Regular narrow-complex tachycardias | Medibuddy
5th May 2025

Regular narrow-complex tachycardias

For patients who are haemodynamically stable and have a regular narrow-complex tachycardia, follow the steps below:

  1. Attempt vagal manoeuvres. This can be sufficient to cardiovert the patient back to sinus rhythm.
  2. If unsuccessful and there is no evidence of a pre-excitation syndrome (e.g. WPW), give adenosine under direct ECG monitoring. The doses are 6mg rapid IV bolus, then 12mg if unsuccessful, then 18mg if unsuccessful.
  3. If unsuccessful, give verapamil or beta-blocker (metoprolol is the drug of choice in acute situations due to its fast onset of action)
  4. If ineffective, attempt DC cardioversion as above (note atrial flutter is unlikely to chemically cardiovert and will often need DC cardioversion if treatment of underlying causes is unsuccessful).

Patients with a pre-excitation syndrome such as Wolff-Parkinson-White should not be given digoxin or verapamil, as these can provoke fatal arrhythmias through blockade of the SA node, encouraging conduction down the aberrant pathway.. If cardioversion is unsuccessful, patients should be referred for consideration of radio-frequency ablation of their aberrant conduction pathway.

Class Mechanism
Class 1 Inhibits fast Na+ channels during depolarisation, reducing depolarisation and conduction velocity. Membrane stabilisers
Class 1a

e.g. quinidine, procainamide

Prolonged action potential duration by reducing the excitability of non-nodal regions of the heart during phase 0 depolarisation
Class 1b

e.g. lignocaine, phenytoin

Reduce action potential duration by decreasing the rate of spontaneous phase 4 in myocardial cells (reduces automaticity)
Class 1c

e.g. flecainide, encainide

Potent Na+ channel blockers – little effect on duration of action potential in ventricular myocardium, shortens action potential in Purkinje fibres. Decreases speed of conduction of cardiac impulses.
Class 2 (beta-blockers)

e.g. metoprolol, esmolol

Decrease rate of depolarisation and increase effective refractory period of AV node & decreased automaticity, decreased QT duration. Decreases heart rate and oxygen consumption.
Class 3

e.g. amiodarone, sotalol

Inhibit K+ channels to prolong the refractory period, cardiac depolarisation and action potential duration. Effectively decreases the amount of time cardiac cells are excitable.

Note amiodarone has some class 1, 2, 3 and 4 effects.

Class 4 (calcium-channel block)

e.g. verapamil, diltiazem, nifedipine

Inhibit slow Ca2+ channels – slow calcium ion currents may contribute towards development of VT. Block L-type Ca2+ channels to impair SA node pacemaker activity. Decrease duration of action potential but no effect on automaticity.

Table 4: Vaughan-Williams classification of anti-arrhythmic drugs.

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