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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.
The main symptom of AVNRT is the sudden development of rapid regular palpitations. [1] These palpitations may be associated with a fluttering sensation in the neck, caused by near-simultaneous contraction of the atria and ventricles against a closed tricuspid valve leading to the pressure or atrial contraction being transmitted backwards into the venous system. [2]
Re-entry is also responsible for most paroxysmal supraventricular tachycardia, and dangerous ventricular tachycardia. These types of re-entry circuits are different from WPW syndromes, which utilize abnormal conduction pathways. Although omega-3 fatty acids from fish oil can be protective against arrhythmias, they can facilitate re-entrant ...
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.
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.
The underlying mechanism typically involves an accessory pathway that results in re-entry. [3] 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. [3] Vagal maneuvers, such as the Valsalva maneuver, are often used as the initial treatment. [4]
(The re-entrant rhythm is less likely to interact with tissue that has become refractory). The class III agents exhibit reverse-use dependence (their potency increases with slower heart rates, and therefore improves maintenance of sinus rhythm). Inhibiting potassium channels results in slowed atrial-ventricular myocyte repolarization.
Cellular conduction and refractory periods are also modified to eliminate re-entry depolarization causing arrhythmia. Factors contributing to the generation of arrhythmia include: ischemia, hypoxia, acidosis and drug toxicity. If untreated, arrhythmias may present as bradycardia, tachycardia, or progress to atrial/ventricular fibrillation. [3]
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