What is the pathophysiology of accelerated idioventricular rhythm (AIVR)?
In most cases, the mechanism of AIVR appears to be related to the enhanced automaticity in His-Purkinje fibers and/or myocardium, sometimes accompanied with vagal excess and decreased sympathetic activity. Ischemia, reperfusion, hypoxia, drugs, and electrolyte abnormalities can all accelerate the phase 4 action potential depolarization rates in His-Purkinje fiber and myocardium, leading to faster spontaneous cell depolarization (enhanced automaticity). When the enhanced automaticity in His-Purkinje fiber or myocardium surpasses that of sinus node, AIVR manifests as the dominant rhythm of the heart. Sinus bradycardia may facilitate the appearance of AIVR.
@papan Most AIVRs originate from a single focus. Occasionally, in patients with acute myocardial ischemia and myocarditis, AIVR can originate from multiple foci. The ventricular rate of AIVR is generally between 40 to 100-120 bpm. Usually, AIVR is hemodynamically well tolerated due to its slow ventricular rate. It is self-limited and resolves as sinus rate surpasses the rate of AIVR. Rarely, AIVR can degenerate into ventricular tachycardia or ventricular fibrillation. In patients with severe myocardial dysfunction, AIVR may lead to hemodynamic instability due to the loss of AV synchrony or relatively rapid ventricular rate.