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A 12-lead ECG showing paroxysmal supraventricular tachycardia at about 180 beats per minute. 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 ...
In-between episodes there is normal electrical conduction in the heart. During an episode of AVRT caused by PJRT, the accessory pathway conducts electrical activity from the ventricles directly back to the atria at the end of systole, which triggers the atria to contract, and the current to pass back to the ventricles again via the atrioventricular node (AV node); see diagram.
Mechanism of AVRT compared with other supraventricular arrhythmias. Two distinct pathways are involved: the normal atrioventricular conduction system, and an accessory pathway. During AVRT, the electrical signal passes in the normal manner from the AV node into the ventricles.
Atrial flutter was first identified as an independent medical condition in 1920 by the British physician Sir Thomas Lewis (1881–1945) and colleagues. [5] AFL is the second most common pathologic supraventricular tachycardia but occurs at a rate less than one-tenth of the most common supraventricular tachycardia (atrial fibrillation).
Paroxysmal supraventricular tachycardia (PSVT) is a type of supraventricular tachycardia, named for its intermittent episodes of abrupt onset and termination. [3] [6] Often people have no symptoms. [1] Otherwise symptoms may include palpitations, feeling lightheaded, sweating, shortness of breath, and chest pain. [2] The cause is not known. [3]
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.
LGL syndrome was originally thought to be due to an abnormal electrical connection between the atria and the ventricles, but is now thought to be due to accelerated conduction through the atrioventricular node in the majority of cases. [1] The syndrome is named after Bernard Lown, William Francis Ganong, Jr., and Samuel A. Levine. [2] [3]
The majority of time symptomatic WPW fits the definition of AVRT (Supraventricular tachycardia) however AVNRT (dual AV nodal physiology) exist in ~10% of patients with WPW syndrome creating the possibility of spontaneous atrial fibrillation degenerating into ventricular fibrillation (VF). The fact that WPW patients are young and do not have ...
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