Supraventricular Tachycardia

 

• Background

  Definition

  • Tachycardia due to faulty impulse formation or conduction which is sustained by tissue above the ventricle.
  • Though this technically includes AF and atrial flutter, SVT usually refers to other causes, especially atrial tachycardia, AVRT, and AVNRT.

  Classification by origin

  • Sinus tachycardia: from the SA node.
  • Atrial tachycardia: from the atrial tissue. Can be focal – as in ectopic atrial tachycardia or multifocal atrial tachycardia – or non-focal – as in AF or macro re-entrant atrial tachycardia.
  • Nodal or junctional tachycardia: from the AV node. Due to a re-entrant pathway – AVNRT, AVRT – or (rarely), due to enhanced automaticity of the node – automatic junctional rhythm.

• Signs and symptoms

  Paroxysmal tachycardia:

  • Palpitations
  • Dizzy
  • SOB
  • Chest pain

  Onset is usually sudden if re-entrant tachycardia, but more gradual if sinus tachycardia.

• Investigations

  ECG

  HR >100 bpm.

  QRS:

  • Narrow QRS complex, as there is a normal spread of depolarization through the bundle of His and bundle branches.
  • Wide QRS in WPW – except during runs of AVRT – due to the delta wave.

  P-waves:

  • Sinus tachycardia → usual positive pattern in all leads except for aVR.
  • Atrial tachycardia → inverted (ectopic atrial tachycardia), varying morphology (multifocal atrial tachycardia), sawtooth (atrial flutter), or absent (AF).
  • Junctional tachycardia → inverted, hidden within QRS, and/or following QRS.

  Echo

  • Usually normal
  • If there is LVF, then increased risk of sudden cardiac death and class 1 drugs are contraindicated.

• AV nodal re-entrant tachycardia (AVNRT)

  Pathophysiology and epidemiology

  • 25% of population have both a slow and fast pathway in the AV node and are at risk.
  • In these predisposed individuals, episodes of AVNRT occur due to premature atrial ectopic beats.
  • Between episodes, individuals are well and have a normal ECG.

  ECG

  • HR is usually >140 bpm.
  • Narrow QRS.
  • The atrial depolarisation impulse is closer to the ventricles than in sinus rhythm. Atrial and ventricular depolarisation is thus much closer or even concurrent or reversed, appearing as a reduced PR interval, a P wave within the QRS (often hidden), or a P wave after the QRS. When the P wave follows the start of the QRS, the distance between is the 'RP interval'.
  • If the P wave is visible, it is inverted, especially in the inferior leads, as atrial depolarisation spreads upwards.
  • Junctional tachycardia due to enhanced automaticity in the node may look similar, with an inverted or hidden P-wave, but is usually slightly slower at 100-130 bpm.

  Typical AVNRT (slow-fast)

  • Atrial ectopic impulse travels down slow path – while the fast is refractory from sinus rhythm – and onwards into the ventricles. As the current reaches the ventricles, it also moves back up the fast pathway – which is no longer refractory – and into the atria, leading to simultaneous atrial and ventricular contraction. The current then moves back down the slow path and a micro re-entrant loop is established.
  • Short RP interval: P wave usually hidden in QRS, or pseudo-R in V1-V2 or pseudo-S in II, III, or aVF.

  Atypical AVNRT (fast-slow)

  • Impulse goes down fast path and up slow, leading to atrial contraction after ventricular contraction.
  • Long RP interval: inverted P wave visible between QRS and T.

• AV re-entrant tachycardia (AVRT) and Wolff-Parkinson White syndrome (WPW)

  WPW pattern

  • A developmental abnormality gives rise to conductive myocardial fibres – bidirectional accessory pathways – which connect the atrium to the ipsilateral ventricle across the mitral/tricuspid annulus.
  • This can lead to pre-excitation of the ventricle, appearing as a delta wave on ECG, which is then joined by the normal depolarization wave. This does not cause problems.
  • This sign alone is the 'WPW pattern', seen in 1/500 individuals. Commoner in males.

  WPW syndrome

  WPW syndrome is when there are also symptomatic episodes of tachycardia (AVRT), due to the following mechanisms:

  • Orthodromic AVRT (95% of cases): If an atrial ectopic occurs when the accessory pathway is refractory, it will go down through the AV node and back through the now repolarized accessory pathway. Can also be caused by a ventricular ectopic.
  • Antidromic AVRT: goes the other way i.e. down accessory pathway, up AV.
  • Concealed WPW: in rare cases there is a unidirectional pathway (ventricle → atrium) and no delta-wave, but still a risk of AVRT.

  ECG

  At rest:

  • Short PR.
  • Slurred upstroke of QRS (delta wave).
  • Broad QRS

  During AVRT:

  • Orthodromic: no delta-wave, narrow QRS, and hidden or inverted P-waves.
  • Antidromic: delta-wave, broad QRS, and hidden or inverted P-waves.

  Complications

  Individuals with WPW who experience an episode of AF are at risk of developing VF and sudden cardiac death. This is rare, however, especially if asymptomatic.

• Atrial tachycardia

  Ectopic atrial tachycardia

  • Rhythm arising from an ectopic focus within the atrium.
  • ECG: P is inverted, reflecting an origin below (inversion in inferior leads) or to the right (inversion in the lateral leads) of the SA node, spreading up or to the right. Unlike in junctional tachycardias, the PR interval is normal.

  Multifocal atrial tachycardia

  • Rhythm arising from multiple ectopic foci in the atrium, with irregular conduction to ventricles.
  • Irregularly irregular RR interval and pulse.
  • Unlike in AF, distinct P waves are seen, though with multiple morphologies (at least 3), directions, and PR intervals.
  • Usually associated with COPD or HF.

  Atrial flutter

  • A type of macro re-entrant atrial tachycardia, in which large areas form a depolarisation circuit within the right atrium, discharging into the left atrium at around 300 bpm.
  • Often occurs in the context of structural heart disease or after cardiac surgery.
  • Causes 'sawtooth' F-waves on ECG instead of P waves.
  • Usually 2:1 or 4:1 conduction to the ventricle, giving HR of 150 or 75 bpm. Occasionally, conduction is irregular, causing an irregularly irregular pulse.
  • Sometimes F waves are ambiguous, so suspect atrial flutter in any ECG at 150 bpm.

• Management of SVT

  Acute treatment

  Slow the AV node while on ECG monitoring. For nodal tachycardia, this terminates the arrhythmia, and for atrial tachycardia, this aids diagnosis as the P wave morphology becomes clear. Approach:

  • First try vagal maneuvers: modified Valsalva manoeuvre or carotid sinus massage.
  • Then IV drugs: 1st-line adenosine, 2nd-line verapamil, and 3rd-line β-blocker, amiodarone, or flecainide.

  Synchronised electrical cardioversion is 1st line if haemodynamically unstable or in atrial flutter. Stable atrial flutter patients should first receive appropriate anticoagulation (unless <48h duration).

  Prevention

  Based on symptom severity and patient preference. Options:

  • Teach Valsalva: breath out forcefully with mouth and nose closed.
  • Medication if there is no pre-excitation: 1st line verapamil, propranolol, or digoxin; 2nd line flecainide, sotalol; 3rd line amiodarone, especially if structural heart disease present.
  • Medication if there is pre-excitation (WPW): flecainide if no structural disease, amiodarone or sotalol if there is structural disease. Digoxin is contraindicated.
  • Catheter ablation (under local anaesthetic) is curative. 1st line in symptomatic WPW or recurrent atrial flutter.