Supraventricular Tachycardia

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Supraventricular tachycardia’ (SVT)

Supraventricular Tachycardia

  • These are usually associated with a narrow QRS complex and are characterised by a re-entry circuit or automatic focus involving the atria.
  • The term SVT is misleading, as in many cases the ventricles also form part of the re-entry circuit, such as in patients with AV re-entrant tachycardia.

Atrioventricular nodal re-entranttachycardia (AVNRT)

  • This is due to re-entry in a circuit involving the AV node and its two right atrial input pathways: a superior ‘fast’ pathway and an inferior ‘slow’ pathway
  • This produces a regular tachycardia with a rate of 120–240/min.
  • It tends to occur in hearts that are otherwise normal
  • Episodes may last from a few seconds to many hours.
  • The patient is usually aware of a fast heart beat and may feel faint or breathless.
  • Polyuria, mainly due to the release of atrial natriuretic peptide, is sometimes a feature, and cardiac pain or heart failure may occur if there is coexisting structural heart disease.
  • The ECG usually shows a tachycardia with normal QRS complexes but occasionally there may be rate-dependent bundle branch block

Management

  • Treatment is not always necessary. However, an episode may be terminated by carotid sinus pressure or other measures that increase vagal tone (e.g. Valsalvamanœuvre).
  • Intravenous adenosine or verapamil will restore sinus rhythm in most cases.
  •  Suitable alternative drugs include β-blockersor flecainide.
  • In rare cases when there is severe haemodynamic compromise, the tachycardia should be terminated by DC cardioversion

Wolff–Parkinson–White syndromeand Atrioventricular re-entranttachycardia (AVRT)

In these conditions, an abnormal band of conducting tissue connects the atria and ventricles. It resembles Purkinje tissue in that it conducts very rapidly, and is known as an accessory pathway

Manifest accessory pathway VS Concealed accessory pathway

  • In around half of cases, this pathway only conducts in the retrograde direction (from ventricles to atria) and thus does not alter the appearance of the ECG in sinus rhythm. This is known as a concealed accessory pathway.
  • In the remainder, conduction takes place partly through the AV node and partly through the accessory pathway. Premature acti- vation of ventricular tissue via the pathway produces a short PR interval and a ‘slurring’ of the QRS com- plex, called a delta wave This is known as a manifest accessory pathway.

AV node re-entrant tachycardia vs WPW syndrome

As the AV node and accessory pathway have different conduction speeds and refractory periods, a re-entry circuit can develop, causing tachycardia; when this is associated with symptoms, the condition is known as Wolff– Parkinson–White syndrome.

  • AV node re-entrant tachycardia.
    • The mechanism of AVNRT occurs via two right atrial AV nodal input pathways: the slow (S) and fast (F) pathways.
    • Antegrade conduction occurs via the slow pathway; the wavefront enters the AV node and passes into the ventricles, at the same time re-entering the atria via the fast pathway
  • WPW syndrome
    • In WPW syndrome there is a strip of accessory conducting tissue that allows electricity to bypass the AV node and spread from the atria to the ventricles rapidly and without delay.
    • When the ventricles are depolarised through the AV node the ECG is normal, but when the ventricles are depolarised through the accessory conducting tissue the ECG shows a very short PR interval and a broad QRS complex

 

The ECG appearance of this tachycardia may be indistinguishable from that of AVNRT .

3 ECG appearences

Sinus rhythm.

  • In sinus rhythm the ventricles are depolarised through (1) the AV node and (2) the         accessory pathway, producing an ECG with a short PR interval and broadened                 QRS complexes; the characteristic slurring of the upstroke of the QRS complex                 is known as a delta wave.

Orthodromic tachycardia.

    • This is the most common form of tachycardia in WPW.
    • The re-entry circuit passes antegradely through the AV node and retrogradely               through the accessory pathway.
    • The ventricles are therefore depolarised in the normal way, producing a narrow-          complex tachycardia that is indistinguishable from other forms of SVT.

Atrial fibrillation.

  • In this rhythm the ventricles are largely depolarised through the accessory   pathway, producing an irregular broad-complex tachycardia which is often more          rapid.

Clinical presentation and treatment

  • Carotid sinus pressure or intra- venous adenosine can terminate the tachycardia. If atrial fibrillation occurs, it may produce a dangerously rapid ventricular rate because the accessory pathway lacks the rate-limiting properties of the AVnode .This is known as pre-excited atrial fibrillation and may cause collapse, syncope and even death.
  • It should be treated as an emergency, usually with DC cardioversion.
  • Catheter ablation is first-line treatment in symptomatic patients and is nearly always curative.
  • Prophylactic anti-arrhythmic drugs, such as flecainide, propafenone or amiodarone, can also be used. These slow the conduction rate and prolong the refractory period of the accessory pathway.
  • Digoxin and verapamil shorten the refractory period of the accessory pathway and should be avoided.


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