36. Forms and consequences of paroxysmal tachycardia

General

A paroxysmal tachycardia is a tachycardia which begins and ends suddenly and violently. Most of these are supraventricular, meaning that the stimulus originates at above the level of the ventricle.

We distinguish three types of paroxysmal supraventricular tachycardias:

  • Atrioventricular re-entry tachycardia (AVRT)
  • Atrioventricular nodal re-entry tachycardia (AVNRT)
  • Atrial tachycardia

We distinguish two types of paroxysmal ventricular tachycardias:

  • Ventricular tachycardia
  • Torsade-de-pointes

Supraventricular and ventricular tachycardias can be differentiated by looking at the response of carotid massage. Supraventricular tachycardias should have their frequency decreased by carotid massage, while ventricular tachycardias don’t.

Clinical features:

Episodes of paroxysmal supraventricular tachycardia cause symptoms like palpitations, dizziness, chest pain, dyspnoea and potentially syncope.

Treatment:

Haemodynamically unstable patients may require cardioversion. Haemodynamically stable patients can be treated with carotid massage or can perform the Valsalva manoeuvre.

Patients with identifiable accessory conducting fibres can have these fibres burnt off with catheter ablation.

Re-entry

Re-entry is an important mechanism in paroxysmal tachycardias. Not all conducting fibres in the conducting system of the heart has the same properties; some have higher conduction speed than others, and some have longer refractory period than others. This creates the basis for a re-entry circuit.

In a re-entry circuit an extrasystole occurs at a specific time, which causes the action potential to go in an endless cycle, essentially producing a new pacemaker that excites tissues around it.

This re-entry circuit can exist entirely within the AV node. In this case it’s called micro re-entry. If the re-entry circuit involves an accessory conducting fibre (like the bundle of Kent), it’s called macro re-entry.

The re-entry circuit most commonly lies between the atria and ventricles, so the four chambers of the heart contract almost simultaneously.

The reason a re-entry circuit develops is hard to explain in words. This video explains it better than I could:

https://www.teachingmedicine.com/Lesson.aspx?l_id=133

Atrioventricular re-entry tachycardia

AVRT is a macro re-entry, so for it to develop an accessory conducting fibre between the atria and ventricles must be present. Because of this, they’re most commonly associated with the pre-excitation syndrome WPW. A supraventricular extrasystole is necessary to trigger AVRT.

We distinguish two types of AVRT:

  • Orthodromic AVRT
  • Antidromic AVRT

Orthodromic AVRT is the type that’s usually seen in WPW.

Pathomechanism:

In orthodromic AVRT the stimulus is conducted in anterograde direction (down) through the AV node and in retrograde direction (up) through the accessory fibre. The ventricles will be depolarized normally, so the QRS will be normal.

In antidromic AVRT the stimulus is conducted in retrograde direction (up) through the AV node and in anterograde direction (down) through the accessory fibre. The ventricles will not be depolarized normally, so the QRS will be wide.

ECG morphology:

  • Tachycardia
  • P-wave can be before, inside or after QRS
  • In orthodromic AVRT – QRS is normal
  • In antidromic AVRT – QRS is wide (> 120 ms)

Antidromic AVRT can be difficult to differentiate from ventricular tachycardia.

Atrioventricular nodal re-entry tachycardia

AVNRT is a micro re-entry, meaning that it develops within the AV node. It develops because some conducting fibres in the AV node have different conduction speed and refractory period than others. A supraventricular extrasystole is necessary to trigger AVNRT.

ECG morphology:

  • Tachycardia
  • P-wave can be before, inside or after QRS
  • Negative P-wave in leads II, III, aVF
  • QRS complex is normal
Atrial tachycardia

In atrial tachycardia the atria are stimulated by a heterotopic focus inside the atria, most commonly due to re-entry. It can occur in people with healthy hearts. The heterotopic focus often requires time to “warm-up”, so tachycardia takes some time to develop.

ECG morphology:

  • The P-wave morphology is abnormal
  • Frequency is between 100 – 250/min
  • QRS complex normal
Ventricular tachycardia

Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia that originates from the ventricles. A re-entry circuit lies in the background. It’s often initiated by a ventricular extrasystole.

As the atria and ventricles are beating asynchronously ventricular filling is impaired. As the ventricles are contracting with such high frequency (100 – 250/min) the contractions are no longer haemodynamically significant. The result is that the cardiac output decreases significantly.

Ventricular tachycardia can progress into ventricular flutter or fibrillation.

Etiology:

  • Ischaemic heart disease
  • Cardiomyopathy
  • Long QT syndrome
  • Electrolyte abnormalities
    • Hypokalaemia
    • Hyperkalaemia

Classification:

  • Based on duration
    • Non-sustained – stops within 30 seconds
    • Sustained – lasts more than 30 seconds
  • Based on QRS morphology
    • Monomorphic – only one heterotopic focus, all QRS look similar
    • Polymorphic – more than one heterotopic focus, all QRS look different
      • Torsade de pointes

ECG morphology:

  • Wide QRS complexes
  • Ventricular frequency 100 – 250/min

Torsade de pointes:

Torsade de pointes (TdP) is a type of polymorphic ventricular tachycardia. The QRS axis changes continuously, giving the ECG an irregular spindle-like morphology.

Treatment:

Cardioversion or defibrillation should be performed.


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35. Pre-excitation syndromes

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37. Signs of chronic or acute overload in the ECG (hypertrophy, strain)

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