Paroxysmal supraventricular tachycardia is a regular heart rate pattern, originating from the anatomical location which if found above the ventricles, namely in the atrial space. This deviation from the normal ventricular heart rate has a sudden beginning and end, with the heart rate ranging between 160-220 bpm.
PSVT symptomatology depends on the general medical status of a patient and their heart rate. Patients with heart conditions or other types of diseases do exhibit severer symptomatology than otherwise healthy individuals. Some remain asymptomatic.
Symptoms arise abruptly and may resolve by themselves, lasting from a few minutes to 1-2 days. The fast heartbeat does not allow for the full amount of blood to accumulate in the ventricle; in this way, less than the required blood is forwarded to the rest of the body and the heart loses its proper functionality. The symptoms described below are those displayed when the heartbeat reaches the levels of 140-250 bpm:
A detailed medical and surgical history, including PSVT-related symptomatology, habits and medications is the first step towards a successful diagnosis. Physical examination should center around the heart and other organs that could account for the same clinical manifestations (eg. lungs).
Other tests that can be carried out to confirm the diagnosis of PSVT and to determine the most appropriate treatment scheme include an electrocardiogram (ECG), an echocardiogram (ECHO), a stress test, electrophysiologic studies, coronary angiography and blood tests.
Electrocardiogram (ECG): The ECG is the first step towards diagnosing any type of arrhythmia and sometimes may also provide a clue toward its causes, primarily when there is an underlying heart disease. PSVT is easy to observe on a 12-lead ECG strip, when the test is carried out at the time that an individual is experiencing tachycardic symptomatology. In some cases, further tests or even therapeutic schemes depend on the results of the ECG .
Ambulatory ECG: A basic disadvantage of ECG is that one can observe real-time irregularities; once the heart rate is restored to normal, the ECG strip will also produce normal results. Since PSVT has a sudden onset and equally sudden resolution, ambulatory monitoring is required in order to monitor the heart continually over a period of time (1-2 days). A Holter monitor  is continuously worn by the patient, who will also be required to keep a diary at the same time, to allow their physician to diagnose any irregularities on the ECG results during times when the patient is symptomatic.
Echocardiogram (ECHO): The echo is capable of depicting the heart walls and valves and also detects the left ventricle's pumping capacity. It is used to identify structural problems in the heart, valves, or muscles. However, an echocardiogram is mostly reserved for patients with irregular SVT's.
Stress test: The stress test helps to identify a potential coronary heart disease, monitoring a patient both at rest and while exercising. Since coronary heart disease hinders blood flow through the arteries due to the accumulation of fat deposits, it can cause abnormal heart rhythms. This test is carried out in patients with a possible PSVT caused by stress and for other conditions, such as myocardial ischemia. The stress test does not provide the physician with a positive or negative result, but needs to be evaluated together with a detailed medical history, clinical examination and further tests.
Cardiac catheterization and coronary angiography: When stress test results are pathologic or the patient experiences chest pain, shortness of breath, or fainting, they are candidates for cardiac catheterization under local anesthesia. Angiography can detect arterial obstruction and damage to the arteries or valves, with the use of dye. It is performed on patients with a high risk of coronary heart disease or severe symptomatology, due to its invasiveness and potential subsequent complications.
Electrophysiologic study: This test utilizes pacemaker electrodes placed intracardially to monitor electrical activity. Electrodes are placed via a catheter that accesses the heart via the veins under local anesthesia. This test is rarely performed in patients with PSVT and may be required in cases of patients with profound symptomatology and little response to treatment or in cases of kown pathologic electrical pathways.
Lab tests: Blood tests can exclude thyroid disease and can also detect heart muscle damage due to infarction, by measuring certain enzymes. Urine and blood tests can also be carried out to identify drugs or illegal substances, possibly responsible for a rapid heartbeat.
Instances of PSVT can be treated either medicinally or with simple tactics that patients can learn to carry out on their own and can be employed in their everyday lives. Tactics aim at the stimulation of the vagus nerve, which is known to reduce an increased heart rate, and include:
It is important that these tactics are most beneficial if they are employed just after an arrhythmia is first experienced.
There are, however, some cases when a patient should seek medical help for an arrhythmic episode. These cases include:
In such occasions, an arrhythmia can be stopped by administering adenosine or verapamil (IV). In some rare occasions, drugs fail to control an arrhythmia and cardioversion may be required .
Prevention of an arrhythmic attack poses certain challenges. Patients who experience frequent or severe episodes are usually candidates for radiofrequency ablation: an electrical current is delivered through an catheter inserted in the heart. In this way tissue producing paroxysmal supraventricular tachycardia is permanently destroyed. As an alternative to radiofrequency ablation, nearly any antiarrhythmic drug can also be used, including beta-blockers, digoxin, diltiazem, verapamil, propafenone, and flecainide  .
However, paroxysmal SVT can lead to heart failure, ischemia, pulmonary edema, or infarction; complications such as there are mainly reserved for patients with inadequate left ventricular output . A study has shown that 1/3 of SVT patients experienced a syncoptic event or required medical intervention to stop the tachycardia . Persistent SVT can also lead to cardiomyopathy.
On the other hand, patients with WPW syndrome do have a slight risk of sudden death. If the syndrome is complicated by atrial fibrillation or flutter on the grounds of an extra electrical pathway with increased conductibility, it is possible that they will go into cardiac arrest. This phenomenon is quite rare and is most of the times observed in patients who have already experienced symptoms due to the syndrome. Another possibility is sudden death without any prior indication of WPW; however the frequency of this phenomenon is unknown.
In the absence of Wolf-Parkinson-White syndrom, the risk of PSVT-induced sudden death is very small.
Most of the times, supraventricular tachycardia is accompanied by no other symptomatology. Nevertheless, it may be linked to a wide variety of other diseases, such as  :
Heart and vessel conditions:
PSVT may also develop on the grounds of digitalis, asthma treatment with relative drugs, or cold remedies. There are also patients who do not meet any of the aforementioned criteria, in which case PSVT causes remain unclear.
PSVT is the most frequent arrhythmia in infants, children, and women during the course of pregnancy.
PSVT features an incidence of approximately 1-3 per 1000 persons and a subsequent prevalence of 0.2%. Of the supraventricular arrhythmias, atrial fibrillation is the most frequently observed one, affecting 3 million people in the United States, with prevalence of 0.4-1%. Researchers expect atrial fibrillation to be affecting more than 7.5 million individuals by 2050  .
Atrial tachycardia is a condition originating either from the atrium or from adjacent regions, such as the superior vena cava or the pulmonary veins. It is the least frequent and difficult to treat arrhythmia amongst the regular supraventricular tachycardias.
The initiation of an arrhythmia is primarily rendered possible due to the atrial anatomy and the ability of many types of cardiac cells to produce electrical impulses. Electrophysiological testing has identified 3 possible mechanisms responsible for PSVT:
Atrial cardial cells found in the crista terminalis and pulmonary veins, are the regions usually responsible for automaticity or triggered activity. Once these cells start producing impulses faster than the sinoatrial node, they dominate heartbeat control, causing an abnormal heart function. On the other hand, signals can pathologically return to the atrium because of a coexistent disease, tissue scarring or medications, through the mitral and tricuspid annuli, pulmonary veins, orifices of the vena cava and coronary sinus.
In people with no coexistent heart disease, the mechanism most often involved cause is increased automaticity from a single atrial region. It usually arises due to elevated catecholamine levels, relapses of chronic lung disease, alcohol abuse and electrolyte imbalances. Heart rate tends to remain at less than 200 beats per minute, it follows an accelerated pattern and displays a certain fluctuation in each beat during warm-up. Beats eventually slow down and, in contradistinction to re-entry mechanisms, no premature atrial beat triggers the tachycardia. Automatic atrial tachycardia is usually persistent, especially in children.
On the other hand, patients with coexistent heart disease or those who have undergone cardiac surgery, usually experience PSVT as a result of signal re-entry. Surgical scars may constitute a signal blockage, in which case heart cells find a different path in order to conduct electricity. Conduction in one pathway is usually slow, and the other pathway provides unhindered conductibility, initiated by a premature beat; this results in tachycardic phenomena. This mechanism is responsible for the sudden onset and end.
Triggered activity usually causes atrial tachyarrhythmia in cardiomyopathy patients who are under treatment with digoxin. The abnormality often lasts long and is challenging to treat. Triggered activity tachycardias feature a warm-up period (beginning) and a cool-down period (end), devoid of the sudden onset and resolution of phenomena caused by re-entry. Atrial tachycardias caused by digoxin toxicity are usually accompanied by an atrioventricular block.
The heart utilizes its electrical conductibility in order to produce each heartbeat and generate the blood flow necessary for the body to function. The simplest way to understand the heart's functionality, is to consider it an electrical, two-stage pump. Under normal circumstances, specific cells located in the sinoatrial node (found in the right atrium) produce the first electrical signal, the frequency of which determines the heartbeat rate. This signal is transmitted to the whole atrial muscle; the latter contracts in order to push blood forward to the ventricles. The electrical impulse is then conducted to the atrioventricular node, which essentially connects the atrium and ventricle. The atrioventricular node (AV node) determines when the signal will eventually be transmitted to the ventricles, causing them to pump the blood into the aorta. In order to accomplish this, the AV node slightly delays signal transmission to the ventricles, allowing them to fill with the proper amount of blood.
Paroxysmal supraventricular tachycardia (PSVT) is a heart condition which causes irregular electricity transmission, resulting in faster contraction of the atrium and subsequently, of the ventricles, as the two of them are connected via the chain effect. This phenomenon occurs intermittently, often resolving without intervention. It can have a duration of seconds, or even hours.
One possible mechanism resulting in PSVT involves defective electrical structures of the AV node. Healthy individuals feature only one transmission pathway from the atrioventricular node and signal travels exclusively to the ventricles. In PSVT patients, however, one of the possible mechanisms involves a dual pathway, through which electrical impulses can return to the atrium, where they were originally produced, causing faster heartbeats.
Any heartbeat pattern that does not follow the normal electrical transmission pathway described above is classified as an arrhythmia, including abnormalities in rate or the signal production site. During the past years, electrophysiologic studies have made the accurate classification of all arrhythmias possible, including supraventricular tachycardia (SVT), with intracardiac studies labelling the mechanisms responsible for the generation of the tachyarrhythmia. Because of the anatomic region that produces the arrhythmia (or dysrhythmia), SVT is classified as a "supraventricular" arrhythmia, namely originating from a location other than the ventricles. Supraventricular arrhythmias can either be atrial or AV arrhythmias. Another possible classification of the arrhythmias is achieved by dividing them into conditions with regular or irregular rhythms  .
Atrial tachyarrhythmias (originating from the atrium) include the following:
AV tachyarrhythmias (originating from the atrioventricular node) include the following:
Paroxysmal supraventricular tachycardia (PSVT) is a condition involving episodes of fast heartbeat originating in the section of the heart which is located just above the ventricles. "Paroxysmal" is used to convey the meaning of periodical.
In healthy individuals the muscles of the different heart sections (atria and ventricles) follow a coordinated contraction.
Risk factors for PSVT include:
Symptoms have a characteristical abrupt start and ending, with a duration of minutes or even hours. Symptoms can potentially include:
Other symptoms that can occur with this condition:
The first step towards a diagnosis is the physical exam. This will show a faster than normal heart rate, ranging from 100 to even 250 beats per minute. Very high heart rate is a characteristic finding in children. Pulses in the neck may also be observable, alongside other symptoms related to poor circulation (dizziness, pallor).
An ECG conducted while one is having an attack will show PSVT. An electrophysiological study (EPS) may be required for a definite diagnosis and in order to plan the most succesful treatment scheme.
Because PSVT is an intermittent phenomenon, patients may need to wear a Holter monitor for 24 hours in order to diagnose it, or another device for longer periods of time.
A Holter monitor records cardiac electrical activity. During the 24-hour period that the patient wears it, they also keep a diary with their activities. The diary helps the physician decide whether any abnormal heart rate seen on the Holter monitor is indicative of a disease, or can be traced to normal situations that alter any person's heart rate suddenly (fear, anxiety etc).
PSVT that arises solely sporadically may not require intervention if you don't have symptoms or other conditions.
You may attempt the following maneuvers to stop a rapid heartbeat during an episode of PSVT:
Failure of the above means that a patient requires some type of medical intervention to decrease the heartbeat, which may include:
Long-term treatment for patients with frequent episodes of PSVT or a coexistent heart condition, may include:
Surgical treatment is also an option, primarily for people who have a coexistent heart condition for which they need surgery as well. Surgery aims at destroying abnormal electrical pathways that cause rapid heart rates.