These arrhythmias are common in otherwise healthy individuals and may be debilitating, because of their unpredictable occurrence and speed during daily life, but are generally not life threatening.
There are two common types which account for more than 90 % of SVTs. These are AV node junctional reentrant tachycardia (AVJRT) and those due to an accessory or additional electrical connection between the atria and ventricles (Wolff-Parkinson-White syndrome). And there are other, much rarer, types.
The basic mechanism which causes this and many other heart arrhythmias is called ‘re-entry’. After a heart beat occurs there is time when the heart cannot beat again as it is recharging itself (absolute refractory period), then there is a period when a particularly vigorous electrical impulse can initiate a heartbeat (relative refractory period) followed by normal electrical function.
The electrical function of the heart is different in different areas. When there are areas with different electrical function close to each other, the normal even conduction of electrical impulses can be disrupted, especially if a normal beat is followed by an extra beat coming from another area of the heart or ectopic beat. The ectopic beat precipitates re-entry via the slower pathway.
In AVJRT the re-entry occurs in and around the AV node. Drugs which slow conduction such as beta-blockers or calcium channel blockers can be used to treat it but acutely we give a naturally occurring substance, adenosine, which shows electrical activity throughout the heart briefly stopping the rhythm and allowing normal rhythm to resume. As in all heart arrythmias we can use an external electrical shock to reset the heart’s rhythm (cardioversion) but this is not usually needed in SVT. This arrhythmia is readily cured by an electrical ablation procedure which eliminates the slow pathway and therefore the re-entry circuit.
In normal subjects the only way electrical impulses travel from atria to ventricles is via the AV node but in SVT due to an accessory A-V connection there is an alternative way for electrical impulses to travel from atria to the ventricles. This accessory connection may be obvious on the resting ECG but in other cases is not obvious or ‘concealed’. Conduction can be much more rapid via the accessory pathway than through the AV node (up to 250/min) and this can be dangerous, as atrial fibrillation can lead to ventricular fibrillation when the pathway is able to conduct from atrium to ventricles.
Treatment of this is similar to AVJRT but can be more urgent if the patient is compromised. Curing this arrhythmia involves finding the location of the accessory pathways as they may be multiple and then ablating them using high frequency alternating current applied by special catheters under a general anaesthetic or sedation.