2000. Ann Intern Med. 133(11):864