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Re-entry ventricular arrhythmia is a type of paroxysmal tachycardia occurring in the ventricle where the cause of the arrhythmia is due to the electric signal not completing the normal circuit, but rather an alternative circuit looping back upon itself. [1] There develops a self-perpetuating rapid and abnormal activation.
AV-nodal reentrant tachycardia (AVNRT) is a type of abnormal fast heart rhythm. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia.
Atrioventricular reentrant tachycardia (AVRT), or atrioventricular reciprocating tachycardia, is a type of heart arrhythmia with an abnormally fast rhythm (tachycardia); it is classified as a type of supraventricular tachycardia (SVT).
Ventricular tachycardia (V-tach or VT) is a cardiovascular disorder in which fast heart rate occurs in the ventricles of the heart. [3] Although a few seconds of VT may not result in permanent problems, longer periods are dangerous; and multiple episodes over a short period of time are referred to as an electrical storm.
Atrioventricular nodal re-entry tachycardia, [11] which is caused by a dual AV node physiology and AVNRT can only occur in people with it, however almost half of the population have it, though only a few of them will develop AVNRT at some point in life.
Arrhythmia may be classified by rate (tachycardia, bradycardia), mechanism (automaticity, re-entry, triggered) or duration (isolated premature beats; couplets; runs, that is 3 or more beats; non-sustained = less than 30 seconds or sustained = over 30 seconds). [citation needed] Arrhythmias are also classified by site of origin: [citation needed]
Reentry can produce single ectopic beats, or it can trigger paroxysmal tachycardia. Triggered beats are considered to be due to after-depolarizations triggered by the preceding action potential. These are often seen in patients with ventricular arrhythmias due to digoxin toxicity and reperfusion therapy after myocardial infarction (MI).
Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry ventricular arrhythmia. [citation needed] Most myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of membrane potential.
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