Paroxysmal supraventricular tachycardia (PSVT) is a type of supraventricular tachycardia, named for its intermittent episodes of abrupt onset and termination. Often people have no symptoms. Otherwise symptoms may include palpitations, feeling lightheaded, sweating, shortness of breath, and chest pain. The cause is not known. Risk factors include alcohol, psychostimulants such as caffeine, nicotine, and amphetamines, psychological stress, and Wolff-Parkinson-White syndrome, which often is inherited. The underlying mechanism typically involves an accessory pathway that results in re-entry. Diagnosis is typically by an electrocardiogram (ECG) which shows narrow QRS complexes and a fast heart rhythm typically between 150 and 240 beats per minute. Vagal maneuvers, such as the Valsalva maneuver, are often used as the initial treatment. If not effective and the person has a normal blood pressure the medication adenosine may be tried. If adenosine is not effective a calcium channel blocker or beta blocker may be used. Otherwise synchronized cardioversion is the treatment. Future episodes can be prevented by catheter ablation. About 2.3 per 1000 people have paroxysmal supraventricular tachycardia. Problems typically begin in those 12 to 45 years old. Women are more often affected than men. Outcomes are generally good in those who otherwise have a normal heart. An ultrasound of the heart may be done to rule out underlying heart problems.
Signs and symptoms Symptoms may include palpitations, feeling faint, sweating, shortness of breath, and chest pain. Episodes start and end suddenly.
Types AV nodal re-entrant tachycardia (AVNRT) makes up 56% of cases Atrioventricular reentrant tachycardia (AVRT) makes up 27% of cases Wolff-Parkinson-White syndrome Paroxysmal atrial tachycardia makes up 17% of cases
Anatomy Paroxysmal supraventricular tachycardia is a type of arrhythmia that originates in the atrioventricular (AV) junction. The most common underlying anatomical cause of PSVT is atrioventricular nodal reentry, which accounts for more than half of the cases. The underlying anatomical causes of PSVT, specifically atrioventricular nodal reentry, involve the presence of two functionally distinct conduction pathways within the AV node and the formation of a reentrant circuit that sustains the tachycardia. These pathways within the AV node are known as the fast pathway and the slow pathway. The AV node is the structure that controls how electrical signals travel between the upper chambers (atria) and lower chambers (ventricles). During normal sinus rhythm, these signals pass through only one pathway, known as the fast pathway. The fast pathway conducts signals quickly but has a longer rest period before it can send another signal. However, in people with PSVT caused by atrioventricular nodal reentry, both the fast and the slow pathways are activated. The slow pathway conducts signals more slowly but has a shorter rest period. In a healthy heart during normal sinus rhythm, only either the fast pathway or the slow pathway is used at any given moment for conducting electrical signals through the AV node, not both simultaneously. During PSVT episodes, an irregular heartbeat is triggered by an early electrical signal from one of the atria. This premature signal enters both pathways simultaneously. It encounters no problem traveling along the slow pathway because its conduction speed matches up well with this specific arrhythmia type. However, it faces difficulty passing through effectively down the faster path since it takes slightly longer for that path to be ready following the conduction of a recent signal. At this point, if retrograde or backward flow overcomes the forward movement's pace in the fast pathway, then unwanted feedback further intensifies the rapid heartbeat until something intervenes to stop the episode. There is currently no solid understanding on what stops the episode in PSVT.
Treatment Treatment depends on the type of heart rhythm shown on an electrocardiogram test, and the stability of the patient's blood circulation. If a patient has low blood pressure, difficulty breathing, chest pain, shock, or confusion, they are considered unstable and must have an electrocardiogram result checked to determine if the heart is beating normally. If this is not the case, cardioversion, which uses electricity to reset the heartbeat, should be performed urgently. If an electrocardiogram shows that the high heart rate is caused by something other than PSVT itself (such as a reduction in blood flow to the heart), injections of drugs called beta-blockers may help. The same medication can also be used if someone is found to be unstable due to inappropriate sinus tachycardia (a fast but unexplained normal heartbeat). AV nodal blocking can be achieved in at least three ways:
Physical maneuvers A number of physical maneuvers increase the resistance of the AV node to transmit impulses (AV nodal block), principally through activation of the parasympathetic nervous system, conducted to the heart by the vagus nerve. These manipulations are collectively referred to as vagal maneuvers. The Valsalva maneuver should be the first vagal maneuver tried and works by increasing intra-thoracic pressure and affecting baroreceptors (pressure sensors) within the arch of the aorta. It is carried out by asking the patient to hold his/her breath while trying to exhale forcibly as if straining during a bowel movement. Holding the nose and exhaling against the obstruction has a similar effect. Pressing down gently on the top of closed eyes may also bring heartbeat back to normal rhythm for some people with atrial or supraventricular tachycardia (SVT). This is known as the oculocardiac reflex. A 2023 review confirms the success of the Valsalva maneuver as a non-pharmaceutical intervention in PSVT.
Medications
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