Paroxysmal supraventricular tachycardia (PSVT) is an intermittent arrhythmia that is characterized by a sudden onset and offset and a regular ventricular response. Epi­sodes may last from a few seconds to several hours or lon­ger. PSVT often occurs in patients without structural heart disease.

The most common mechanism for PSVT is reen­try, which may be initiated or terminated by a fortuitously timed atrial or ventricular premature beat. The reentrant circuit usually involves dual pathways (a slow and a fast pathway) within the AV node; this is referred to as AV nodal reentrant tachycardia (AVNRT)

and accounts for 60% of cases of PSVT. Less commonly (30% of cases), reen­try is due to an accessory pathway between the atria and ventricles, referred to as atrioventricular reciprocating tachycardia (AVRT).


Symptoms most often start and stop suddenly. They can last for a few minutes or several hours. Symptoms may include:

  • Anxiety
  • Chest tightness
  • Palpitations (a sensation of feeling the heartbeat), often with an irregular or fast rate (racing)
  • Rapid pulse
  • Shortness of breath

Other symptoms that can occur with this condition include:

  • Dizziness
  • Fainting

Exams and Tests

A physical exam during a PSVT episode will show a rapid heart rate. It may also show forceful pulses in the neck.

The heart rate may be over 100, and even more than 250 beats per minute (bpm). In children, the heart rate tends to be very high. There may be signs of poor blood circulation such as lightheadedness. Between episodes of PSVT, the heart rate is normal (60 to 100 bpm).

An ECG during symptoms shows PSVT. An electrophysiology study (EPS) may be needed for an accurate diagnosis and to find the best treatment.

Because PSVT comes and goes, to diagnose it people may need to wear a 24-hour Holter monitor. For longer periods of time, another tape of the rhythm recording device may be used.


AV nodal blocking agents are the medications of choice as first-line medical therapy. Beta-blockers or non-dihydropyridine calcium channel blockers, such as diltiazem and verapamil, are typically used first. Patients who do not respond to agents that increase refractoriness of the AV node may be treated with antiarrhythmics. The class Ic agents (flecainide, propafenone) can be used in patients without underlying structural heart disease. In patients with evidence of structural heart disease, class III agents, such as sotalol or amiodarone, should be used because of the lower incidence of ventricular proarrhythmiaduring long-term therapy.


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