Supraventricular tachycardia

Supraventricular tachycardia is an arrhythmia with a mechanism involving at least one atrium and/or the atrioventricular node



Parts of the heart’s physiology

Tachycardia is a generic term meaning that the heart is beating too quickly. It is the opposite of bradycardia, where the heart beats too slowly.

Too quickly relative to what?

The heart normally beats at a variable rate that suits the needs of the body. This rate may go down to 45–50 beats per minute (bpm) at rest, or even less in very athletic patients or in those on heart-slowing treatment, and may rise to 150 bpm or even up to 200 bpm in young people, often when taking part in very intense activity. This is all perfectly normal.

The “normal” heart rhythm is determined by an area of the heart, a small bundle of cells located in the right atrium, called the “sinus node”. The sinus node receives messages from the whole body, allowing it to dictate the ideal heart rate to the heart, that allows it to provide an adequate flow rate for optimal blood flow to the organs according to their needs.

The sinus node delivers “electrochemical” pulses at a variable rate that suits the needs of the body. It acts a bit like the conductor of an orchestra. The electrochemical message delivered with each pulse of the sinus node spreads to the whole heart muscle via routes that could be likened to electrical circuits. This message circulates very quickly so as to activate all the heart cells at the same time.

This allows all the heart cells to contract in synchrony; first of all in the atria, then in the ventricles.

There is in fact a “filter” between the atria and ventricles called the “atrioventricular node”, or “AV node”, which induces a phase shift between the contraction of the atria and that of the ventricles. This phase shift allows the atria to contract first of all and fill the ventricles, which will then contract once filled.

Classification of tachycardia

Tachycardia is normally classified into 2 groups according to the anatomical origin

  • “Ventricular tachycardia”, which, as the name suggests, is tachycardia that originates in the ventricles.
  • “Supraventricular tachycardia”, which originates above the ventricles, namely:

Either from the atria (e.g. atrial tachycardia, atrial fibrillation, atrial flutter)

Or the junction between the atria and the ventricles – this is known as junctional tachycardia: AV-nodal reciprocating tachycardia (AVNRT) or atrioventricular reciprocating tachycardia (sometimes called Wolff-Parkinson-White syndrome)

Beyond this anatomical classification, tachycardia is differentiated according to its mechanisms, of which there are 2:

  • “Automatic” tachycardia: the mechanism consists of one or more foci of cells that inappropriately discharge regular and rapid electrical pulses. For example: Focal atrial tachycardia, Atrial fibrillation
  • “Reciprocating” tachycardia: in this case there is “looping” electrical activation often caused by the presence of an area of cells in the heart which short-circuits the normal electrical pathway. For example: Atrial flutter: when we talk about “common” flutter (the most common), the short circuit is the cavotricuspid isthmus, an anatomical area located between the right atrium and the right ventricle. In the event of “atypical” flutter, it can even be a different area.

AV-nodal reciprocating tachycardia (AVNRT): the short circuit is the slow pathway, a bundle of cells located in the AV node. This is sometimes referred to as Bouveret-Hoffmann syndrome.
Atrioventricular reciprocating tachycardia: the short circuit is the accessory pathway, often called the bundle of Kent, which is a supernumerary connection. This is sometimes called Wolff-Parkinson-White syndrome.


Most of the time, no cause is found in patients with SVT. We refer to this as SVT in a healthy heart, it is most often the case.

However, it is customary to carry out a basic assessment of cardiac morphology (at least an echocardiography) because in rare cases an associated heart disease is found, which must be thoroughly investigated.


It is commonly said that SVT does not threaten the patient’s life. This is true in the vast majority of cases. The main complications that SVT patients are exposed to are:

  • Discomfort associated with palpitations
  • Experiencing dizziness or loss of consciousness during or after an episode
  • Onset of shortness of breath or dyspnoea secondary to heart failure, if the episode is rapid and lasting
  • Appearance of a clot in the heart which can then be ejected into the bloodstream and create an embolism (cerebral => stroke or other). This complication is encountered only in special cases: in cases of atrial fibrillation, atrial flutter or atrial tachycardia, and in high-risk patients.


The only way to diagnose SVT with certainty is to carry out an electrocardiogram (ECG) at the moment when an episode is occurring. The problem is that most of the time, patients who visit the cardiologist are not experiencing an episode and the electrocardiogram is usually normal, except in rare cases when it can provide guidance.

We can therefore use various diagnostic tools, including:

ECG during an episode: in the event of an episode, do not hesitate to visit your cardiologist or the emergency department to undergo an electrocardiogram during an episode, which will allow a diagnosis (please remember to take a copy of the emergency ECG trace to your cardiologist)
24 or 48-hours loop recorder: This is a small, portable device that automatically records your heart’s activity over 24 or 48 hours, allowing your doctor to examine your heart rhythm more closely.

Event recorder: When you experience symptoms, you press a button and a short ECG recording is carried out. The recorder, which can be used for several weeks, allows your doctor to see your heart rhythm at the moment your symptoms occur.
Exercise ECG: This test uses an ECG to record your heart’s electrical activity while you are walking on a treadmill or pedalling on an exercise bike. It can help determine whether exercise triggers your palpitations.
Implantable loop recorder: when the intervals between episodes are long and we are unable to obtain a trace using the above tests, we may suggest the implantation of a subcutaneous Holter, which is a kind of electronic chip that is implanted under the skin at chest level in front of the heart in a operating theatre (the procedure is carried out on an outpatient basis under local anaesthesia and takes around ten minutes). This chip makes it possible to record the heart’s activity for around 3 years and is easily controlled using specific machines used by heart rhythm specialists. Note that this chip can be very easily removed (always in an operating theatre) at any time.

Electrophysiology study (EP study): This is a procedure carried out in an operating theatre, usually on an outpatient basis, under local anaesthetic and sedation. It consists of placing recording leads directly in the heart to allow more precise tests to be carried out and to try to trigger episodes by stimulating the heart and recording its internal electrical activity. This investigation is not painful. In some cases, depending on the diagnosis, it allows the tachycardia to be treated immediately afterwards by burning ( = catheter ablation) using heat (radiofrequency ablation) or by cold (cryoablation).


2 strategies can be considered for treating SVT. These strategies will be discussed with your cardiologist depending on the type of SVT, your symptoms, and the frequency of your episodes.


This strategy involves leaving the focus or arrhythmogenic circuit in place.

Several options can then be offered to the patient:

Therapeutic abstention and education: this strategy does not prevent episodes from occurring, and no long-term treatment is offered. In some cases we can teach the patient certain manoeuvres capable of stopping the attacks (but not preventing them from occurring), such as in Bouveret-Hoffmann syndrome (in which case we teach them the Valsava manoeuvre), or we prescribe a treatment capable of stopping the attacks. This treatment would only be taken during an episode and takes a certain amount of time to take effect (generally around 1 hour).

Preventive drug treatment: this strategy involves prevent new episodes from occurring by administering long-term antiarrhythmia treatment, the aim of which is to “put to sleep” the focus of the diseased heart cells without destroying it. This strategy may be effective in some patients. Its disadvantage is that it requires long-term treatment and patients therefore run the risk of experiencing side effects of these treatments (fatigue and bradycardia, often in young people). It’s also not effective in 100% of cases.


This strategy aims to cure tachycardia permanently by “getting rid” of the diseased focus or short-circuit. This is done using a procedure called “ablation”.


The term catheter ablation is actually incorrect because strictly speaking, nothing is removed.

Instead, the term ablation means “burning” the diseased areas of the heart responsible for tachycardia. These are micro burns that can either be done using heat (radiofrequency ablation) or cold (cryoablation).

This procedure is most often performed during a short outpatient visit: the patient arrives at the hospital in the morning and leaves in the afternoon.

Most of the time it requires a local anaesthetic (general anaesthetic in rare cases), which is why each patient must have a consultation with an anaesthetist before this procedure.

The ablation procedure is performed without any skin incision, simply by performing infusions (under local anaesthetic) into a large vein located in the crease of the thigh, called the femoral vein. More rarely, an arterial puncture may be necessary in the femoral artery. Through these infusions, we place small leads in the heart, guided by a fluoroscopy device (= x-ray). These leads, once positioned in the heart, allow direct recording of the electrical circuits, to trigger tachycardia, if necessary, and to carry out ablation of the affected areas

The advantage of this procedure is that it usually allows a permanent cure for tachycardia with a very high success rate (greater than 90–95% for common flutters, Bouveret-Hoffman syndrome and accessory pathways, Wolff-Parkinson-White syndrome, and slightly lower for other types of tachycardia) and above all the possibility of stopping all treatment. Very rarely, in the event of recurrence, it may be necessary to carry out an additional, second procedure.

The disadvantage of this procedure is the risk of complication, which is nevertheless very low and depends on the type of tachycardia. Examples include:

Bruising at the puncture site (by far the most common complication, which occurs in around 5% of cases)
Recurrent tachycardia with the need for a second procedure.

Risk of injury to the main electrical pathway (= risk of complete atrioventricular block), which would require implantation of a pacemaker: very rare, around 0.5 out of 100 cases and only present in very specific cases where the ablation carried out is located near the main electrical circuit of the heart (bundle of His). This risk is encountered in the case of Bouveret-Hoffman syndrome (AV-nodal reciprocating tachycardia) and particularly in the case of “parahissian” accessory pathways. It is in these cases that we can offer the patient cold treatment (cryoablation), which is a little less effective but carries less risk.
Risk of pericardial effusion, very rare (1/1000). Pericardial effusion means the presence of fluid (usually blood) around the heart, which can impair the relaxation of the heart and require drainage.
Risks associated with anaesthesia.