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Abnormally fast heart rhythm
These abnormal rhythms start from either the atria or atrioventricular node. Diagnosis is typically by electrocardiogram (ECG), Holter monitor, or event monitor. A normal resting heart rate is 60 to 100 beats per minute. A resting heart rate of more than 100 beats per minute is defined as a tachycardia. During an episode of SVT, the heart beats about 150 to 220 times per minute. Specific treatment depends on the type of SVT Atrial fibrillation affects about 25 per 1000 people, paroxysmal supraventricular tachycardia 2.3 per 1000, Wolff Parkinson White syndrome 2 per 1000, and atrial flutter 0.8 per 1000.

The main pumping chamber, the ventricle, is protected (to a certain extent) against excessively high rates arising from the supraventricular areas by a "gating mechanism" at the atrioventricular node, which allows only a proportion of the fast impulses to pass through to the ventricles. An accessory "bypass tract" can avoid the AV node and its protection so that the fast rate may be directly transmitted to the ventricles. This situation has characteristic findings on ECG. A congenital heart lesion, Ebstein's anomaly, is most commonly associated with supraventricular tachycardia.

Subtypes of SVT can often be distinguished by their electrocardiogram (ECG) characteristics. Most have a narrow QRS complex, although, occasionally, electrical conduction abnormalities may produce a wide QRS complex that may mimic ventricular tachycardia (VT). In the clinical setting, the distinction between narrow and wide complex tachycardia (supraventricular vs. ventricular) is fundamental since they are treated differently. In addition, ventricular tachycardia can quickly degenerate into ventricular fibrillation and death and merits different consideration. In the less common situation in which a wide complex tachycardia may be supraventricular, a number of algorithms have been devised to assist in distinguishing between them. In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin. Sinus tachycardia is physiologic when a reasonable stimulus, such as the catecholamine surge associated with fright, stress, or physical activity, provokes the tachycardia. It is identical to a normal sinus rhythm, except for its faster rate (>100 beats per minute in adults). However, sinus tachycardia is considered part of the diagnoses included in SVT by most sources. Sinoatrial node reentrant tachycardia (SANRT) is caused by a reentry circuit localised to the SA node, resulting in a P wave of normal shape and size (morphology) that falls before a regular, narrow QRS complex. It cannot be distinguished electrocardiographically from sinus tachycardia unless the sudden onset is observed (or recorded on a continuous monitoring device). It may sometimes be distinguished by its prompt response to vagal maneuvers. Ectopic (unifocal) atrial tachycardia arises from an independent focus within the atria, distinguished by a consistent P wave of abnormal shape and/or size that falls before a narrow, regular QRS complex. It can be caused by automaticity, which means that some cardiac muscle cells, which have the primordial (primitive, inborn, inherent) ability to generate electrical impulses that are common to all cardiac muscle cells, have established themselves as a 'rhythm center' with a natural rate of electrical discharge that is faster than the normal SA node. Some atrial tachycardias, rather than being a result of increased automaticity may be a result of a micro reentrant circuit (defined by some as less than 2 cm in longest diameter to distinguish it from macro reentrant atrial flutter). Still other atrial tachycardias may be due to triggered activity caused by after depolarizations. Multifocal atrial tachycardia (MAT) is tachycardia arising from at least three ectopic foci within the atria, distinguished by P waves of at least three different morphologies that all fall before irregular, narrow QRS complexes. This rhythm is most commonly seen in elderly people with COPD. Atrial fibrillation meets the definition of SVT when associated with a ventricular response greater than 100 beats per minute. It is characterized as an "irregularly, irregular rhythm" both in its atrial and ventricular depolarizations and is distinguished by its fibrillatory atrial waves that, at some point in their chaos, stimulate a response from the ventricles in the form of irregular, narrow QRS complexes. Atrial flutter, is caused by a re entry rhythm in the atria, with a regular atrial rate often of about 300 beats per minute. On the ECG this appears as a line of "sawtooth" waves preceding the QRS complex. The AV node will not usually conduct 300 beats per minute so the P:QRS ratio is usually 2:1 or 4:1 pattern, (though rarely 3:1, and sometimes 1:1 where class IC antiarrhythmic drug are in use). Because the ratio of P to QRS is usually consistent, A flutter is often regular in comparison to its irregular counterpart, atrial fibrillation. Atrial flutter is also not necessarily a tachycardia by definition unless the AV node permits a ventricular response greater than 100 beats per minute. AV nodal reentrant tachycardia (AVNRT) involves a reentry circuit forming next to, or within, the AV node. The circuit most often involves two tiny pathways one faster than the other. Because the node is immediately between the atria and ventricle, the re entry circuit often stimulates both, appearing as a backward (retrograde) conducted P wave buried within or occurring just after the regular, narrow QRS complexes. Atrioventricular reciprocating tachycardia (AVRT), also results from a reentry circuit, although one physically much larger than AVNRT. One portion of the circuit is usually the AV node, and the other, an abnormal accessory pathway (muscular connection) from the atria to the ventricle. Wolff Parkinson White syndrome (WPW) is a relatively common abnormality with an accessory pathway, the bundle of Kent crossing the AV valvular ring. In orthodromic AVRT, atrial impulses are conducted down through the AV node and retrogradely re enter the atrium via the accessory pathway. A distinguishing characteristic of orthodromic AVRT can therefore be an inverted P wave (relative to a sinus P wave) that follows each of its regular, narrow QRS complexes, due to retrograde conduction. In antidromic AVRT, atrial impulses are conducted down through the accessory pathway and re enter the atrium retrogradely via the AV node. Because the accessory pathway initiates conduction in the ventricles outside of the bundle of His, the QRS complex in antidromic AVRT is wider than usual. A delta wave is an initial slurred deflection seen in the initial part of an otherwise narrow QRS of a patient at risk for WPW and is an indicator of the presence of an accessory pathway. These beats are a fusion between the conduction down the accessory pathway and the slightly delayed but then dominant conduction via the AV node. Once an antidromic AVRT tachycardia is initiated, it is no longer delta waves but rather a wide complex (>120 ms) tachycardia that is seen. Junctional ectopic tachycardia (JET) is a rare tachycardia caused by increased automaticity of the AV node itself initiating frequent heartbeats. On the ECG, junctional tachycardia often presents with abnormal morphology P waves that may fall anywhere in relation to a regular, narrow QRS complex. It is often due to drug toxicity.

Most SVTs are unpleasant rather than life threatening, although very fast heart rates can be problematic for those with underlying ischemic heart disease, or the elderly. Episodes can be treated when they occur by Valsalva maneuver, adenosine injection or taking a AV node blocking agent as pill in pocket, but regular medication may also be used to prevent or reduce recurrence. While some treatment modalities can be applied to all SVTs, there are specific therapies available to treat some sub types. Effective treatment consequently requires knowledge of how and where the arrhythmia is initiated and its mode of spread. Lifestyle changes, medication and heart procedures may be needed to control or eliminate the rapid heartbeats and related symptoms. Acute attacks of supraventricular tachycardia are treated with Esmolol (i. v.).